Sidney C. Smith

A cluster of risk factors for cardiovascular disease and type 2 diabetes mellitus, which occur together more often than by chance alone, have become known as the metabolic syndrome. The risk factors include raised blood pressure, dyslipidemia (raised triglycerides and lowered high-density lipoprotein cholesterol), raised fasting glucose, and central obesity. Various diagnostic criteria have been proposed by different organizations over the past decade. Most recently, these have come from the International Diabetes Federation and the American Heart Association/National Heart, Lung, and Blood Institute. The main difference concerns the measure for central obesity, with this being an obligatory component in the International Diabetes Federation definition, lower than in the American Heart Association/National Heart, Lung, and Blood Institute criteria, and ethnic specific. The present article represents the outcome of a meeting between several major organizations in an attempt to unify criteria. It was agreed that there should not be an obligatory component, but that waist measurement would continue to be a useful preliminary screening tool. Three abnormal findings out of 5 would qualify a person for the metabolic syndrome. A single set of cut points would be used for all components except waist circumference, for which further work is required. In the interim, national or regional cut points for waist circumference can be used.

The metabolic syndrome has received increased attention in the past few years. This statement from the American Heart Association (AHA) and the National Heart, Lung, and Blood Institute (NHLBI) is intended to provide up-to-date guidance for professionals on the diagnosis and management of the metabolic syndrome in adults. The metabolic syndrome is a constellation of interrelated risk factors of metabolic origin— metabolic risk factors —that appear to directly promote the development of atherosclerotic cardiovascular disease (ASCVD).1 Patients with the metabolic syndrome also are at increased risk for developing type 2 diabetes mellitus. Another set of conditions, the underlying risk factors , give rise to the metabolic risk factors. In the past few years, several expert groups have attempted to set forth simple diagnostic criteria to be used in clinical practice to identify patients who manifest the multiple components of the metabolic syndrome. These criteria have varied somewhat in specific elements, but in general they include a combination of both underlying and metabolic risk factors. The most widely recognized of the metabolic risk factors are atherogenic dyslipidemia, elevated blood pressure, and elevated plasma glucose. Individuals with these characteristics commonly manifest a prothrombotic state and a pro-inflammatory state as well. Atherogenic dyslipidemia consists of an aggregation of lipoprotein abnormalities including elevated serum triglyceride and apolipoprotein B (apoB), increased small LDL particles, and a reduced level of HDL cholesterol (HDL-C). The metabolic syndrome is often referred to as if it were a discrete entity with a single cause. Available data suggest that it truly is a syndrome, ie, a grouping of ASCVD risk factors, but one that probably has more than one cause. Regardless of cause, the syndrome identifies individuals at an elevated risk for ASCVD. The magnitude of the increased risk can vary according to which components of the syndrome are …

Hypertension is the most common condition seen in primary care and leads to myocardial infarction, stroke, renal failure, and death if not detected early and treated appropriately. Patients want to be assured that blood pressure (BP) treatment will reduce their disease burden, while clinicians want guidance on hypertension management using the best scientific evidence. This report takes a rigorous, evidence-based approach to recommend treatment thresholds, goals, and medications in the management of hypertension in adults. Evidence was drawn from randomized controlled trials, which represent the gold standard for determining efficacy and effectiveness. Evidence quality and recommendations were graded based on their effect on important outcomes. There is strong evidence to support treating hypertensive persons aged 60 years or older to a BP goal of less than 150/90 mm Hg and hypertensive persons 30 through 59 years of age to a diastolic goal of less than 90 mm Hg; however, there is insufficient evidence in hypertensive persons younger than 60 years for a systolic goal, or in those younger than 30 years for a diastolic goal, so the panel recommends a BP of less than 140/90 mm Hg for those groups based on expert opinion. The same thresholds and goals are recommended for hypertensive adults with diabetes or nondiabetic chronic kidney disease (CKD) as for the general hypertensive population younger than 60 years. There is moderate evidence to support initiating drug treatment with an angiotensin-converting enzyme inhibitor, angiotensin receptor blocker, calcium channel blocker, or thiazide-type diuretic in the nonblack hypertensive population, including those with diabetes. In the black hypertensive population, including those with diabetes, a calcium channel blocker or thiazide-type diuretic is recommended as initial therapy. There is moderate evidence to support initial or add-on antihypertensive therapy with an angiotensin-converting enzyme inhibitor or angiotensin receptor blocker in persons with CKD to improve kidney outcomes. Although this guideline provides evidence-based recommendations for the management of high BP and should meet the clinical needs of most patients, these recommendations are not a substitute for clinical judgment, and decisions about care must carefully consider and incorporate the clinical characteristics and circumstances of each individual patient.

The Adult Treatment Panel III (ATP III) of the National Cholesterol Education Program issued an evidence-based set of guidelines on cholesterol management in 2001. Since the publication of ATP III, 5 major clinical trials of statin therapy with clinical end points have been published. These trials addressed issues that were not examined in previous clinical trials of cholesterol-lowering therapy. The present document reviews the results of these recent trials and assesses their implications for cholesterol management. Therapeutic lifestyle changes (TLC) remain an essential modality in clinical management. The trials confirm the benefit of cholesterol-lowering therapy in high-risk patients and support the ATP III treatment goal of low-density lipoprotein cholesterol (LDL-C) <100 mg/dL. They support the inclusion of patients with diabetes in the high-risk category and confirm the benefits of LDL-lowering therapy in these patients. They further confirm that older persons benefit from therapeutic lowering of LDL-C. The major recommendations for modifications to footnote the ATP III treatment algorithm are the following. In high-risk persons, the recommended LDL-C goal is <100 mg/dL, but when risk is very high, an LDL-C goal of <70 mg/dL is a therapeutic option, ie, a reasonable clinical strategy, on the basis of available clinical trial evidence. This therapeutic option extends also to patients at very high risk who have a baseline LDL-C <100 mg/dL. Moreover, when a high-risk patient has high triglycerides or low high-density lipoprotein cholesterol (HDL-C), consideration can be given to combining a fibrate or nicotinic acid with an LDL-lowering drug. For moderately high-risk persons (2+ risk factors and 10-year risk 10% to 20%), the recommended LDL-C goal is <130 mg/dL, but an LDL-C goal <100 mg/dL is a therapeutic option on the basis of recent trial evidence. The latter option extends also to moderately high-risk persons with a baseline LDL-C of 100 to 129 mg/dL. When LDL-lowering drug therapy is employed in high-risk or moderately high-risk persons, it is advised that intensity of therapy be sufficient to achieve at least a 30% to 40% reduction in LDL-C levels. Moreover, any person at high risk or moderately high risk who has lifestyle-related risk factors (eg, obesity, physical inactivity, elevated triglycerides, low HDL-C, or metabolic syndrome) is a candidate for TLC to modify these risk factors regardless of LDL-C level. Finally, for people in lower-risk categories, recent clinical trials do not modify the goals and cutpoints of therapy.

In 1998, the American Heart Association convened Prevention Conference V to examine strategies for the identification of high-risk patients who need primary prevention. Among the strategies discussed was the measurement of markers of inflammation.1 The Conference concluded that “many of these markers (including inflammatory markers) are not yet considered applicable for routine risk assessment because of: (1) lack of measurement standardization, (2) lack of consistency in epidemiological findings from prospective studies with endpoints, and (3) lack of evidence that the novel marker adds to risk prediction over and above that already achievable through the use of established risk factors.” The National Cholesterol Education Program Adult Treatment Panel III Guidelines identified these markers as emerging risk factors,1a which could be used as an optional risk factor measurement to adjust estimates of absolute risk obtained using standard risk factors. Since these publications, a large number of peer-reviewed scientific reports have been published relating inflammatory markers to cardiovascular disease (CVD). Several commercial assays for inflammatory markers have become available. As a consequence of the expanding research base and availability of assays, the number of inflammatory marker tests ordered by clinicians for CVD risk prediction has grown rapidly. Despite this, there has been no consensus from professional societies or governmental agencies as to how these assays of markers of inflammation should be used in clinical practice. On March 14 and 15, 2002, a workshop titled “CDC/AHA Workshop on Inflammatory Markers and Cardiovascular Disease: Applications to Clinical and Public Health Practice” was convened in Atlanta, Ga, to address these issues. The goals of this workshop were to determine which of the currently available tests should be used; what results should be used to define high risk; which patients should be tested; and the indications for which the tests would be most useful. These …

In 2004, the first American Heart Association scientific statement on "Air Pollution and Cardiovascular Disease" concluded that exposure to particulate matter (PM) air pollution contributes to cardiovascular morbidity and mortality. In the interim, numerous studies have expanded our understanding of this association and further elucidated the physiological and molecular mechanisms involved. The main objective of this updated American Heart Association scientific statement is to provide a comprehensive review of the new evidence linking PM exposure with cardiovascular disease, with a specific focus on highlighting the clinical implications for researchers and healthcare providers. The writing group also sought to provide expert consensus opinions on many aspects of the current state of science and updated suggestions for areas of future research. On the basis of the findings of this review, several new conclusions were reached, including the following: Exposure to PM <2.5 microm in diameter (PM(2.5)) over a few hours to weeks can trigger cardiovascular disease-related mortality and nonfatal events; longer-term exposure (eg, a few years) increases the risk for cardiovascular mortality to an even greater extent than exposures over a few days and reduces life expectancy within more highly exposed segments of the population by several months to a few years; reductions in PM levels are associated with decreases in cardiovascular mortality within a time frame as short as a few years; and many credible pathological mechanisms have been elucidated that lend biological plausibility to these findings. It is the opinion of the writing group that the overall evidence is consistent with a causal relationship between PM(2.5) exposure and cardiovascular morbidity and mortality. This body of evidence has grown and been strengthened substantially since the first American Heart Association scientific statement was published. Finally, PM(2.5) exposure is deemed a modifiable factor that contributes to cardiovascular morbidity and mortality.

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HomeCirculationVol. 129, No. 25_suppl_22013 ACC/AHA Guideline on the Treatment of Blood Cholesterol to Reduce Atherosclerotic Cardiovascular Risk in Adults Open AccessResearch ArticlePDF/EPUBAboutView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissionsDownload Articles + Supplements ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toSupplemental MaterialOpen AccessResearch ArticlePDF/EPUB2013 ACC/AHA Guideline on the Treatment of Blood Cholesterol to Reduce Atherosclerotic Cardiovascular Risk in AdultsA Report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines Neil J. Stone, MD, MACP, FAHA, FACC, Jennifer G. Robinson, MD, MPH, FAHA, Alice H. Lichtenstein, DSc, FAHA, C. Noel Bairey Merz, MD, FAHA, FACC, Conrad B. Blum, MD, FAHA, Robert H. Eckel, MD, FAHA, Anne C. Goldberg, MD, FACP, FAHA, David Gordon, MD, Daniel Levy, MD, Donald M. Lloyd-Jones, MD, SCM, FACC, FAHA, Patrick McBride, MD, MPH, FAHA, J. Sanford Schwartz, MD, Susan T. Shero, MS, RN, Sidney C. SmithJr, MD, FACC, FAHA, Karol Watson, MD, PhD, FACC, FAHA and Peter W. F. Wilson, MD, FAHA Neil J. StoneNeil J. Stone Search for more papers by this author , Jennifer G. RobinsonJennifer G. Robinson Search for more papers by this author , Alice H. LichtensteinAlice H. Lichtenstein Search for more papers by this author , C. Noel Bairey MerzC. Noel Bairey Merz Search for more papers by this author , Conrad B. BlumConrad B. Blum Search for more papers by this author , Robert H. EckelRobert H. Eckel Search for more papers by this author , Anne C. GoldbergAnne C. Goldberg Search for more papers by this author , David GordonDavid Gordon Search for more papers by this author , Daniel LevyDaniel Levy *Ex-Officio Members. Search for more papers by this author , Donald M. Lloyd-JonesDonald M. Lloyd-Jones Search for more papers by this author , Patrick McBridePatrick McBride Search for more papers by this author , J. Sanford SchwartzJ. Sanford Schwartz Search for more papers by this author , Susan T. SheroSusan T. Shero *Ex-Officio Members. Search for more papers by this author , Sidney C. SmithJrSidney C. SmithJr Search for more papers by this author , Karol WatsonKarol Watson Search for more papers by this author and Peter W. F. WilsonPeter W. F. Wilson Search for more papers by this author Originally published12 Nov 2013https://doi.org/10.1161/01.cir.0000437738.63853.7aCirculation. 2014;129:S1–S45is corrected byCorrectionCorrectionOther version(s) of this articleYou are viewing the most recent version of this article. Previous versions: January 1, 2013: Previous Version 1 Table of ContentsPreamble and Transition to ACC/AHA Guidelines to Reduce Cardiovascular Risk S21. Introduction S31.1 Organization of the Panel S31.2 Document Review and Approval S31.3 Scope of Guideline S31.4 Methodology and Evidence Review S52. Overview of the Guideline S62.1. Lifestyle as the Foundation for ASCVD Risk-Reduction Efforts S62.2. Initiation of Statin Therapy S73. Critical Questions and Conclusions S103.1. Identification of CQs S103.1.1. CQ1: LDL-C and Non–HDL-C Goals in Secondary Prevention S103.1.2. CQ2: LDL-C and Non–HDL-C Goals in Primary Prevention S103.1.3. CQ3: Efficacy and Safety of Cholesterol-Lowering Medications S104. Statin Treatment: Recommendations S104.1. Intensity of Statin Therapy in Primary and Secondary Prevention S124.2. LDL-C and Non–HDL-C Treatment Goals S124.3. Secondary Prevention S134.4. Primary Prevention in Individuals ≥21 Years of Age With LDL-C ≥190 mg/dL S144.5. Primary Prevention in Individuals With Diabetes S164.6. Primary Prevention in Individuals Without Diabetes and With LDL-C 70 to 189 mg/dL S164.7. Risk Assessment in Primary Prevention S174.8. Heart Failure and Hemodialysis S175. Safety: Recommendations S186. Managing Statin Therapy: Recommendations S216.1. Monitoring Statin Therapy S216.2. Optimizing Statin Therapy S216.3. Insufficient Response to Statin Therapy S216.3.1 Testing S216.3.2 Nonstatins Added to Statins or in Statin-Intolerant Individuals S227. Selected Clinical and Population Subgroups S237.1. Sex and Racial and Ethnic Subgroups S237.2. Individuals >75 Years of Age S238. Limitations S249. Evidence Gaps and Future Research Needs S2410. Conclusions S24References S25Appendix 1. Author Relationships With Industry and Other Entities (Relevant) S28Appendix 2. Expert Reviewer Relationships With Industry and Other Entities S32Appendix 3. Abbreviations S33Appendix 4. Evidence Statements S33Appendix 5. Expanded Discussion of What’s New in the Guideline S43Preamble and Transition to ACC/AHA Guidelines to Reduce Cardiovascular RiskThe goals of the American College of Cardiology (ACC) and the American Heart Association (AHA) are to prevent cardiovascular diseases; improve the management of people who have these diseases through professional education and research; and develop guidelines, standards, and policies that promote optimal patient care and cardiovascular health. Toward these objectives, the ACC and AHA have collaborated with the National Heart, Lung, and Blood Institute (NHLBI) and stakeholder and professional organizations to develop clinical practice guidelines for assessment of cardiovascular risk, lifestyle modifications to reduce cardiovascular risk, management of blood cholesterol in adults, and management of overweight and obesity in adults.In 2008, the NHLBI initiated these guidelines by sponsoring rigorous systematic evidence reviews for each topic by expert panels convened to develop critical questions (CQs), interpret the evidence, and craft recommendations. In response to the 2011 report from the Institute of Medicine on the development of trustworthy clinical guidelines,1 the NHLBI Advisory Council recommended that the NHLBI focus specifically on reviewing the highest-quality evidence and partner with other organizations to develop recommendations.2,3 Accordingly, in June 2013 the NHLBI initiated collaboration with the ACC and AHA to work with other organizations to complete and publish the 4 guidelines noted above and make them available to the widest possible constituency. Recognizing that the Expert Panels/Work Groups did not consider evidence beyond 2011 (except as specified in the methodology), the ACC, AHA, and collaborating societies plan to begin updating these guidelines starting in 2014.The joint ACC/AHA Task Force on Practice Guidelines (Task Force) appointed a subcommittee to shepherd this transition, communicate the rationale and expectations to the writing panels and partnering organizations, and expeditiously publish the documents. The ACC/AHA and partner organizations recruited a limited number of expert reviewers for fiduciary examination of content, recognizing that each document had undergone extensive peer review by representatives of the NHLBI Advisory Council, key federal agencies, and scientific experts. Each writing panel responded to comments from these reviewers. Clarifications were incorporated where appropriate, but there were no substantive changes because the bulk of the content was undisputed.Although the Task Force led the final development of these prevention guidelines, they differ from other ACC/AHA guidelines. First, as opposed to an extensive compendium of clinical information, these documents are significantly more limited in scope and focus on selected CQs on each topic, based on the highest-quality evidence available. Recommendations were derived from randomized trials, meta-analyses, and observational studies evaluated for quality and were not formulated when sufficient evidence was not available. Second, the text accompanying each recommendation is succinct, summarizing the evidence for each question. The Full Panel/Work Group Reports include more detailed information about the evidence statements that serve as the basis for recommendations. Third, the format of the recommendations differs from other ACC/AHA guidelines. Each recommendation has been mapped from the NHLBI grading format to the ACC/AHA Classification of Recommendation/Level of Evidence (COR/LOE) construct (Table 1) and is expressed in both formats. Because of the inherent differences in grading systems and the clinical questions driving the recommendations, alignment between the NHLBI and ACC/AHA formats is in some cases imperfect. Explanations of these variations are noted in the recommendation tables, where applicable.Table 1. Applying Classification of Recommendation and Level of EvidenceTable 1. Applying Classification of Recommendation and Level of EvidenceIn consultation with NHLBI, the policies adopted by the writing panels to manage relationships of authors with industry and other entities (RWI) are outlined in the methods section of each panel report. These policies were in effect when this effort began in 2008 and throughout the writing process and voting on recommendations, until the process was transferred to ACC/AHA in 2013. In the interest of transparency, the ACC/AHA requested that panel authors resubmit RWI disclosures as of July 2013. Relationships relevant to this guideline are disclosed in Appendix 1. None of the ACC/AHA expert reviewers had relevant RWI (Appendix 2). See Appendix 3 for a list of abbreviations used in the guideline.Systematic evidence reports and accompanying summary tables were developed by the expert panels and NHLBI. The guideline was reviewed by the ACC/AHA Task Force and approved by the ACC Board of Trustees, and the AHA Science Advisory and Coordinating Committee. In addition, ACC/AHA sought endorsement from other stakeholders, including professional organizations. It is the hope of the writing panels, stakeholders, professional organizations, NHLBI, and Task Force that the guidelines will garner the widest possible readership for the benefit of patients, providers, and the public health.These guidelines are meant to define practices that meet the needs of patients in most circumstances and are not a replacement for clinical judgment. The ultimate decision about care of a particular patient must be made by the healthcare provider and patient in light of the circumstances presented by that patient. As a result, situations might arise in which deviations from these guidelines may be appropriate. These considerations notwithstanding, in caring for most patients, clinicians can employ the recommendations confidently to reduce the risks of atherosclerotic cardiovascular disease (ASCVD) events.See Tables 1a and 1b for an explanation of the NHLBI recommendation grading methodology.Table 1a. NHLBI Grading of the Strength of RecommendationsGradeStrength of Recommendation*AStrong recommendationThere is high certainty based on evidence that the net benefit‡ is substantial.BModerate recommendationThere is moderate certainty based on evidence that the net benefit is moderate to substantial, or there is high certainty that the net benefit is moderate.CWeak recommendationThere is at least moderate certainty based on evidence that there is a small net benefit.DRecommendation againstThere is at least moderate certainty based on evidence that there is no net benefit or that risks/harms outweigh benefits.EExpert opinion (“There is insufficient evidence or evidence is unclear or conflicting, but this is what the Work Group recommends.”)Net benefit is unclear. Balance of benefits and harms cannot be determined because of no evidence, insufficient evidence, unclear evidence, or conflicting evidence, but the Work Group thought it was important to provide clinical guidance and make a recommendation. Further research is recommended in this area.NNo recommendation for or against (“There is insufficient evidence or evidence is unclear or conflicting.”)Net benefit is unclear. Balance of benefits and harms cannot be determined because of no evidence, insufficient evidence, unclear evidence, or conflicting evidence, and the Work Group thought no recommendation should be made. Further research is recommended in this area.*In most cases, the strength of the recommendation should be closely aligned with the quality of the evidence; however, under some circumstances, there may be valid reasons for making recommendations that are not closely aligned with the quality of the evidence (eg, strong recommendation when the evidence quality is moderate, such as smoking cessation to reduce cardiovascular disease risk or ordering an ECG as part of the initial diagnostic work-up for a patient presenting with possible MI). Those situations should be limited and the rationale explained clearly by the Work Group.†Net benefit is defined as benefits minus risks/harms of the service/intervention.ECG indicates electrocardiogram; MI, myocardial infarction; and NHLBI, National Heart, Lung, and Blood Institute.Table 1b. NHLBI Quality Rating of the Strength of EvidenceType of EvidenceQuality Rating*Well-designed, well-executed‡ RCT that adequately represent populations to which the results are applied and directly assess effects on health outcomes.Meta-analyses of such studies.Highly certain about the estimate of effect. Further research is unlikely to change our confidence in the estimate of effect.>HighRCT with minor limitations‡ affecting confidence in, or applicability of, the results.Well-designed, well-executed nonrandomized controlled studies§ and well-designed, well-executed observational studies‖.Meta-analyses of such studies.Moderately certain about the estimate of effect. Further research may have an impact on our confidence in the estimate of effect and may change the estimate.>ModerateRCT with major limitations.Nonrandomized controlled studies and observational studies with major limitations affecting confidence in, or applicability of, the results.Uncontrolled clinical observations without an appropriate comparison group (eg, case series, case reports).Physiological studies in humans.Meta-analyses of such studies.Low certainty about the estimate of effect. Further research is likely to have an impact on our confidence in the estimate of effect and is likely to change the estimate.Low*In some cases, other evidence, such as large all-or-none case series (eg, jumping from airplanes or tall structures), can represent high- or moderate-quality evidence. In such cases, the rationale for the evidence rating exception should be explained by the Work Group and clearly justified.†“Well-designed, well-executed” refers to studies that directly address the question; use adequate randomization, blinding, and allocation concealment; are adequately powered; use intention-to-treat analyses; and have high follow-up rates.‡Limitations include concerns with the design and execution of a study that result in decreased confidence in the true estimate of the effect. Examples of such limitations include but are not limited to: inadequate randomization, lack of blinding of study participants or outcome assessors, inadequate power, outcomes of interest that are not prespecified for the primary outcomes, low follow-up rates, and findings based on subgroup analyses. Whether the limitations are considered minor or major is based on the number and severity of flaws in design or execution. Rules for determining whether the limitations are considered minor or major and how they will affect rating of the individual studies will be developed collaboratively with the methodology team.§Nonrandomized controlled studies refer to intervention studies where assignment to intervention and comparison groups is not random (eg, quasi-experimental study design).‖Observational studies include prospective and retrospective cohort, case-control, and cross-sectional studies.NHLBI indicates National Heart, Lung, and Blood Institute; and RCT, randomized controlled trials.1. Introduction1.1. Organization of the PanelThe Blood Cholesterol Expert Panel (Expert Panel) was originally convened as the Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults (Adult Treatment Panel IV) appointed by the NHLBI. The Expert Panel was composed of 13 members and 3 ex-officio members, which included primary care physicians, cardiologists, endocrinologists, and experts in clinical lipidology, clinical trials, cardiovascular epidemiology and nutrition, and guideline development. The Expert Panel chair asked all panel members to disclose any conflict-of-interest information to the full panel in advance of the deliberations; members with conflicts were asked to recuse themselves from voting on any aspect of the guideline for which a conflict might exist. All 16 members of the NHLBI Adult Treatment Panel IV Panel transitioned to the ACC/AHA guideline Expert Panel. Independent contractors performed the systematic review with the assistance of the Expert Panel and provided methodological guidance to the Expert Panel.1.2. Document Review and ApprovalA formal peer review process was initially completed under the auspices of the NHLBI and included 23 expert reviewers and representatives of federal agencies. This document was also reviewed by 4 expert reviewers nominated by the ACC and the AHA when the management of the guideline transitioned to the ACC/AHA. The ACC and AHA reviewers’ RWI information is published in this document (Appendix 2).This document was approved for publication by the governing bodies of the ACC and AHA and endorsed by the American Academy of Physician Assistants, American Association of Cardiovascular and Pulmonary Rehabilitation, American Pharmacists Association, American Society for Preventive Cardiology, Association of Black Cardiologists, Preventive Cardiovascular Nurses Association, and WomenHeart: The National Coalition for Women with Heart Disease.1.3. Scope of GuidelineThis guideline is based on the Full Panel Report, which is provided as an online-only data supplement to the guideline. The Full Panel Report contains background and additional material related to content, methodology, evidence synthesis, rationale, and references and is supported by the NHLBI Systematic Evidence Review, which can be found at http://www.nhlbi.nih.gov/guidelines/cholesterol/ser/. Table 2 provides an overview to facilitate understanding what is new in the present guideline.Table 2. What’s New in the Guideline?*Focus on ASCVD Risk Reduction: 4 Statin Benefit GroupsThis guideline is based on a comprehensive set of data from RCTs from which 4 statin benefit groups were identified that focus efforts to reduce ASCVD events in secondary and primary prevention.This guideline identifies high-intensity and moderate-intensity statin therapy for use in secondary and primary prevention.A New Perspective on LDL-C and/or Non–HDL-C Treatment GoalsThe Expert Panel was unable to find RCT evidence to support continued use of specific LDL-C or non–HDL-C treatment targets.The appropriate intensity of statin therapy should be used to reduce ASCVD risk in those most likely to benefit.Nonstatin therapies, as compared with statin therapy, do not provide acceptable ASCVD risk-reduction benefits relative to their potential for adverse effects in the routine prevention of ASCVD.Global Risk Assessment for Primary PreventionThis guideline recommends use of the new Pooled Cohort Equations to estimate 10-year ASCVD risk in both white and black men and women.By more accurately identifying higher-risk individuals for statin therapy, the guideline focuses statin therapy on those most likely to benefit.It also indicates, on the basis of RCT data, those high-risk groups that might not benefit.This guideline recommends a discussion between clinicians and patients before initiation of statin therapy.Safety RecommendationsThis guideline used RCTs to identify important safety considerations in individuals receiving treatment of blood cholesterol to reduce ASCVD risk.Using RCTs to determine statin adverse effects facilitates understanding of the net benefit from statin therapy.This guideline provides expert guidance on management of statin-associated adverse effects, including muscle symptoms.Role of Biomarkers and Noninvasive TestsTreatment decisions in selected individuals who are not included in the 4 statin benefit groups may be informed by other factors as recommended by the Risk Assessment Work Group and Blood Cholesterol Expert Panel.Future Updates to the Blood Cholesterol GuidelineThis is a comprehensive guideline for the evidence-based treatment of blood cholesterol to reduce ASCVD risk.Future updates will build on this foundation to provide expert guidance on the management of complex lipid disorders and incorporate refinements in risk stratification based on critical review of emerging data.RCTs comparing alternative treatment strategies are needed in order to inform future evidence-based guidelines for the optimum ASCVD risk-reduction approach.*See Appendix 5, for an expanded discussion of what’s new in the guideline.ASCVD indicates atherosclerotic cardiovascular disease; HDL-C, high-density lipoprotein cholesterol; LDL-C, low-density lipoprotein cholesterol; and RCT, randomized controlled trial.The Expert Panel was charged with using data from randomized controlled trials (RCTs) and systematic reviews and meta-analyses of RCTs to update the clinical practice recommendations for the treatment of blood cholesterol levels to reduce ASCVD risk. For this guideline, ASCVD includes coronary heart disease (CHD), stroke, and peripheral arterial disease, all of presumed atherosclerotic origin. These recommendations are intended to provide a strong, evidence-based foundation for the treatment of cholesterol for the primary and secondary prevention of ASCVD in women and men.Because RCT data were used to identify those most likely to benefit from cholesterol-lowering statin therapy, the recommendations will be of value to primary care clinicians as well as specialists concerned with ASCVD prevention. Importantly, the recommendations were designed to be easy to use in the clinical setting, facilitating the implementation of a strategy of risk assessment and treatment focused on the prevention of ASCVD. The present guideline is intended to address treatment of adults (≥21 years of age) to complement the NHLBI cardiovascular health risk-reduction guideline for children and adolescents.4The members of the Expert Panel acknowledge the important contributions arising from decades of genetic and biochemical studies, observational epidemiological and ecological studies, and in vitro and animal experiments that associated higher low-density lipoprotein cholesterol (LDL-C) levels with greater ASCVD risk. These studies provided the rationale for RCTs, which in turn demonstrated that lowering cholesterol levels reduced ASCVD events and thereby established a central, causal role of atherogenic cholesterol-containing lipoprotein particles, particularly LDL, in the genesis of CHD and ASCVD.Other strategies for using drug therapy to reduce ASCVD events have been advocated, including treat-to-cholesterol target, lowest-is-best, and risk-based treatment approaches. However, only 1 approach has been evaluated in multiple RCTs—the use of fixed doses of cholesterol-lowering drugs to reduce ASCVD risk. Because the overwhelming body of evidence came from statin RCTs, the Expert Panel appropriately focused on these statin RCTs to develop evidence-based guidelines for the reduction of ASCVD risk. We recognize that this represents a significant departure from current strategies. This should not come as a surprise to clinicians. The recent guideline on heart failure has changed long-standing paradigms on the basis of the evidence, and this guideline does as well.5 Future RCTs will be needed to determine the optimal treatment strategy to provide the greatest reduction in ASCVD events with best margin of safety.The Expert Panel acknowledges that our process did not provide for a comprehensive approach to the detection, evaluation, and treatment of lipid disorders as was done in the prior Adult Treatment Panel III Report.6 However, the present guideline was never intended to be a comprehensive approach to lipid management for purposes other than ASCVD risk reduction. A limited number of expert opinion recommendations were made only when RCT evidence was not present and after a thorough consideration of what the Expert Panel had learned from the RCTs. For the many questions about complex lipid disorders that are beyond the scope of our systematic evidence review, or for which little or no RCT data are available, it is anticipated that clinicians with lipid expertise can contribute to their management.1.4. Methodology and Evidence ReviewAlthough the Expert Panel was convened before the Institute of Medicine reports on practice guidelines, our evidence-based process followed most of the standards from the Institute of Medicine report, “Clinical Practice Guidelines We Can Trust.”1 The systematic review was limited to RCTs with ASCVD outcomes and systematic reviews and meta-analyses of RCTs with ASCVD outcomes. Observational studies and those with <18 months (CQ1 and CQ2) or <12 months (CQ3) of follow-up were excluded. Support was provided by a methodology contractor and a systematic review and general support contractor and included the following steps:The Expert Panel constructed CQs relevant to clinical practice.The Expert Panel identified (a priori) inclusion/exclusion criteria for each CQ.An independent contractor developed a literature search strategy, based on inclusion/exclusion criteria, for each CQ.An independent contractor executed a systematic electronic search of the published literature from relevant bibliographic databases for each CQ. The date range for the overall literature search was January 1, 1995, through December 1, 2009. However, RCTs with hard ASCVD outcomes of myocardial infarction (MI), stroke, and cardiovascular death published after that date range were eligible for consideration until the Expert Panel began deliberations on relevant recommendations.RCTs that met the inclusion criteria and were independently graded as fair or good quality were included in the evidence tables for the consideration of the Expert Panel. RCTs that were graded as poor quality were excluded.With the assistance of independent methodologists, this evidence base was used to develop a series of evidence statements graded on the level of the evidence (high, medium, or low).The Expert Panel then synthesized the evidence statements into treatment recommendations/summaries graded as A (strong), B (moderate), C (weak), D (recommend against), E (expert), and N (no recommendation).The final evidence statements and treatment recommendations were approved by at least a majority of voting members of the Expert Panel.Guideline implementability appraisals, planned and coordinated by the NHLBI Implementation Work Group, were performed to identify and address barriers to guideline implementation.In addition, the Expert Panel was able to include major RCTs and meta-analyses of RCTs published through July 2013 in our discussion and as part of the process of determining ACC/AHA grading of the NHLBI expert-level recommendations.2. Overview of the GuidelineThe RCTs identified in the systematic evidence review indicated a consistent reduction in ASCVD events from 3-hydroxy-3-methylglutaryl-coenzyme A reductase inhibitor (statin) therapy in secondary- and primary-prevention populations, with the exception of no ASCVD event reduction when statin therapy was initiated in those with New York Heart Association class II to IV heart failure or those receiving maintenance hemodialysis. The RCTs either compared fixed doses of statins with placebo or untreated controls, or compared fixed doses of higher-intensity statins with moderate-intensity statins. These trials were not designed to evaluate the effect of titrated (dose-adjusted) statin treatment to achieve prespecified LDL-C or non–HDL-C goals.Therefore, the Expert Panel was unable to find RCT evidence to support titrating cholesterol-lowering drug therapy to achieve target LDL-C or non–HDL-C levels, as recommended by Adult Treatment Panel III.6–8 Notably, the Expert Panel did find RCT evidence that use of therapy (eg, niacin) to additionally lower non–HDL-C, once an LDL-C target was achieved, did not further reduce ASCVD outcomes.9 The Expert Panel also found extensive RCT evidence that the appropriate intensity of statin therapy should be used to reduce ASCVD risk in those most likely to benefit. The work of the Expert Panel was informed by the reports of the Lifestyle Management10 and Risk Assessment Work Groups11 (Figure 1). A summary of the major recommendations for the treatment of cholesterol to reduce ASCVD risk are provided in Table 3.Table 3. Summary of Key Recommendations for the Treatment of Blood Cholesterol to Reduce ASCVD Risk in Adults (See Tables 4, 8, 9, and 10 for the complete recommendations; and Table 5 for definition of statin intensity)Table 3. Summary of Key Recommendations for the Treatment of Blood Cholesterol to Reduce ASCVD Risk in Adults (See Tables 4, 8, 9, and 10 for the complete recommendations; and Table 5 for definition of statin intensity)Table 4. Recommendations for Treatment of Blood Cholesterol to Reduce Atherosclerotic Cardiovascular Risk in Adults—Statin Treatment (High, Moderate, and Low Statin Intensities are Defined in Table 5)Table 4. Recommendations for Treatment of Blood Cholesterol to Reduce Atherosclerotic Cardiovascular Risk in Adults—Statin Treatment (High, Moderate, and Low Statin Intensities are Defined in Table 5)Table 5. High-, Moderate-, and Low-Intensity Statin Therapy (Used in the RCTs Reviewed by the Expert Panel)*High-Intensity Statin TherapyModerate-Intensity Statin TherapyLow-Intensity Statin TherapyDaily dose lowers LDL-C, on average, by approximately ≥50%

Glenn N. Levine, MD, FACC, FAHA, Chair Patrick T. O’Gara, MD, MACC, FAHA, Chair-Elect Jonathan L. Halperin, MD, FACC, FAHA, Immediate Past Chair Sana M. Al-Khatib, MD, MHS, FACC, FAHA Joshua A. Beckman, MD, MS, FAHA Kim K. Birtcher, MS, PharmD, AACC Biykem Bozkurt, MD, PhD, FACC, FAHA

Harmon S. Jordan, ScD, Lev Nevo, MD, Janusz Wnek, PhD Jeffrey L. Anderson, MD, FACC, FAHA, Chair , Jonathan L. Halperin, MD, FACC, FAHA, Chair-Elect , Nancy M. Albert, PhD, CCNS, CCRN, FAHA, Biykem Bozkurt, MD, PhD, FACC, FAHA, Ralph G. Brindis, MD, MPH, MACC, Lesley H. Curtis, PhD, FAHA, David

Kristian Thygesen∗ (Denmark) Joseph S. Alpert∗ (USA) Allan S. Jaffe (USA) Bernard R. Chaitman (USA) Jeroen J. Bax (The Netherlands) David A. Morrow (USA) Harvey D. White∗ (New Zealand) Hans Mickley (Denmark) Filippo Crea (Italy) Frans Van de Werf (Belgium) Chiara Bucciarelli-Ducci (

HomeCirculationVol. 139, No. 252018 AHA/ACC/AACVPR/AAPA/ABC/ACPM/ADA/AGS/APhA/ASPC/NLA/PCNA Guideline on the Management of Blood Cholesterol: A Report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines Free AccessReview ArticlePDF/EPUBAboutView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissionsDownload Articles + Supplements ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toSupplemental MaterialFree AccessReview ArticlePDF/EPUB2018 AHA/ACC/AACVPR/AAPA/ABC/ACPM/ADA/AGS/APhA/ASPC/NLA/PCNA Guideline on the Management of Blood Cholesterol: A Report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines Scott M. Grundy, MD, PhD, FAHA, Chair, Neil J. Stone, MD, FACC, FAHA, Vice Chair, Alison L. Bailey, MD, FACC, FAACVPR, Craig Beam, CRE, Kim K. Birtcher, MS, PharmD, AACC, FNLA, Roger S. Blumenthal, MD, FACC, FAHA, FNLA, Lynne T. Braun, PhD, CNP, FAHA, FPCNA, FNLA, Sarah de Ferranti, MD, MPH, Joseph Faiella-Tommasino, PhD, PA-C, Daniel E. Forman, MD, FAHA, Ronald Goldberg, MD, Paul A. Heidenreich, MD, MS, FACC, FAHA, Mark A. Hlatky, MD, FACC, FAHA, Daniel W. Jones, MD, FAHA, Donald Lloyd-Jones, MD, SCM, FACC, FAHA, Nuria Lopez-Pajares, MD, MPH, Chiadi E. Ndumele, MD, PhD, FAHA, Carl E. Orringer, MD, FACC, FNLA, Carmen A. Peralta, MD, MAS, Joseph J. Saseen, PharmD, FNLA, FAHA, Sidney C. Smith Jr, MD, MACC, FAHA, Laurence Sperling, MD, FACC, FAHA, FASPC, Salim S. Virani, MD, PhD, FACC, FAHA and Joseph Yeboah, MD, MS, FACC, FAHA Scott M. GrundyScott M. Grundy Search for more papers by this author , Neil J. StoneNeil J. Stone Search for more papers by this author , Alison L. BaileyAlison L. Bailey Search for more papers by this author , Craig BeamCraig Beam Search for more papers by this author , Kim K. BirtcherKim K. Birtcher Search for more papers by this author , Roger S. BlumenthalRoger S. Blumenthal Search for more papers by this author , Lynne T. BraunLynne T. Braun Search for more papers by this author , Sarah de FerrantiSarah de Ferranti Search for more papers by this author , Joseph Faiella-TommasinoJoseph Faiella-Tommasino Search for more papers by this author , Daniel E. FormanDaniel E. Forman Search for more papers by this author , Ronald GoldbergRonald Goldberg Search for more papers by this author , Paul A. HeidenreichPaul A. Heidenreich Search for more papers by this author , Mark A. HlatkyMark A. Hlatky Search for more papers by this author , Daniel W. JonesDaniel W. Jones Search for more papers by this author , Donald Lloyd-JonesDonald Lloyd-Jones Search for more papers by this author , Nuria Lopez-PajaresNuria Lopez-Pajares Search for more papers by this author , Chiadi E. NdumeleChiadi E. Ndumele Search for more papers by this author , Carl E. OrringerCarl E. Orringer Search for more papers by this author , Carmen A. PeraltaCarmen A. Peralta Search for more papers by this author , Joseph J. SaseenJoseph J. Saseen Search for more papers by this author , Sidney C. Smith JrSidney C. Smith Jr Search for more papers by this author , Laurence SperlingLaurence Sperling Search for more papers by this author , Salim S. ViraniSalim S. Virani Search for more papers by this author and Joseph YeboahJoseph Yeboah Search for more papers by this author Originally published10 Nov 2018https://doi.org/10.1161/CIR.0000000000000625Circulation. 2019;139:e1082–e1143is corrected byCorrection to: 2018 AHA/ACC/AACVPR/AAPA/ABC/ACPM/ADA/AGS/APhA/ASPC/NLA/PCNA Guideline on the Management of Blood Cholesterol: A Report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice GuidelinesOther version(s) of this articleYou are viewing the most recent version of this article. Previous versions: November 10, 2018: Ahead of Print Table of ContentsTop 10 Take-Home Messages to Reduce Risk of Atherosclerotic Cardiovascular Disease Through Cholesterol Management e1083Preamble e10841. Introduction e10851.1. Methodology and Evidence Review e10851.2. Organization of the Writing Committee e10861.3. Document Review and Approval e10861.4. Scope of the Guideline e10861.5. Class of Recommendation and Level of Evidence e10871.6. Abbreviations e10872. High Blood Cholesterol and ASCVD e10872.1. Serum Cholesterol, Lipoproteins, and ASCVD e10872.1.1. Cholesterol, Lipoproteins, and Apolipoprotein B e10872.1.2. Cholesterol, LDL-C, and ASCVD e10872.1.3. LDL-C and Other Risk Factors e10872.2. Measurements of LDL-C and Non–HDL-C e10882.3. Measurements of Apolipoprotein B and Lipoprotein (a) e10892.4. Monitoring Response of LDL-C to Statin Therapy e10903. Therapeutic Modalities e10903.1. Lifestyle Therapies e10903.1.1. Diet Composition, Weight Control, and Physical Activity e10903.1.2. Lifestyle Therapies and Metabolic Syndrome e10903.2. Lipid-Lowering Drugs e10903.2.1. Statin Therapy e10903.2.2. Nonstatin Therapies e10913.2.3. Nonstatin Add-on Drugs to Statin Therapy e10914. Patient Management Groups e10914.1. Secondary ASCVD Prevention e10914.2. Severe Hypercholesterolemia (LDL-C ≥190 mg/dL [≥4.9 mmol/L]) e10954.3. Diabetes Mellitus in Adults e10974.4. Primary Prevention e10994.4.1. Evaluation and Risk Assessment e10994.4.2. Primary Prevention Adults 40 to 75 Years of Age With LDL-C Levels 70 to 189 mg/dL (1.7 to 4.8 mmol/L) e11024.4.3. Monitoring in Response to LDL-C–Lowering Therapy e11064.4.4. Primary Prevention in Other Age Groups e11074.5. Other Populations at Risk e11114.5.1. Ethnicity e11114.5.2. Hypertriglyceridemia e11125. Statin Safety and Statin-Associated Side Effects e11176. Implementation e11207. Cost and Value Considerations e11217.1. Economic Value Considerations: PCSK9 Inhibitors e11218. Limitations and Knowledge Gaps e11228.1. Randomized Controlled Trials e11228.2. Risk Assessment e11228.2.1. Continuing Refinement of PCE e11238.2.2. Improvement in Lifetime Risk Estimate e11238.2.3. Refinement of Clinician–Patient Risk Discussion e11238.2.4. Monitoring and Adjustment of Treatment e11238.2.5. Prognostic Significance of CAC e1123References e1124Appendix 1: Author Relationships With Industry and Other Entities (Relevant)—2018 AHA/ACC/AACVPR/AAPA/ABC/ACPM/ADA/AGS/APhA/ASPC/NLA/PCNA Guideline on the Management of Blood Cholesterol (August 2018) e1139Appendix 2: Reviewer Relationships With Industry and Other Entities (Comprehensive)—2018 AHA/ACC/AACVPR/AAPA/ABC/ACPM/ADA/AGS/APhA/ASPC/NLA/PCNA Guideline on the Management of Blood Cholesterol (August 2018) e1141Top 10 Take-Home Messages to Reduce Risk of Atherosclerotic Cardiovascular Disease Through Cholesterol ManagementIn all individuals, emphasize a heart-healthy lifestyle across the life course. A healthy lifestyle reduces atherosclerotic cardiovascular disease (ASCVD) risk at all ages. In younger individuals, healthy lifestyle can reduce development of risk factors and is the foundation of ASCVD risk reduction. In young adults 20 to 39 years of age, an assessment of lifetime risk facilitates the clinician–patient risk discussion (see No. 6) and emphasizes intensive lifestyle efforts. In all age groups, lifestyle therapy is the primary intervention for metabolic syndrome.In patients with clinical ASCVD, reduce low-density lipoprotein cholesterol (LDL-C) with high-intensity statin therapy or maximally tolerated statin therapy. The more LDL-C is reduced on statin therapy, the greater will be subsequent risk reduction. Use a maximally tolerated statin to lower LDL-C levels by ≥50%.In very high-risk ASCVD, use a LDL-C threshold of 70 mg/dL (1.8 mmol/L) to consider addition of nonstatins to statin therapy. Very high-risk includes a history of multiple major ASCVD events or 1 major ASCVD event and multiple high-risk conditions. In very high-risk ASCVD patients, it is reasonable to add ezetimibe to maximally tolerated statin therapy when the LDL-C level remains ≥70 mg/dL (≥1.8 mmol/L). In patients at very high risk whose LDL-C level remains ≥70 mg/dL (≥1.8 mmol/L) on maximally tolerated statin and ezetimibe therapy, adding a PCSK9 inhibitor is reasonable, although the long-term safety (>3 years) is uncertain and cost effectiveness is low at mid-2018 list prices.In patients with severe primary hypercholesterolemia (LDL-C level ≥190 mg/dL [≥4.9 mmol/L]), without calculating 10-year ASCVD risk, begin high-intensity statin therapy. If the LDL-C level remains ≥100 mg/dL (≥2.6 mmol/L), adding ezetimibe is reasonable. If the LDL-C level on statin plus ezetimibe remains ≥100 mg/dL (≥2.6 mmol/L) and the patient has multiple factors that increase subsequent risk of ASCVD events, a PCSK9 inhibitor may be considered, although the long-term safety (>3 years) is uncertain and economic value is uncertain at mid-2018 list prices.In patients 40 to 75 years of age with diabetes mellitus and LDL-C ≥70 mg/dL (≥1.8 mmol/L), start moderate-intensity statin therapy without calculating 10-year ASCVD risk. In patients with diabetes mellitus at higher risk, especially those with multiple risk factors or those 50 to 75 years of age, it is reasonable to use a high-intensity statin to reduce the LDL-C level by ≥50%.In adults 40 to 75 years of age evaluated for primary ASCVD prevention, have a clinician–patient risk discussion before starting statin therapy. Risk discussion should include a review of major risk factors (eg, cigarette smoking, elevated blood pressure, LDL-C, hemoglobin A1C [if indicated], and calculated 10-year risk of ASCVD); the presence of risk-enhancing factors (see No. 8); the potential benefits of lifestyle and statin therapies; the potential for adverse effects and drug–drug interactions; consideration of costs of statin therapy; and patient preferences and values in shared decision-making.In adults 40 to 75 years of age without diabetes mellitus and with LDL-C levels ≥70 mg/dL (≥1.8 mmol/L), at a 10-year ASCVD risk of ≥7.5%, start a moderate-intensity statin if a discussion of treatment options favors statin therapy. Risk-enhancing factors favor statin therapy (see No. 8). If risk status is uncertain, consider using coronary artery calcium (CAC) to improve specificity (see No. 9). If statins are indicated, reduce LDL-C levels by ≥30%, and if 10-year risk is ≥20%, reduce LDL-C levels by ≥50%.In adults 40 to 75 years of age without diabetes mellitus and 10-year risk of 7.5% to 19.9% (intermediate risk), risk-enhancing factors favor initiation of statin therapy (see No. 7). Risk-enhancing factors include family history of premature ASCVD; persistently elevated LDL-C levels ≥160 mg/dL (≥4.1 mmol/L); metabolic syndrome; chronic kidney disease; history of preeclampsia or premature menopause (age <40 years); chronic inflammatory disorders (eg, rheumatoid arthritis, psoriasis, or chronic HIV); high-risk ethnic groups (eg, South Asian); persistent elevations of triglycerides ≥175 mg/dL (≥1.97 mmol/L); and, if measured in selected individuals, apolipoprotein B ≥130 mg/dL, high-sensitivity C-reactive protein ≥2.0 mg/L, ankle-brachial index <0.9 and lipoprotein (a) ≥50 mg/dL or 125 nmol/L, especially at higher values of lipoprotein (a). Risk-enhancing factors may favor statin therapy in patients at 10-year risk of 5-7.5% (borderline risk).In adults 40 to 75 years of age without diabetes mellitus and with LDL-C levels ≥70 mg/dL to 189 mg/dL (≥1.8-4.9 mmol/L), at a 10-year ASCVD risk of ≥7.5% to 19.9%, if a decision about statin therapy is uncertain, consider measuring CAC. If CAC is zero, treatment with statin therapy may be withheld or delayed, except in cigarette smokers, those with diabetes mellitus, and those with a strong family history of premature ASCVD. A CAC score of 1 to 99 favors statin therapy, especially in those ≥55 years of age. For any patient, if the CAC score is ≥100 Agatston units or ≥75th percentile, statin therapy is indicated unless otherwise deferred by the outcome of clinician–patient risk discussion.Assess adherence and percentage response to LDL-C–lowering medications and lifestyle changes with repeat lipid measurement 4 to 12 weeks after statin initiation or dose adjustment, repeated every 3 to 12 months as needed. Define responses to lifestyle and statin therapy by percentage reductions in LDL-C levels compared with baseline. In ASCVD patients at very high-risk, triggers for adding nonstatin drug therapy are defined by threshold LDL-C levels ≥70 mg/dL (≥1.8 mmol/L) on maximal statin therapy (see No. 3).PreambleSince 1980, the American College of Cardiology (ACC) and American Heart Association (AHA) have translated scientific evidence into clinical practice guidelines with recommendations to improve cardiovascular health. These guidelines, which are based on systematic methods to evaluate and classify evidence, provide a foundation for the delivery of quality cardiovascular care. The ACC and AHA sponsor the development and publication of clinical practice guidelines without commercial support, and members volunteer their time to the writing and review efforts.Clinical practice guidelines provide recommendations applicable to patients with or at risk of developing cardiovascular disease (CVD). The focus is on medical practice in the United States, but these guidelines are relevant to patients throughout the world. Although guidelines may be used to inform regulatory or payer decisions, the intent is to improve quality of care and align with patients’ interests. Guidelines are intended to define practices meeting the needs of patients in most, but not all, circumstances, and should not replace clinical judgment.Recommendations for guideline-directed management and therapy, which encompasses clinical evaluation, diagnostic testing, and both pharmacological and procedural treatments, are effective only when followed by both practitioners and patients. Adherence to recommendations can be enhanced by shared decision-making between clinicians and patients, with patient engagement in selecting interventions on the basis of individual values, preferences, and associated conditions and comorbidities.The ACC/AHA Task Force on Clinical Practice Guidelines strives to ensure that the guideline writing committee both contains requisite expertise and is representative of the broader medical community by selecting experts from a broad array of backgrounds, representing different geographic regions, sexes, races, ethnicities, intellectual perspectives/biases, and scopes of clinical practice, and by inviting organizations and professional societies with related interests and expertise to participate as partners or collaborators. The ACC and AHA have rigorous policies and methods to ensure that documents are developed without bias or improper influence. The complete policy on relationships with industry and other entities (RWI) can be found online.Beginning in 2017, numerous modifications to the guidelines have been and continue to be implemented to make guidelines shorter and enhance “user friendliness.” Guidelines are written and presented in a modular knowledge chunk format, in which each chunk includes a table of recommendations, a brief synopsis, recommendation-specific supportive text and, when appropriate, flow diagrams or additional tables. Hyperlinked references are provided for each modular knowledge chunk to facilitate quick access and review. More structured guidelines—including word limits (“targets”) and a web guideline supplement for useful but noncritical tables and figures—are 2 such changes. This Preamble is an abbreviated version, with the detailed version available online.Glenn N. Levine, MD, FACC, FAHAChair, ACC/AHA Task Force on Clinical Practice Guidelines1. Introduction1.1. Methodology and Evidence ReviewThe recommendations listed in the present guideline are, whenever possible, evidence based. An initial extensive evidence review, which included literature derived from research involving human subjects, published in English, and indexed in MEDLINE (through PubMed), EMBASE, the Cochrane Library, the Agency for Healthcare Research and Quality, and other selected databases relevant to the present guideline, was conducted from May 1980 to July 2017. Key search words included but were not limited to the following: hyperlipidemia, cholesterol, LDL-C, HDL-C, ezetimibe, bile acid sequestrants, PCSK9 inhibitors, lifestyle, diet, exercise, medications, child, adolescent, screening, primary prevention, secondary prevention, cardiovascular disease, coronary artery calcium, familial hypercholesterolemia. ASCVD risk-enhancing factors, statin therapy, diabetes mellitus, women, adherence, Hispanic/Latino, South Asian, African American. Additional relevant studies published through August 2018 during the guideline writing process, were also considered by the writing committee and added to the evidence tables when appropriate. The final evidence tables are included in the Online Data Supplement and summarize the evidence used by the writing committee to formulate recommendations. References selected and published in the present document are representative and not all-inclusive.As noted in the detailed version of the Preamble, an independent evidence review committee was commissioned to perform a formal systematic review of critical clinical questions related to cholesterol (Table 1), the results of which were considered by the writing committee for incorporation into the present guideline. Concurrent with this process, writing committee members evaluated study data relevant to the rest of the guideline. The findings of the evidence review committee and the writing committee members were formally presented and discussed, and then recommendations were developed. The systematic review for the 2018 Cholesterol Clinical Practice GuidelinesS1.1-1 is published in conjunction with the present guideline, and includes its respective data supplements.Table 1. ERC QuestionsQuestionSection NumberIn adults ≥20 years of age with clinical atherosclerotic disease (eg, CHD, peripheral artery disease, or CVD) or at high-risk of ASCVD, what are the magnitude of benefit (absolute reduction; NNT) in individual endpoints and composite ischemic events (eg, fatal cardiovascular event, nonfatal MI, nonfatal stroke, unstable angina/revascularization) and magnitude of harm (absolute increase; NNH) in terms of adverse events (eg, cancer, rhabdomyolysis, diabetes mellitus) derived from LDL-C lowering in large RCTs (>1 000 participants and originally designed to last >12 months) with statin therapy plus a second lipid-modifying agent compared with statin alone?4.1Clinical atherosclerotic cardiovascular disease (ASCVD) includes acute coronary syndrome (ACS), those with history of myocardial infarction (MI), stable or unstable angina or coronary or other arterial revascularization, stroke, transient ischemic attack (TIA), or peripheral artery disease (PAD) including aortic aneurysm, all of atherosclerotic origin.ASCVD indicates atherosclerotic cardiovascular disease; CHD, coronary heart disease; CVD, cardiovascular disease; ERC, Evidence Review Committee; LDL-C, low-density lipoprotein cholesterol; MI, myocardial infarction; NNH, number needed to harm; NNT number needed to treat; and RCT, randomized controlled trial.Numerical values for triglycerides, total cholesterol (TC), low-density lipoprotein cholesterol (LDL-C), high-density lipoprotein cholesterol (HDL-C), and non–HDL-C are given in both mg/dL and mmol/L. To convert to mmol/L, the values in mg/dL for TC, LDL-C, HDL-C, and non–HDL-C were divided by 38.6 and for triglycerides, by 88.6.On May 10, 2018 a writing committee member discussed their participation in an industry-supported, multicenter study, which they had thought was not relevant to this prevention guideline. However, when this was reviewed using specific ACC/AHA criteria it was considered to represent a relevant relationship with industry. Given the current policy that a prevention guideline writing committee member must be free of any relevant relationships with industry, this member was removed from the committee. The 2 sections authored by the writing committee member were removed and replaced by new material written by the guideline chairs, and the revised sections reviewed and approved by all remaining writing committee members. The writing committee member did not participate in any further guideline discussions or review of the manuscript or recommendations.1.2. Organization of the Writing CommitteeThe writing committee consisted of medical experts including cardiologists, internists, interventionalists, a nurse practitioner, pharmacists, a physician assistant, a pediatrician, a nephrologist, and a lay/patient representative. The writing committee included representatives from the American Heart Association (AHA), American College of Cardiology (ACC), American Association of Cardiovascular and Pulmonary Rehabilitation (AACVPR), American Association Academy of Physician Assistants (AAPA), Association of Black Cardiologists (ABC), American College of Preventive Medicine (ACPM), American Diabetes Association (ADA), American Geriatrics Society (AGS), American Pharmacists Association (APhA), American Society for Preventive Cardiology (ASPC), National Lipid Association (NLA), and Preventive Cardiovascular Nurses Association (PCNA). Appendix 1 of the present document lists writing committee members’ relevant relationships with industry and other entities. For the purposes of full transparency, the writing committee members’ comprehensive disclosure information is available online.1.3. Document Review and ApprovalThis document was reviewed by 21 official reviewers each nominated by the ACC, AHA, AAPA, ABC, ACPM, ADA, AGS, APhA, ASPC, NLA, and PCNA, as well as 27 individual content reviewers. Reviewers’ RWI information was distributed to the writing committee and is published in this document (Appendix 2).This document was approved for publication by the governing bodies of the AHA, the ACC, AAPA, ABC, ACPM, ADA, AGS, APhA, ASPC, NLA, and PCNA.1.4. Scope of the GuidelineThe purpose of the present guideline is to address the practical management of patients with high blood cholesterol and related disorders. The writing committee reviewed previously published guidelines, evidence reviews, and related statements. Table S1 in the Web Supplement contains a list of publications and statements deemed pertinent. The primary sources of evidence are randomized controlled trials (RCTs). Most RCTs in this area have been performed with statins as the only cholesterol-lowering drug.S1.4-1–S1.4-3 Since the 2013 ACC/AHA cholesterol guideline,S1.4-4 newer cholesterol-lowering agents (nonstatin drugs) have been introduced and subjected to RCTs. They include ezetimibe and PCSK9 inhibitors, and their use is limited mainly to secondary prevention in patients at very high-risk of new atherosclerotic cardiovascular disease (ASCVD) events. Most other patients with ASCVD are treated with statins alone. In primary prevention, statins are recommended for patients with severe hypercholesterolemia and in adults 40 to 75 years of age either with diabetes mellitus or at higher ASCVD risk. Throughout these guidelines similar to the 2013 guidelines, consistent attention is given to a clinician–patient risk discussion for making shared decisions. Besides major risk factors of the pooled cohort equations (PCE), the clinician–patient risk discussion can include other risk-enhancing factors, and when risk status is uncertain, a coronary artery calcium (CAC) score is an option to facilitate decision-making in adults ≥40 years of age. In children, adolescents, and young adults, identifying those with familial hypercholesterolemia (FH) is a priority. However, most attention is given to reducing lifetime ASCVD risk through lifestyle therapies.1.5. Class of Recommendation and Level of EvidenceRecommendations are designated with both a class of recommendation (COR) and a level of evidence (LOE). The class of recommendation indicates the strength of recommendation, encompassing the estimated magnitude and certainty of benefit in proportion to risk. The level of evidence rates the quality of scientific evidence supporting the intervention on the basis of the type, quantity, and consistency of data from clinical trials and other sources (Table 2).S1.5-1Table 2. Applying Class of Recommendation and Level of Evidence to Clinical Strategies, Interventions, Treatments, or Diagnostic Testing in Patient Care* (Updated August 2015)Table 2. Applying Class of Recommendation and Level of Evidence to Clinical Strategies, Interventions, Treatments, or Diagnostic Testing in Patient Care* (Updated August 2015)1.6. AbbreviationsAbbreviationMeaning/PhraseABIankle-brachial indexACSacute coronary syndromeAIDSacquired immunodeficiency syndromeapoBapolipoprotein BARRabsolute risk reductionASCVDatherosclerotic cardiovascular diseaseCACcoronary artery calciumCHDcoronary heart diseaseCKcreatine kinaseCKDchronic kidney diseaseCORClass of RecommendationCTTCholesterol Treatment TrialistsCVDcardiovascular diseaseeGFRestimated glomerular filtration rateFHfamilial hypercholesterolemiaHDLhigh-density lipoproteinHFheart failureHIVhuman immunodeficiency virusLDL-Clow-density lipoprotein cholesterolLOELevel of EvidenceLp(a)lipoprotein (a)MImyocardial infarctionPCEpooled cohort equationsQALYquality-adjusted life-yearRArheumatoid arthritisRCTrandomized controlled trialsRRRrelative risk reductionRWIrelationships with industry and other entitiesSAMSstatin-associated muscle symptomsSRsystematic reviewTCtotal cholesterolVLDLvery low-density lipoproteinVLDL-Cvery low-density lipoprotein cholesterol2. High Blood Cholesterol and ASCVD2.1. Serum Cholesterol, Lipoproteins, and ASCVD2.1.1. Cholesterol, Lipoproteins, and Apolipoprotein BSerum cholesterol and its lipoprotein carriers (LDL, very low-density lipoprotein [VLDL], and HDL) are known to be related to ASCVD. LDL-C is the dominant form of atherogenic cholesterol. VLDL is the chief carrier of triglycerides, and VLDL cholesterol (VLDL-C) is also atherogenic. HDL-C is seemingly not atherogenic. Chylomicrons transport dietary fat; chylomicron atherogenicity is uncertain. The combination of LDL-C and VLDL-C is called non–HDL-C and is more atherogenic than either lipoprotein alone. The main protein embedded in LDL and VLDL is apolipoprotein B (apoB), and like non–HDL-C, apoB is a stronger indicator of atherogenicity than LDL-C alone.2.1.2. Cholesterol, LDL-C, and ASCVDEvidence that serum cholesterol contributes to ASCVD comes from several sources: animal studies, genetic forms of hypercholesterolemia, epidemiological studies, and RCTs. US population studiesS2.1.2-1,S2.1.2-2 suggest that optimal total cholesterol levels are about 150 mg/dL (3.8 mmol/L), which corresponds to an LDL-C level of about 100 mg/dL (2.6 mmol/L). Adult populations with cholesterol concentrations in this range manifest low rates of ASCVD.S2.1.2-3 RCTs of cholesterol-lowering drugs in high-risk patients confirm that LDL-C lowering produces marked reductions in ASCVD. This confirms the general principle that “lower is better” for LDL-C.S2.1.2-4–S2.1-6 The present guideline looks to evidence from new RCTs to aid in the translation of RCT data to the individual patient to provide net benefit.S2.1.2-72.1.3. LDL-C and Other Risk FactorsAlthough LDL-C is a primary cause of atherosclerosis, other risk factors contribute, as well. The major risk factors include cigarette smoking, hypertension, dysglycemia, and other lipoprotein abnormalities. Because atherosclerosis progresses with advancing age, a person’s age also counts as a risk factor. By combining all major risk factors into a prediction equation, an individual’s probability of developing ASCVD can be estimated. The Framingham Heart StudyS2.1.3-1 took the lead in creating risk-prediction equations. These were improved in the 2013 ACC/AHA cholesterol guidelinesS2.1.3-2 by compiling data from 5 community-based cohorts that were broadly representative of the US population. These so-called population cohort equations have been validated in a large community-based US population.S2.1.3-3 Initially, data from the Women’s Health Initiative, a contemporary multiethnic cohort of postmenopausal women, appeared to indicate that these pooled cohort equations overestimated ASCVD risk. However, when event surveillance was improved by data from Centers for Medicare & Medicaid Services, the authors found that the equations discriminated risk well.S2.1.3-4Several other factors associate with ASCVD, and in the present document these are called risk-enhancing factors. Projections of future risk derived from major risk factors and risk-enhancing factors can be used to adjust the intensity of LDL-lowering therapy.2.2. Measurements of LDL-C and Non–HDL-CSynopsisThe standard calculation method for LDL-C is the Friedewald formula: LDL-C=(TC)–(triglycerides/5)– (HDL-C). When triglyceride levels are not elevated, this equation is sufficiently accurate. In hypertriglyceridemia, however, Friedewald-calculated LDL-C can be erroneous. After normal food intake, LDL-C differs minimally with time.S2.2-10 Fasting and nonfasting TC and HDL-C levels appear to have fairly similar prognostic value and associations with CVD outcomes.S2.2-1–S2.2-6,S2.2-11 Thus, nonfasting samples can be used for risk assessment in primary prevention and for assessment of baseline LDL-C levels before the initiation of a statin in primary and secondary prevention. If more precision is necessary, fasting lipids can be measured, but a nonfasting sample is reasonable for most situations. The unreliability of the Friedewald-calculated LDL-C levels appears to be greatest at lower levels of LDL-C, particularly <70 mg/dL (<1.8 mmol/L).S2.2-7 Martin

Since 1980, the American College of Cardiology (ACC) and American Heart Association (AHA) have translated scientific evidence into clinical practice guidelines (guidelines) with recommendations to improve cardiovascular health.In 2013, the National Heart, Lung, and Blood Institute (NHLBI) Advisory Council recommended that the NHLBI focus specifically on reviewing the highest-quality evidence and partner with other organizations to develop recommendations.P-1,P-2 Accordingly, the ACC and AHA collaborated with the NHLBI and stakeholder and professional organizations to complete and publish 4 guidelines (on assessment of cardiovascular risk, lifestyle modifications to reduce cardiovascular risk, management of blood cholesterol in adults, and management of overweight and obesity in adults) to make them available to the widest possible constituency.In 2014, the ACC and AHA, in partnership with several other professional societies, initiated a guideline on the prevention, detection, evaluation, and management of high blood pressure (BP) in adults.Under the management of the ACC/ AHA Task Force, a Prevention Subcommittee was appointed to help guide development of the suite of guidelines on prevention of cardiovascular disease (CVD).These guidelines, which are based on systematic methods to evaluate and classify evidence, provide a cornerstone for quality cardiovascular care.The ACC and AHA sponsor the development and publication of guidelines without commercial support, and members of each organization volunteer their time to the writing and review efforts.Guidelines are official policy of the ACC and AHA. HypertensionJune 2018of clinical practice.The Task Force may also invite organizations and professional societies with related interests and expertise to participate as partners, collaborators, or endorsers. Relationships With Industry and Other EntitiesThe ACC and AHA have rigorous policies and methods to ensure that guidelines are developed without bias or improper influence.The complete relationships with industry and other entities (RWI) policy can be found online.Appendix 1 of the present document lists writing committee members' relevant RWI.For the purposes of full transparency, writing committee members' comprehensive disclosure information is available online.Comprehensive disclosure information for the Task Force is available online. Evidence Review and Evidence Review CommitteesIn developing recommendations, the writing committee uses evidence-based methodologies that are based on all available data.P-6-P-9 Literature searches focus on randomized controlled trials (RCTs) but also include registries, nonrandomized comparative and descriptive studies, case series, cohort studies, systematic reviews, and expert opinion.Only key references are cited.An independent evidence review committee (ERC) is commissioned when there are 1 or more questions deemed of utmost clinical importance that merit formal systematic review.The systematic review will determine which patients are most likely to benefit from a drug, device, or treatment strategy and to what degree.Criteria for commissioning an ERC and formal systematic review include: a) the absence of a current authoritative systematic review, b) the feasibility of defining the benefit and risk in a time frame consistent with the writing of a guideline, c) the relevance to a substantial number of patients, and d) the likelihood that the findings can be translated into actionable recommendations.ERC members may include methodologists, epidemiologists, healthcare providers, and biostatisticians.The recommendations developed by the writing committee on the basis of the systematic review are marked with "SR." Guideline-Directed Management and TherapyThe term guideline-directed management and therapy (GDMT) encompasses clinical evaluation, diagnostic testing, and pharmacological and procedural treatments.For these and all recommended drug treatment regimens, the reader should confirm the dosage by reviewing product insert material and evaluate the treatment regimen for contraindications and interactions.The recommendations are limited to drugs, devices, and treatments approved for clinical use in the United States. Class of Recommendation and Level of EvidenceThe Class of Recommendation (COR) indicates the strength of the recommendation, encompassing the estimated magnitude and certainty of benefit in proportion to risk.The Level of Evidence (LOE) rates the quality of scientific evidence that supports the intervention on the basis of the type, quantity, and consistency of data from clinical trials and other sources (Table 1).P-6-P-8

HomeCirculationVol. 129, No. 25_suppl_22013 ACC/AHA Guideline on the Assessment of Cardiovascular Risk Open AccessResearch ArticlePDF/EPUBAboutView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissionsDownload Articles + Supplements ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toSupplementary MaterialsOpen AccessResearch ArticlePDF/EPUB2013 ACC/AHA Guideline on the Assessment of Cardiovascular RiskA Report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines David C. GoffJr, MD, PhD, FACP, FAHA, Donald M. Lloyd-Jones, MD, ScM, FACC, FAHA, Glen Bennett, MPH, Sean Coady, MS, Ralph B. D’Agostino, Sr, PhD, FAHA, Raymond Gibbons, MD, FACC, FAHA, Philip Greenland, MD, FACC, FAHA, Daniel T. Lackland, DrPH, FAHA, Daniel Levy, MD, Christopher J. O’Donnell, MD, MPH, Jennifer G. Robinson, MD, MPH, FAHA, J. Sanford Schwartz, MD, Susan T. Shero, MS, RN, Sidney C. SmithJr, MD, FACC, FAHA, Paul Sorlie, PhD, Neil J. Stone, MD, FACC, FAHA and Peter W. F. Wilson, MD, FAHA David C. GoffJrDavid C. GoffJr Search for more papers by this author , Donald M. Lloyd-JonesDonald M. Lloyd-Jones Search for more papers by this author , Glen BennettGlen Bennett *Ex-Officio Members. Search for more papers by this author , Sean CoadySean Coady *Ex-Officio Members. Search for more papers by this author , Ralph B. D’AgostinoRalph B. D’Agostino Search for more papers by this author , Raymond GibbonsRaymond Gibbons Search for more papers by this author , Philip GreenlandPhilip Greenland Search for more papers by this author , Daniel T. LacklandDaniel T. Lackland Search for more papers by this author , Daniel LevyDaniel Levy *Ex-Officio Members. Search for more papers by this author , Christopher J. O’DonnellChristopher J. O’Donnell *Ex-Officio Members. Search for more papers by this author , Jennifer G. RobinsonJennifer G. Robinson Search for more papers by this author , J. Sanford SchwartzJ. Sanford Schwartz Search for more papers by this author , Susan T. SheroSusan T. Shero *Ex-Officio Members. Search for more papers by this author , Sidney C. SmithJrSidney C. SmithJr Search for more papers by this author , Paul SorliePaul Sorlie *Ex-Officio Members. Search for more papers by this author , Neil J. StoneNeil J. Stone Search for more papers by this author and Peter W. F. WilsonPeter W. F. Wilson Search for more papers by this author Originally published12 Nov 2013https://doi.org/10.1161/01.cir.0000437741.48606.98Circulation. 2014;129:S49–S73is corrected byCorrectionOther version(s) of this articleYou are viewing the most recent version of this article. Previous versions: January 1, 2013: Previous Version 1 Table of ContentsPreamble and Transition to ACC/AHA Guidelines to Reduce Cardiovascular Risk S501. Introduction S521.1. Organization of the Work Group S521.2. Document Review and Approval S521.3. Charge to the Work Group S531.4. Methodology and Evidence Review S532. Risk Assessment: Recommendations S533. Approach to Risk Assessment S534. Development of New Pooled Cohort ASCVD Risk Equations S554.1. Recommendations for Assessment of 10-Year Risk of a First Hard ASCVD Event S555. Implications for Risk Assessment S556. CQs and Systematic Evidence Review S566.1. Critical Question 1 S566.1.1. Summary of Systematic Reviews and Meta-Analyses for CQ1 S566.1.2. Recommendations for CQ1: Use of Newer Risk Markers After Quantitative Risk Assessment S586.2. Critical Question 2 S586.2.1. Summary of Evidence for CQ2 S596.2.2. Recommendations for CQ2: Long-Term Risk Assessment S597. Implementation Considerations for Risk Assessment S598. Evidence Gaps and Future Research Needs S599. Conclusions S60References S60Appendix 1. Author Relationships With Industry and Other Entities (Relevant) S62Appendix 2. Expert Reviewer Relationships With Industry and Other Entities S65Appendix 3. Abbreviations S65Appendix 4. Evidence Statements for CQ1 S66Appendix 5. Evidence Statements for CQ2 S69Appendix 6. Characteristics of Previously Published Risk Scores and Current Pooled Cohort Equations S70Appendix 7. Development and Steps for Implementation of the ASCVD Pooled Cohort Risk Equations S71Preamble and Transition to ACC/AHA Guidelines to Reduce Cardiovascular RiskThe goals of the American College of Cardiology (ACC) and the American Heart Association (AHA) are to prevent cardiovascular diseases (CVD); improve the management of people who have these diseases through professional education and research; and develop guidelines, standards, and policies that promote optimal patient care and cardiovascular health. Toward these objectives, the ACC and AHA have collaborated with the National Heart, Lung, and Blood Institute (NHLBI) and stakeholder and professional organizations to develop clinical practice guidelines for assessment of cardiovascular risk, lifestyle modifications to reduce cardiovascular risk, management of blood cholesterol in adults, and management of overweight and obesity in adults.In 2008, the NHLBI initiated these guidelines by sponsoring rigorous systematic evidence reviews for each topic by expert panels convened to develop critical questions (CQs), interpret the evidence, and craft recommendations. In response to the 2011 report from the Institute of Medicine on the development of trustworthy clinical guidelines,1 the NHLBI Advisory Council recommended that the NHLBI focus specifically on reviewing the highest-quality evidence and partner with other organizations to develop recommendations.2,3 Accordingly, in June 2013 the NHLBI initiated collaboration with the ACC and AHA to work with other organizations to complete and publish the 4 guidelines noted above and make them available to the widest possible constituency. Recognizing that the Expert Work Group/Work Groups did not consider evidence beyond 2011 (except as specified in the methodology), the ACC, AHA, and collaborating societies plan to begin updating these guidelines starting in 2014.The joint ACC/AHA Task Force on Practice Guidelines (Task Force) appointed a subcommittee to shepherd this transition, communicate the rationale and expectations to the writing panels and partnering organizations, and expeditiously publish the documents. The ACC/AHA and partner organizations recruited a limited number of expert reviewers for fiduciary examination of content, recognizing that each document had undergone extensive peer review by representatives of the NHLBI Advisory Council, key federal agencies, and scientific experts. Each writing panel responded to comments from these reviewers. Clarifications were incorporated where appropriate, but there were no substantive changes because the bulk of the content was undisputed.Although the Task Force led the final development of these prevention guidelines, they differ from other ACC/AHA guidelines. First, as opposed to an extensive compendium of clinical information, these documents are significantly more limited in scope and focus on selected CQs on each topic, based on the highest-quality evidence available. Recommendations were derived from randomized trials, meta-analyses, and observational studies evaluated for quality and were not formulated when sufficient evidence was not available. Second, the text accompanying each recommendation is succinct, summarizing the evidence for each question. The Full Panel/Work Group Reports include more detailed information about the evidence statements that serve as the basis for recommendations. Third, the format of the recommendations differs from other ACC/AHA guidelines. Each recommendation has been mapped from the NHLBI grading format to the ACC/AHA Classification of Recommendation/Level of Evidence (COR/LOE) construct (Table 1) and is expressed in both formats. Because of the inherent differences in grading systems and the clinical questions driving the recommendations, alignment between the NHLBI and ACC/AHA formats is in some cases imperfect. Explanations of these variations are noted in the recommendation tables, where applicable.Table 1. Applying Classification of Recommendation and Level of EvidenceTable 1. Applying Classification of Recommendation and Level of EvidenceIn consultation with NHLBI, the policies adopted by the writing panels to manage relationships of authors with industry and other entities (RWI) are outlined in the methods section of each panel report. These policies were in effect when this effort began in 2008 and throughout the writing process and voting on recommendations, until the process was transferred to ACC/AHA in 2013. In the interest of transparency, the ACC/AHA requested that panel authors resubmit RWI disclosures as of July 2013. Relationships relevant to this guideline are disclosed in Appendix 1. None of the ACC/AHA expert reviewers had relevant RWI (Appendix 2). See Appendix 3 for a list of abbreviations used in the guideline.Systematic evidence reports and accompanying summary tables were developed by the expert panels and NHLBI. The guideline was reviewed by the ACC/AHA Task Force and approved by the ACC Board of Trustees, and the AHA Science Advisory and Coordinating Committee. In addition, ACC/AHA sought endorsement from other stakeholders, including professional organizations. It is the hope of the writing panels, stakeholders, professional organizations, NHLBI, and Task Force that the guidelines will garner the widest possible readership for the benefit of patients, providers, and the public health.These guidelines are meant to define practices that meet the needs of patients in most circumstances and are not a replacement for clinical judgment. The ultimate decision about care of a particular patient must be made by the healthcare provider and patient in light of the circumstances presented by that patient. As a result, situations might arise in which deviations from these guidelines may be appropriate. These considerations notwithstanding, in caring for most patients, clinicians can employ the recommendations confidently to reduce the risks of atherosclerotic cardiovascular disease (ASCVD) events.See Tables 2 and 3 for an explanation of the NHLBI recommendation grading methodology.Table 2. NHLBI Grading of the Strength of RecommendationsGradeStrength of Recommendation*AStrong recommendationThere is high certainty based on evidence that the net benefit† is substantial.BModerate recommendationThere is moderate certainty based on evidence that the net benefit is moderate to substantial, or there is high certainty that the net benefit is moderate.CWeak recommendationThere is at least moderate certainty based on evidence that there is a small net benefit.DRecommendation againstThere is at least moderate certainty based on evidence that there is no net benefit or that risks/harms outweigh benefits.EExpert opinion (“There is insufficient evidence or evidence is unclear or conflicting, but this is what the Work Group recommends.”)Net benefit is unclear. Balance of benefits and harms cannot be determined because of no evidence, insufficient evidence, unclear evidence, or conflicting evidence, but the Work Group thought it was important to provide clinical guidance and make a recommendation. Further research is recommended in this area.NNo recommendation for or against (“There is insufficient evidence or evidence is unclear or conflicting.”)Net benefit is unclear. Balance of benefits and harms cannot be determined because of no evidence, insufficient evidence, unclear evidence, or conflicting evidence, and the Work Group thought no recommendation should be made. Further research is recommended in this area.*In most cases, the strength of the recommendation should be closely aligned with the quality of the evidence; however, under some circumstances, there may be valid reasons for making recommendations that are not closely aligned with the quality of the evidence (eg, strong recommendation when the evidence quality is moderate, such as smoking cessation to reduce cardiovascular disease risk or ordering an ECG as part of the initial diagnostic work-up for a patient presenting with possible MI). Those situations should be limited and the rationale explained clearly by the Work Group.†Net benefit is defined as benefits minus risks/harms of the service/intervention.ECG indicates electrocardiogram; MI, myocardial infarction; and NHLBI, National Heart, Lung, and Blood Institute.Table 3. NHLBI Quality Rating of the Strength of EvidenceType of EvidenceQuality Rating*Well-designed, well-executed† RCT that adequately represent populations to which the results are applied and directly assess effects on health outcomes.Meta-analyses of such studies.Highly certain about the estimate of effect.Further research is unlikely to change our confidence in the estimate of effect.HighRCT with minor limitations‡ affecting confidence in, or applicability of, the results.Well-designed, well-executed nonrandomized controlled studies§ and well-designed, well-executed observational studies‖.Meta-analyses of such studies.Moderately certain about the estimate of effect.Further research may have an impact on our confidence in the estimate of effect and may change the estimate.ModerateRCT with major limitations.Nonrandomized controlled studies and observational studies with major limitations affecting confidence in, or applicability of, the results.Uncontrolled clinical observations without an appropriate comparison group (eg, case series, case reports).Physiological studies in humans.Meta-analyses of such studies.Low certainty about the estimate of effect. Further research is likely to have an impact on our confidence in the estimate of effect and is likely to change the estimate.Low*In some cases, other evidence, such as large all-or-none case series (eg, jumping from airplanes or tall structures), can represent high- or moderate-quality evidence. In such cases, the rationale for the evidence rating exception should be explained by the Work Group and clearly justified.†“Well-designed, well-executed” refers to studies that directly address the question; use adequate randomization, blinding, and allocation concealment; are adequately powered; use intention-to-treat analyses; and have high follow-up rates.‡Limitations include concerns with the design and execution of a study that result in decreased confidence in the true estimate of the effect. Examples of such limitations include but are not limited to: inadequate randomization, lack of blinding of study participants or outcome assessors, inadequate power, outcomes of interest that are not prespecified for the primary outcomes, low follow-up rates, and findings based on subgroup analyses. Whether the limitations are considered minor or major is based on the number and severity of flaws in design or execution. Rules for determining whether the limitations are considered minor or major and how they will affect rating of the individual studies will be developed collaboratively with the methodology team.§Nonrandomized controlled studies refer to intervention studies where assignment to intervention and comparison groups is not random (eg, quasi-experimental study design).‖Observational studies include prospective and retrospective cohort, case-control, and cross-sectional studies.NHLBI indicates National Heart, Lung, and Blood Institute; and RCT, randomized controlled trials.1. Introduction1.1. Organization of the Work GroupThe Risk Assessment Work Group (Work Group) was composed of 11 members and 5 ex-officio members, including internists, cardiologists, endocrinologists, and experts in cardiovascular epidemiology, biostatistics, healthcare management and economics, and guideline development.1.2. Document Review and ApprovalA formal peer review process, which included 12 expert reviewers and representatives of federal agencies, was initially completed under the auspices of the NHLBI. This document was also reviewed by 3 expert reviewers nominated by the ACC and the AHA when the management of the guideline transitioned to the ACC/AHA. The ACC and AHA Reviewers’ RWI information is published in this document (Appendix 2).This document was approved for publication by the governing bodies of the ACC and AHA and endorsed by the American Association of Cardiovascular and Pulmonary Rehabilitation, American Society for Preventive Cardiology, American Society of Hypertension, Association of Black Cardiologists, National Lipid Association, Preventive Cardiovascular Nurses Association, and WomenHeart: The National Coalition for Women With Heart Disease.1.3. Charge to the Work GroupThe Work Group was 1 of 3 work groups appointed by the NHLBI to develop its own recommendations and provide cross-cutting input to 3 Panels for updating guidelines on blood cholesterol, blood pressure (BP), and overweight/obesity. The Work Group was asked to examine the scientific evidence on risk assessment for initial ASCVD events and to develop an approach for quantitative risk assessment that could be used in practice and used or adapted by the risk factor panels (blood cholesterol, hypertension, and obesity) in their guidelines and algorithms. Specifically, the Work Group was charged with 2 tasks:To develop or recommend an approach to quantitative risk assessment that could be used to guide care; andTo use systematic review methodology to pose and address a small number of questions judged to be critical to refining and adopting risk assessment in clinical practice.1.4. Methodology and Evidence ReviewThis guideline is based on the Full Work Group Report supplement, which is provided as a supplement to the guideline. The Full Work Group Report supplement contains background and additional material related to content, methodology, evidence synthesis, rationale, and references and is supported by the NHLBI Systematic Evidence Review, which can be found at (http://www.nhlbi.nih.gov/guidelines/cvd_adult/risk_assessment/). These documents also describe the process for the development of novel, comprehensive multivariable risk equations for the prediction of 10-year risk of development of ASCVD in non-Hispanic African-American and non-Hispanic white men and women from 40 to 79 years of age. These equations were developed from several long-standing population-based cohort studies funded by the NHLBI. Ten-year risk was defined as the risk of developing a first ASCVD event, defined as nonfatal myocardial infarction or coronary heart disease (CHD) death or fatal or nonfatal stroke, over a 10-year period among people free from ASCVD at the beginning of the period.In addition, through evaluation of evidence developed by systematic reviews of the literature, the Work Group addressed the following 2 CQs:CQ1. “What is the evidence with regard to reclassification or contribution to risk assessment when high-sensitivity C-reactive protein (hs-CRP), apolipoprotein B (ApoB), glomerular filtration rate, microalbuminuria, family history, cardiorespiratory fitness, ankle-brachial index (ABI), carotid intima-media thickness (CIMT), or coronary artery calcium (CAC) score is considered in addition to the variables that are in the traditional risk scores?”CQ2. “Are models constructed to assess the long-term (≥15 years or lifetime) risk of a first cardiovascular disease (CVD) event in adults effective in assessing variation in long-term risk among adults at low and/or intermediate short-term risk, whether analyzed separately or in combination?”The evidence and recommendations in the guideline focus on the large proportion of the adult population without clinical signs or symptoms of ASCVD who merit evaluation for the primary prevention of ASCVD. They do not apply to those with clinically manifest ASCVD, who require secondary prevention approaches, or to highly-selected patient subgroups, such as those with symptoms suggestive of CVD, who require diagnostic strategies rather than risk assessment. Furthermore, these recommendations were not developed for use in specific subgroups of asymptomatic individuals at unusually high risk, such as those with genetically determined extreme values of traditional risk factors (eg, patients with familial hypercholesterolemia).2. Risk Assessment: RecommendationsSee Table 4 for a summary of the recommendations for risk assessment.Table 4. Summary of Recommendations for Risk AssessmentTable 4. Summary of Recommendations for Risk Assessment3. Approach to Risk AssessmentIn addressing its charge, the Work Group recognized the need for a risk assessment approach that was based on the types of data that primary care providers could easily collect and that could be implemented in routine clinical practice. After deliberation, the Work Group endorsed the existing and widely used paradigm of matching the intensity of preventive efforts with the individual’s absolute risk.23,24 The Work Group acknowledges that none of the risk assessment tools or novel risk markers examined in the present document have been formally evaluated in randomized controlled trials of screening strategies with clinical events as outcomes. Nevertheless, this approach balances an understanding of an individual’s absolute risk of CVD and potential treatment benefits against the potential absolute risks for harm from therapy. With the use of this framework, treatment can be targeted to those most likely to benefit without undue risk of harm, in the context of a “risk discussion.” A risk discussion could include the assessment of the patient’s risk of ASCVD, as well as potential benefits, negative aspects, risks, and patient preferences with regard to initiation of relevant preventive therapies.By its nature, such an approach requires a platform for reliable quantitative estimation of absolute risk based on data from representative population samples. It is important to note that risk estimation is based on group averages, which are then applied to individual patients in practice. This process is admittedly imperfect; no one has 10% or 20% of a heart attack during a 10-year period. Individuals with the same estimated risk will either have or not have the event of interest, and only those patients who are destined to have an event can have their event prevented by therapy. The criticism of the risk-estimation approach to treatment decision making also applies to the alternative, and much less efficient approach, of checking the patient’s characteristics against numerous and complex inclusion and exclusion criteria for a potentially large number of pertinent trials. Only a small fraction of trial participants have events, and only a fraction of these events are prevented by therapy. Using either approach, the clinician must apply the average results obtained from groups of patients to the individual patient in practice.Given the modification and adoption of the Framingham 10-year risk score for CHD risk assessment by the Third Report of the National Cholesterol Education Program Expert Work Group on Diagnosis, Evaluation, and Treatment of High Blood Cholesterol in Adults (Adult Treatment Panel III)24 and the uptake of this algorithm by practice sites across the United States, the Work Group began by discussing the value of retaining this algorithm. In collaboration with other NHLBI panels, the Work Group decided not to use this algorithm in its 2013 recommendations because of the algorithm's derivation in an exclusively white sample population and the limited scope of the outcome (in determining CHD alone). Rather, the Work Group derived risk equations from community-based cohorts that are broadly representative of the US population of whites and African Americans, and the Work Group focused on estimation of first hard ASCVD events (defined as first occurrence of nonfatal myocardial infarction, CHD death, or fatal or nonfatal stroke) as the outcome of interest because they were deemed to be of greater relevance to both patients and providers. The focus on hard ASCVD, rather than CHD alone, is also consistent with evidence reviewed in a statement from the AHA and American Stroke Association calling for the inclusion of ischemic stroke in the outcome of interest for CVD risk assessment.25Numerous multivariable risk scores and equations have been derived and published (Appendix 6; for more details, see the Full Work Group Report supplement). As part of its deliberations, the Work Group considered previously published risk scores with validation in NHLBI cohort data as one possible approach. However, several persistent concerns with existing risk equations were identified, including nonrepresentative or historically dated populations, limited ethnic diversity, narrowly defined endpoints, endpoints influenced by provider preferences (eg, elective revascularizations), and endpoints with poor reliability (eg, angina and heart failure). Given the inherent limitations of existing scores, the Work Group judged that a new risk score was needed to address some of the deficiencies of existing scores—for example, the need for a population sample that approaches, to the degree possible, the ideal sample for algorithm development and closely represents the US population.Data are sparse on the use and impact of absolute risk scores in clinical practice in primary-prevention settings.26 Two systematic reviews, based on few studies, support the conclusion that risk assessment, combined with counseling, is associated with favorable but modest changes in patient knowledge and intention to change and in provider prescribing behavior and risk factor control.27,28 No data are available on hard event outcomes. The Work Group specifically calls for research in this area (Section 8).The Work Group notes that the “2009 ACCF/AHA Performance Measures for the Primary Prevention of Cardiovascular Disease in Adults” specifically recommended use of global CVD risk estimation in clinical practice.29 Likewise, the US Preventive Services Task Force recommendations for aspirin,30 the NHLBI Adult Treatment Panel III recommendations,24 and European31 and Canadian32,33 guidelines for primary prevention of CVD, among others, have all recommended the use of absolute risk assessment for decision making about the intensity of lifestyle and pharmacological preventive interventions. Risk scores have been implemented in practice through paper scoring sheets and, increasingly, through Web sites and downloadable applications. The electronic medical record can be adapted to estimate absolute risks automatically by using patient data and published equations, and it is anticipated that risk estimation with this technology will become a mainstream application of the current and future risk algorithms.4. Development of New Pooled Cohort ASCVD Risk EquationsHaving made the decision to develop new equations to estimate the 10-year risk of developing a first ASCVD event, the Work Group used the best available data from community-based cohorts of adults, with adjudicated endpoints for CHD death, nonfatal myocardial infarction, and fatal or nonfatal stroke. Cohorts that included African-American or white participants with at least 12 years of follow-up were included. Data from other racial/ethnic groups were insufficient, precluding their inclusion in the final analyses. The final pooled cohorts included participants from several large, racially and geographically diverse, modern NHLBI-sponsored cohort studies, including the ARIC (Atherosclerosis Risk in Communities) study,8 the Cardiovascular Health Study,5 and the CARDIA (Coronary Artery Risk Development in Young Adults) study,7 combined with applicable data from the Framingham Original and Offspring Study cohorts.4,6The Work Group used state-of-the-art statistical methods to derive and internally validate the Pooled Cohort Equations, which provide sex- and race-specific estimates of the 10-year risk of ASCVD for African-American and white men and women 40 to 79 years of age. The variables that statistically merit inclusion in the risk assessment equations are age, total cholesterol, high-density lipoprotein cholesterol, systolic BP (including treated or untreated status), diabetes mellitus (diabetes), and current smoking status.An expanded description of the derivation and validation of the Pooled Cohort Equations, as well as the means for implementing them in clinical practice, is provided in Appendix 7. Additional details are provided in the Full Work Group Report supplement. A specific clinical vignette is also provided as an example in Appendix 7. In the clinical vignette, the 10-year risk is calculated for a patient 55 years of age who is a nonsmoker without diabetes, and with total cholesterol level of 213 mg/dL, high-density lipoprotein cholesterol level of 50 mg/dL, and untreated systolic BP of 120 mm Hg. With these values used in the Pooled Cohort Equations, the predicted 10-year ASCVD risks are 2.1% for white women, 3.0% for African-American women, 5.3% for white men, and 6.1% for African-American men.Numerous other potential risk markers were considered for inclusion in the Pooled Cohort Equations: for many, no additional utility was demonstrated when they were included; for others, data are insufficient at the present time to determine their additional value. The equations were also assessed in external validation studies with data from other available cohorts. Other than the Framingham CHD risk score (and its derivative ATP III risk assessment profile) and the European SCORE (System for Cardiac Operative Risk Evaluation) algorithm for CVD death, these equations have been subjected to more rigorous validation than other currently available equations, and they are the only risk assessment equations that include significant numbers of African Americans and that focus on estimation of 10-year risk of the clinically relevant endpoint of ASCVD.

HomeHypertensionVol. 71, No. 62017 ACC/AHA/AAPA/ABC/ACPM/AGS/APhA/ASH/ASPC/NMA/PCNA Guideline for the Prevention, Detection, Evaluation, and Management of High Blood Pressure in Adults: Executive Summary: A Report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines Free AccessReview ArticlePDF/EPUBAboutView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissionsDownload Articles + Supplements ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toSupplemental MaterialFree AccessReview ArticlePDF/EPUB2017 ACC/AHA/AAPA/ABC/ACPM/AGS/APhA/ASH/ASPC/NMA/PCNA Guideline for the Prevention, Detection, Evaluation, and Management of High Blood Pressure in Adults: Executive Summary: A Report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines Paul K. Whelton, MB, MD, MSc, FAHA, Robert M. Carey, MD, FAHA, Wilbert S. Aronow, MD, FACC, FAHA, Donald E. CaseyJr, MD, MPH, MBA, FAHA, Karen J. Collins, MBA, Cheryl Dennison Himmelfarb, RN, ANP, PhD, FAHA, Sondra M. DePalma, MHS, PA-C, CLS, AACC, Samuel Gidding, MD, FAHA, Kenneth A. Jamerson, MD, Daniel W. Jones, MD, FAHA, Eric J. MacLaughlin, PharmD, Paul Muntner, PhD, FAHA, Bruce Ovbiagele, MD, MSc, MAS, MBA, FAHA, Sidney C. SmithJr, MD, MACC, FAHA, Crystal C. Spencer, JD, Randall S. Stafford, MD, PhD, Sandra J. Taler, MD, FAHA, Randal J. Thomas, MD, MS, FACC, FAHA, Kim A. WilliamsSr, MD, MACC, FAHA, Jeff D. Williamson, MD, MHS and Jackson T. WrightJr, MD, PhD, FAHA Paul K. WheltonPaul K. Whelton Search for more papers by this author , Robert M. CareyRobert M. Carey Search for more papers by this author , Wilbert S. AronowWilbert S. Aronow *American Society for Preventive Cardiology Representative. †ACC/AHA Representative. ‡Lay Volunteer/Patient Representative. §Preventive Cardiovascular Nurses Association Representative. ‖American Academy of Physician Assistants Representative. ¶Task Force Liaison. #Association of Black Cardiologists Representative. **American Pharmacists Association Representative. ††ACC/AHA Prevention Subcommittee Liaison. ‡‡American College of Preventive Medicine Representative. §§American Society of Hypertension Representative. ‖‖Task Force on Performance Measures Liaison. ¶¶American Geriatrics Society Representative. ##National Medical Association Representative. ***Former Task Force member; current member during the writing effort. Search for more papers by this author , Donald E. CaseyJrDonald E. CaseyJr *American Society for Preventive Cardiology Representative. †ACC/AHA Representative. ‡Lay Volunteer/Patient Representative. §Preventive Cardiovascular Nurses Association Representative. ‖American Academy of Physician Assistants Representative. ¶Task Force Liaison. #Association of Black Cardiologists Representative. **American Pharmacists Association Representative. ††ACC/AHA Prevention Subcommittee Liaison. ‡‡American College of Preventive Medicine Representative. §§American Society of Hypertension Representative. ‖‖Task Force on Performance Measures Liaison. ¶¶American Geriatrics Society Representative. ##National Medical Association Representative. ***Former Task Force member; current member during the writing effort. Search for more papers by this author , Karen J. CollinsKaren J. Collins *American Society for Preventive Cardiology Representative. †ACC/AHA Representative. ‡Lay Volunteer/Patient Representative. §Preventive Cardiovascular Nurses Association Representative. ‖American Academy of Physician Assistants Representative. ¶Task Force Liaison. #Association of Black Cardiologists Representative. **American Pharmacists Association Representative. ††ACC/AHA Prevention Subcommittee Liaison. ‡‡American College of Preventive Medicine Representative. §§American Society of Hypertension Representative. ‖‖Task Force on Performance Measures Liaison. ¶¶American Geriatrics Society Representative. ##National Medical Association Representative. ***Former Task Force member; current member during the writing effort. Search for more papers by this author , Cheryl Dennison HimmelfarbCheryl Dennison Himmelfarb *American Society for Preventive Cardiology Representative. †ACC/AHA Representative. ‡Lay Volunteer/Patient Representative. §Preventive Cardiovascular Nurses Association Representative. ‖American Academy of Physician Assistants Representative. ¶Task Force Liaison. #Association of Black Cardiologists Representative. **American Pharmacists Association Representative. ††ACC/AHA Prevention Subcommittee Liaison. ‡‡American College of Preventive Medicine Representative. §§American Society of Hypertension Representative. ‖‖Task Force on Performance Measures Liaison. ¶¶American Geriatrics Society Representative. ##National Medical Association Representative. ***Former Task Force member; current member during the writing effort. Search for more papers by this author , Sondra M. DePalmaSondra M. DePalma *American Society for Preventive Cardiology Representative. †ACC/AHA Representative. ‡Lay Volunteer/Patient Representative. §Preventive Cardiovascular Nurses Association Representative. ‖American Academy of Physician Assistants Representative. ¶Task Force Liaison. #Association of Black Cardiologists Representative. **American Pharmacists Association Representative. ††ACC/AHA Prevention Subcommittee Liaison. ‡‡American College of Preventive Medicine Representative. §§American Society of Hypertension Representative. ‖‖Task Force on Performance Measures Liaison. ¶¶American Geriatrics Society Representative. ##National Medical Association Representative. ***Former Task Force member; current member during the writing effort. Search for more papers by this author , Samuel GiddingSamuel Gidding *American Society for Preventive Cardiology Representative. †ACC/AHA Representative. ‡Lay Volunteer/Patient Representative. §Preventive Cardiovascular Nurses Association Representative. ‖American Academy of Physician Assistants Representative. ¶Task Force Liaison. #Association of Black Cardiologists Representative. **American Pharmacists Association Representative. ††ACC/AHA Prevention Subcommittee Liaison. ‡‡American College of Preventive Medicine Representative. §§American Society of Hypertension Representative. ‖‖Task Force on Performance Measures Liaison. ¶¶American Geriatrics Society Representative. ##National Medical Association Representative. ***Former Task Force member; current member during the writing effort. Search for more papers by this author , Kenneth A. JamersonKenneth A. Jamerson *American Society for Preventive Cardiology Representative. †ACC/AHA Representative. ‡Lay Volunteer/Patient Representative. §Preventive Cardiovascular Nurses Association Representative. ‖American Academy of Physician Assistants Representative. ¶Task Force Liaison. #Association of Black Cardiologists Representative. **American Pharmacists Association Representative. ††ACC/AHA Prevention Subcommittee Liaison. ‡‡American College of Preventive Medicine Representative. §§American Society of Hypertension Representative. ‖‖Task Force on Performance Measures Liaison. ¶¶American Geriatrics Society Representative. ##National Medical Association Representative. ***Former Task Force member; current member during the writing effort. Search for more papers by this author , Daniel W. JonesDaniel W. Jones *American Society for Preventive Cardiology Representative. †ACC/AHA Representative. ‡Lay Volunteer/Patient Representative. §Preventive Cardiovascular Nurses Association Representative. ‖American Academy of Physician Assistants Representative. ¶Task Force Liaison. #Association of Black Cardiologists Representative. **American Pharmacists Association Representative. ††ACC/AHA Prevention Subcommittee Liaison. ‡‡American College of Preventive Medicine Representative. §§American Society of Hypertension Representative. ‖‖Task Force on Performance Measures Liaison. ¶¶American Geriatrics Society Representative. ##National Medical Association Representative. ***Former Task Force member; current member during the writing effort. Search for more papers by this author , Eric J. MacLaughlinEric J. MacLaughlin *American Society for Preventive Cardiology Representative. †ACC/AHA Representative. ‡Lay Volunteer/Patient Representative. §Preventive Cardiovascular Nurses Association Representative. ‖American Academy of Physician Assistants Representative. ¶Task Force Liaison. #Association of Black Cardiologists Representative. **American Pharmacists Association Representative. ††ACC/AHA Prevention Subcommittee Liaison. ‡‡American College of Preventive Medicine Representative. §§American Society of Hypertension Representative. ‖‖Task Force on Performance Measures Liaison. ¶¶American Geriatrics Society Representative. ##National Medical Association Representative. ***Former Task Force member; current member during the writing effort. Search for more papers by this author , Paul MuntnerPaul Muntner *American Society for Preventive Cardiology Representative. †ACC/AHA Representative. ‡Lay Volunteer/Patient Representative. §Preventive Cardiovascular Nurses Association Representative. ‖American Academy of Physician Assistants Representative. ¶Task Force Liaison. #Association of Black Cardiologists Representative. **American Pharmacists Association Representative. ††ACC/AHA Prevention Subcommittee Liaison. ‡‡American College of Preventive Medicine Representative. §§American Society of Hypertension Representative. ‖‖Task Force on Performance Measures Liaison. ¶¶American Geriatrics Society Representative. ##National Medical Association Representative. ***Former Task Force member; current member during the writing effort. Search for more papers by this author , Bruce OvbiageleBruce Ovbiagele *American Society for Preventive Cardiology Representative. †ACC/AHA Representative. ‡Lay Volunteer/Patient Representative. §Preventive Cardiovascular Nurses Association Representative. ‖American Academy of Physician Assistants Representative. ¶Task Force Liaison. #Association of Black Cardiologists Representative. **American Pharmacists Association Representative. ††ACC/AHA Prevention Subcommittee Liaison. ‡‡American College of Preventive Medicine Representative. §§American Society of Hypertension Representative. ‖‖Task Force on Performance Measures Liaison. ¶¶American Geriatrics Society Representative. ##National Medical Association Representative. ***Former Task Force member; current member during the writing effort. Search for more papers by this author , Sidney C. SmithJrSidney C. SmithJr *American Society for Preventive Cardiology Representative. †ACC/AHA Representative. ‡Lay Volunteer/Patient Representative. §Preventive Cardiovascular Nurses Association Representative. ‖American Academy of Physician Assistants Representative. ¶Task Force Liaison. #Association of Black Cardiologists Representative. **American Pharmacists Association Representative. ††ACC/AHA Prevention Subcommittee Liaison. ‡‡American College of Preventive Medicine Representative. §§American Society of Hypertension Representative. ‖‖Task Force on Performance Measures Liaison. ¶¶American Geriatrics Society Representative. ##National Medical Association Representative. ***Former Task Force member; current member during the writing effort. Search for more papers by this author , Crystal C. SpencerCrystal C. Spencer *American Society for Preventive Cardiology Representative. †ACC/AHA Representative. ‡Lay Volunteer/Patient Representative. §Preventive Cardiovascular Nurses Association Representative. ‖American Academy of Physician Assistants Representative. ¶Task Force Liaison. #Association of Black Cardiologists Representative. **American Pharmacists Association Representative. ††ACC/AHA Prevention Subcommittee Liaison. ‡‡American College of Preventive Medicine Representative. §§American Society of Hypertension Representative. ‖‖Task Force on Performance Measures Liaison. ¶¶American Geriatrics Society Representative. ##National Medical Association Representative. ***Former Task Force member; current member during the writing effort. Search for more papers by this author , Randall S. StaffordRandall S. Stafford *American Society for Preventive Cardiology Representative. †ACC/AHA Representative. ‡Lay Volunteer/Patient Representative. §Preventive Cardiovascular Nurses Association Representative. ‖American Academy of Physician Assistants Representative. ¶Task Force Liaison. #Association of Black Cardiologists Representative. **American Pharmacists Association Representative. ††ACC/AHA Prevention Subcommittee Liaison. ‡‡American College of Preventive Medicine Representative. §§American Society of Hypertension Representative. ‖‖Task Force on Performance Measures Liaison. ¶¶American Geriatrics Society Representative. ##National Medical Association Representative. ***Former Task Force member; current member during the writing effort. Search for more papers by this author , Sandra J. TalerSandra J. Taler *American Society for Preventive Cardiology Representative. †ACC/AHA Representative. ‡Lay Volunteer/Patient Representative. §Preventive Cardiovascular Nurses Association Representative. ‖American Academy of Physician Assistants Representative. ¶Task Force Liaison. #Association of Black Cardiologists Representative. **American Pharmacists Association Representative. ††ACC/AHA Prevention Subcommittee Liaison. ‡‡American College of Preventive Medicine Representative. §§American Society of Hypertension Representative. ‖‖Task Force on Performance Measures Liaison. ¶¶American Geriatrics Society Representative. ##National Medical Association Representative. ***Former Task Force member; current member during the writing effort. Search for more papers by this author , Randal J. ThomasRandal J. Thomas *American Society for Preventive Cardiology Representative. †ACC/AHA Representative. ‡Lay Volunteer/Patient Representative. §Preventive Cardiovascular Nurses Association Representative. ‖American Academy of Physician Assistants Representative. ¶Task Force Liaison. #Association of Black Cardiologists Representative. **American Pharmacists Association Representative. ††ACC/AHA Prevention Subcommittee Liaison. ‡‡American College of Preventive Medicine Representative. §§American Society of Hypertension Representative. ‖‖Task Force on Performance Measures Liaison. ¶¶American Geriatrics Society Representative. ##National Medical Association Representative. ***Former Task Force member; current member during the writing effort. Search for more papers by this author , Kim A. WilliamsSrKim A. WilliamsSr *American Society for Preventive Cardiology Representative. †ACC/AHA Representative. ‡Lay Volunteer/Patient Representative. §Preventive Cardiovascular Nurses Association Representative. ‖American Academy of Physician Assistants Representative. ¶Task Force Liaison. #Association of Black Cardiologists Representative. **American Pharmacists Association Representative. ††ACC/AHA Prevention Subcommittee Liaison. ‡‡American College of Preventive Medicine Representative. §§American Society of Hypertension Representative. ‖‖Task Force on Performance Measures Liaison. ¶¶American Geriatrics Society Representative. ##National Medical Association Representative. ***Former Task Force member; current member during the writing effort. Search for more papers by this author , Jeff D. WilliamsonJeff D. Williamson *American Society for Preventive Cardiology Representative. †ACC/AHA Representative. ‡Lay Volunteer/Patient Representative. §Preventive Cardiovascular Nurses Association Representative. ‖American Academy of Physician Assistants Representative. ¶Task Force Liaison. #Association of Black Cardiologists Representative. **American Pharmacists Association Representative. ††ACC/AHA Prevention Subcommittee Liaison. ‡‡American College of Preventive Medicine Representative. §§American Society of Hypertension Representative. ‖‖Task Force on Performance Measures Liaison. ¶¶American Geriatrics Society Representative. ##National Medical Association Representative. ***Former Task Force member; current member during the writing effort. Search for more papers by this author and Jackson T. WrightJrJackson T. WrightJr *American Society for Preventive Cardiology Representative. †ACC/AHA Representative. ‡Lay Volunteer/Patient Representative. §Preventive Cardiovascular Nurses Association Representative. ‖American Academy of Physician Assistants Representative. ¶Task Force Liaison. #Association of Black Cardiologists Representative. **American Pharmacists Association Representative. ††ACC/AHA Prevention Subcommittee Liaison. ‡‡American College of Preventive Medicine Representative. §§American Society of Hypertension Representative. ‖‖Task Force on Performance Measures Liaison. ¶¶American Geriatrics Society Representative. ##National Medical Association Representative. ***Former Task Force member; current member during the writing effort. Search for more papers by this author Originally published13 Nov 2017https://doi.org/10.1161/HYP.0000000000000066Hypertension. 2018;71:1269–1324is corrected byCorrection to: 2017 ACC/AHA/AAPA/ABC/ACPM/AGS/APhA/ASH/ASPC/NMA/PCNA Guideline for the Prevention, Detection, Evaluation, and Management of High Blood Pressure in Adults: Executive Summary: A Report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice GuidelinesCorrection to: 2017 ACC/AHA/AAPA/ABC/ACPM/AGS/APhA/ASH/ASPC/NMA/PCNA Guideline for the Prevention, Detection, Evaluation, and Management of High Blood Pressure in Adults: Executive Summary: A Report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice GuidelinesOther version(s) of this articleYou are viewing the most recent version of this article. Previous versions: Previous Version of Record January 1, 2017: Previous Version 1 Table of ContentsPreamble 12701.Introduction 12721.1.Methodology and Evidence Review 12721.2.Organization of the Writing Committee 12731.3.Document Review and Approval 12741.4.Scope of the Guideline 12741.5.Abbreviations and Acronyms 12742.BP and CVD Risk 12742.1.Observational Relationship 12742.2.BP Components 12762.3.Population Risk 12762.4.Coexistence of Hypertension and Related Chronic Conditions 12763.Classification of BP 12763.1.Definition of High BP 12763.2.Lifetime Risk of Hypertension 12773.3.Prevalence of High BP 12774.Measurement of BP 12774.1.Accurate Measurement of BP in the Office 12774.2.Out-of-Office and Self-Monitoring of BP 12784.3.Masked and White Coat Hypertension 12785.Causes of Hypertension 12815.1.Secondary Forms of Hypertension 12815.1.1.Drugs and Other Substances With Potential to Impair BP Control 12835.1.2.Primary Aldosteronism 12835.1.3.Renal Artery Stenosis 12835.1.4.Obstructive Sleep Apnea 12846.Nonpharmacological Interventions 12847.Patient Evaluation 12867.1.Laboratory Tests and Other Diagnostic Procedures 12868.Treatment of High BP 12868.1.Pharmacological Treatment 12868.1.1.Initiation of Pharmacological BP Treatment in the Context of Overall CVD Risk 12868.1.2.BP Treatment Threshold and the Use of CVD Risk Estimation to Guide Drug Treatment of Hypertension 12868.1.3.Follow-Up After Initial BP Evaluation 12878.1.4.General Principles of Drug Therapy 12888.1.5.BP Goal for Patients With Hypertension 12908.1.6.Choice of Initial Medication 12908.2.Follow-Up of BP During Antihypertensive Drug Therapy 12908.2.1.Follow-Up After Initiating Antihypertensive Drug Therapy 12908.2.2.Monitoring Strategies to Improve Control of BP in Patients on Drug Therapy for High BP 12919.Hypertension in Patients With Comorbidities 12919.1.Stable Ischemic Heart Disease 12919.2.Heart Failure 12929.2.1.Heart Failure With Reduced Ejection Fraction 12929.2.2.Heart Failure With Preserved Ejection Fraction 12929.3.Chronic Kidney Disease 12929.3.1.Hypertension After Renal Transplantation 12929.4.Cerebrovascular Disease 12939.4.1.Acute Intracerebral Hemorrhage 12939.4.2.Acute Ischemic Stroke 12939.4.3.Secondary Stroke Prevention 12949.5.Peripheral Artery Disease 12959.6.Diabetes Mellitus 12959.7.Metabolic Syndrome 12969.8.Atrial Fibrillation 12969.9.Valvular Heart Disease 12969.10.Aortic Disease 129610.Special Patient Groups 129610.1.1.Racial and Ethnic Differences in Treatment 129610.2.Sex-Related Issues 129610.2.1.Women 129710.2.2.Pregnancy 129710.3.Age-Related Issues 129710.3.1.Older Persons 129711.Other Considerations 129811.1.Resistant Hypertension 129811.2.Hypertensive Crises—Emergencies and Urgencies 129811.3.Cognitive Decline and Dementia 130111.4.Patients Undergoing Surgical Procedures 130112.Strategies to Improve Hypertension Treatment and Control 130112.1.Adherence Strategies for Treatment of Hypertension 130112.1.1.Antihypertensive Medication Adherence Strategies 130112.1.2.Strategies to Promote Lifestyle Modification 130112.2.Structured, Team-Based Care Interventions for Hypertension Control 130112.3.Health Information Technology–Based Strategies to Promote Hypertension Control 130212.3.1.EHR and Patient Registries 130212.3.2.Telehealth Interventions to Improve Hypertension Control 130212.4.Improving Quality of Care for Patients With Hypertension 130212.4.1.Performance Measures 130212.4.2.Quality Improvement Strategies 130212.5.Financial Incentives 130213.The Plan of Care for Hypertension 130213.1.Health Literacy 130313.2.Access to Health Insurance and Medication Assistance Plans 130313.3.Social and Community Services 130314.Summary of BP Thresholds and Goals for Pharmacological Therapy 1304References 1304Appendix 1.Author Relationships With Industry and Other Entities (Relevant) 1317Appendix 2.Reviewer Relationships With Industry and Other Entities (Comprehensive) 1319PreambleSince 1980, the American College of Cardiology (ACC) and American Heart Association (AHA) have translated scientific evidence into clinical practice guidelines (guidelines) with recommendations to improve cardiovascular health. In 2013, the National Heart, Lung, and Blood Institute (NHLBI) Advisory Council recommended that the NHLBI focus specifically on reviewing the highest-quality evidence and partner with other organizations to develop recommendations.P-1,P-2 Accordingly, the ACC and AHA collaborated with the NHLBI and stakeholder and professional organizations to complete and publish 4 guidelines (on assessment of cardiovascular risk, lifestyle modifications to reduce cardiovascular risk, management of blood cholesterol in adults, and management of overweight and obesity in adults) to make them available to the widest possible constituency. In 2014, the ACC and AHA, in partnership with several other professional societies, initiated a guideline on the prevention, detection, evaluation, and management of high blood pressure (BP) in adults. Under the management of the ACC/AHA Task Force, a Prevention Subcommittee was appointed to help guide development of the suite of guidelines on prevention of cardiovascular disease (CVD). These guidelines, which are based on systematic methods to evaluate and classify evidence, provide a cornerstone for quality cardiovascular care. The ACC and AHA sponsor the development and publication of guidelines without commercial support, and members of each organization volunteer their time to the writing and review efforts. Guidelines are official policy of the ACC and AHA.Intended UsePractice guidelines provide recommendations applicable to patients with or at risk of developing CVD. The focus is on medical practice in the United States, but guidelines developed in collaboration with other organizations can have a global impact. Although guidelines may be used to inform regulatory or payer decisions, they are intended to improve patients’ quality of care and align with patients’ interests. Guidelines are intended to define practices meeting the needs of patients in most, but not all, circumstances and should not replace clinical judgment.Clinical ImplementationManagement in accordance with guideline recommendations is effective only when followed by both practitioners and patients. Adherence to recommendations can be enhanced by shared decision making between clinicians and patients, with patient engagement in selecting interventions on the basis of individual values, preferences, and associated conditions and comorbidities.Methodology and ModernizationThe ACC/AHA Task Force on Clinical Practice Guidelines (Task Force) continuously reviews, updates, and modifies guideline methodology on the basis of published standards from organizations, including the Institute of Medicine,P-3,P-4 and on the basis of internal reevaluation. Similarly, the presentation and delivery of guidelines are reevaluated and modified on the basis of evolving technologies and other factors to facilitate optimal dissemination of information to healthcare professionals at the point of care.Toward this goal, this guideline continues the introduction of an evolved format of presenting guideline recommendations and associated text called the “modular knowledge chunk format.” Each modular “chunk” includes a table of related recommendations, a brief synopsis, recommendation-specific supportive text, and when appropriate, flow diagrams or additional tables. References are provided within the modular chunk itself to facilitate quick review. Additionally, this format will facilitate seamless updating of guidelines with focused updates as new evidence is published, as well as content tagging for rapid electronic retrieval of related recommendations on a topic of interest. This evolved approach format was instituted when this guideline was near completion; therefore, the present document represents a transitional format that best suits the text as written. Future guidelines will fully implement this format, including provisions for limiting the amount of text in a guideline.Recognizing the importance of cost–value considerations in certain guidelines, when appropriate and feasible, an analysis of the value of a drug, device, or intervention may be performed in accordance with the ACC/AHA methodology.P-5To ensure that guideline recommendations remain current, new data are reviewed on an ongoing basis, with full guideline revisions commissioned in approximately 6-year cycles. Publication of new, potentially practice-changing study results that are relevant to an existing or new drug, device, or management strategy will prompt evaluation by the Task Force, in consultation with the relevant guideline writing committee, to determine whether a focused update should be commissioned. For additional information and policies regarding guideline development, we encourage readers to consult the ACC/AHA guideline methodology manualP-6 and other methodology articles.P-7–P-10Selection of Writing Committee MembersThe Task Force strives to avoid bias by selecting experts from a broad array of backgrounds. Writing committee members represent different geographic regions, sexes, ethnicities, races, intellectual perspectives/biases, and scopes of clinical practice. The Task Force may also invite organizations and professional societies with related interests and expertise to participate as partners, collaborators, or endorsers.Relationships With Industry and Other EntitiesThe ACC and AHA have rigorous policies and methods to ensure that guidelines are developed without bias or improper influence. The complete relationships with industry and other entities (RWI) policy can be found online. Appendix 1 of the present document lists writing committee members’ relevant RWI. For the purposes of full transparency, writing committee members’ comprehensive disclosure information is available online. Comprehensive disclosure information for the Task Force is available online.Evidence Review and Evidence Review CommitteesIn developing recommendations, the writing committee uses evidence-based methodologies that are based on all available data.P-6–P-9 Literature searches focus on randomized controlled trials (RCTs) but also include registries, nonrandomized comparative and descriptive studies, case series, cohort studies, systematic reviews, and expert opinion. Only key references are cited.An independent evidence review committee (ERC) is commissioned when there are 1 or more questions deemed of utmost clinical importance that merit formal systematic review. The systematic review will determine which patients are most likely to benefit from a drug, device, or treatment strategy and to what degree. Criteria for commissioning an ERC and formal systematic review include: a) the absence of a current authoritative systematic review, b) the feasibility of defining the benefit and risk in a time frame consistent with the writing of a guideline, c) the relevance to a substantial number of patients, and d) the likelihood that the findings can be translated into actionable recommendations. ERC members may include methodologists, epidemiologists, healthcare providers, and biostatisticians. The recommendations developed by the writing committee on the basis of the systematic review are marked with “SR.”Guideline-Directed Management and TherapyThe term guideline-directed management and therapy (GDMT) encompasses clinical evaluation, diagnostic testing, and pharmacological and procedural treatments. For these and all recommended drug treatment regimens, the reader should confirm the dosage by reviewing product insert material and evaluate the treatment regimen for contraindications and interactions. The recommendations are limited to drugs, devices, and treatments approved for clinical use in the United States.Class of Recommendation and Level of EvidenceThe Class of Recommendation (COR) indicates the strength of the recommendation, encompassing the estimated magnitude and certainty of benefit in proportion t

HomeCirculationVol. 140, No. 112019 ACC/AHA Guideline on the Primary Prevention of Cardiovascular Disease: Executive Summary: A Report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines Free AccessReview ArticlePDF/EPUBAboutView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissionsDownload Articles + Supplements ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toSupplementary MaterialsFree AccessReview ArticlePDF/EPUB2019 ACC/AHA Guideline on the Primary Prevention of Cardiovascular Disease: Executive Summary: A Report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines Donna K. Arnett, PhD, MSPH, FAHA, Co-Chair, Roger S. Blumenthal, MD, FACC, FAHA, Co-Chair, Michelle A. Albert, MD, MPH, FAHA, Andrew B. Buroker, Esq, Zachary D. Goldberger, MD, MS, FACC, FAHA, Ellen J. Hahn, PhD, RN, Cheryl Dennison Himmelfarb, PhD, RN, ANP, FAHA, Amit Khera, MD, MSc, FACC, FAHA, Donald Lloyd-Jones, MD, SCM, FACC, FAHA, J. William McEvoy, MBBCh, MEd, MHS, Erin D. Michos, MD, MHS, FACC, FAHA, Michael D. Miedema, MD, MPH, Daniel Muñoz, MD, MPA, FACC, Sidney C. Smith Jr, MD, MACC, FAHA, Salim S. Virani, MD, PhD, FACC, FAHA, Kim A. Williams Sr, MD, MACC, FAHA, Joseph Yeboah, MD, MS, FACC, FAHA and Boback Ziaeian, MD, PhD, FACC, FAHA Donna K. ArnettDonna K. Arnett Search for more papers by this author , Roger S. BlumenthalRoger S. Blumenthal Search for more papers by this author , Michelle A. AlbertMichelle A. Albert Search for more papers by this author , Andrew B. BurokerAndrew B. Buroker Search for more papers by this author , Zachary D. GoldbergerZachary D. Goldberger Search for more papers by this author , Ellen J. HahnEllen J. Hahn Search for more papers by this author , Cheryl Dennison HimmelfarbCheryl Dennison Himmelfarb Search for more papers by this author , Amit KheraAmit Khera Search for more papers by this author , Donald Lloyd-JonesDonald Lloyd-Jones Search for more papers by this author , J. William McEvoyJ. William McEvoy Search for more papers by this author , Erin D. MichosErin D. Michos Search for more papers by this author , Michael D. MiedemaMichael D. Miedema Search for more papers by this author , Daniel MuñozDaniel Muñoz Search for more papers by this author , Sidney C. Smith JrSidney C. Smith Jr Search for more papers by this author , Salim S. ViraniSalim S. Virani Search for more papers by this author , Kim A. Williams SrKim A. Williams Sr Search for more papers by this author , Joseph YeboahJoseph Yeboah Search for more papers by this author and Boback ZiaeianBoback Ziaeian Search for more papers by this author Originally published17 Mar 2019https://doi.org/10.1161/CIR.0000000000000677Circulation. 2019;140:e563–e595is corrected byCorrection to: 2019 ACC/AHA Guideline on the Primary Prevention of Cardiovascular Disease: Executive Summary: A Report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice GuidelinesCorrection to: 2019 ACC/AHA Guideline on the Primary Prevention of Cardiovascular Disease: Executive Summary: A Report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice GuidelinesCorrection to: 2019 ACC/AHA Guideline on the Primary Prevention of Cardiovascular Disease: Executive Summary: A Report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice GuidelinesOther version(s) of this articleYou are viewing the most recent version of this article. Previous versions: January 27, 2020: Previous Version of Record September 9, 2019: Previous Version of Record March 17, 2019: Ahead of Print Table of ContentsTop 10 Take-Home Messages for the Primary Prevention of Cardiovascular Disease e564Preamble e5641. Introduction e5651.1. Methodology and Evidence Review e5661.2. Organization of the Writing Committee e5661.3. Document Review and Approval e5661.4. Scope of the Guideline e5671.5. Class of Recommendation and Level of Evidence e5671.6. Abbreviations e5682. Overarching Recommendations for ASCVD Prevention Efforts e5682.1. Patient-Centered Approaches to Comprehensive ASCVD Prevention e5682.2. Assessment of Cardiovascular Risk e5693. Lifestyle Factors Affecting Cardiovascular Risk e5703.1. Nutrition and Diet e5703.2. Exercise and Physical Activity e5704. Other Factors Affecting Cardiovascular Risk e5704.1. Adults With Overweight and Obesity e5704.2. Adults With Type 2 Diabetes Mellitus e5704.3. Adults With High Blood Cholesterol e5714.4. Adults With High Blood Pressure or Hypertension e5734.5. Treatment of Tobacco Use e5744.6. Aspirin Use e5755. Cost and Value Considerations e5756. Conclusion e576References e578Appendix 1: Search Criteria e585Appendix 2: Author Relationships With Industry and Other Entities (Relevant) e589Appendix 3 Reviewer Relationships With Industry and Other Entities (Comprehensive) e591Top 10 Take-Home Messages for the Primary Prevention of Cardiovascular DiseaseThe most important way to prevent atherosclerotic vascular disease, heart failure, and atrial fibrillation is to promote a healthy lifestyle throughout life.A team-based care approach is an effective strategy for the prevention of cardiovascular disease. Clinicians should evaluate the social determinants of health that affect individuals to inform treatment decisions.Adults who are 40 to 75 years of age and are being evaluated for cardiovascular disease prevention should undergo 10-year atherosclerotic cardiovascular disease (ASCVD) risk estimation and have a clinician–patient risk discussion before starting on pharmacological therapy, such as antihypertensive therapy, a statin, or aspirin. The presence or absence of additional risk-enhancing factors can help guide decisions about preventive interventions in select individuals, as can coronary artery calcium scanning.All adults should consume a healthy diet that emphasizes the intake of vegetables, fruits, nuts, whole grains, lean vegetable or animal protein, and fish and minimizes the intake of trans fats, red meat and processed red meats, refined carbohydrates, and sweetened beverages. For adults with overweight and obesity, counseling and caloric restriction are recommended for achieving and maintaining weight loss.Adults should engage in at least 150 minutes per week of accumulated moderate-intensity physical activity or 75 minutes per week of vigorous-intensity physical activity.For adults with type 2 diabetes mellitus, lifestyle changes, such as improving dietary habits and achieving exercise recommendations are crucial. If medication is indicated, metformin is first-line therapy, followed by consideration of a sodium-glucose cotransporter 2 inhibitor or a glucagon-like peptide-1 receptor agonist.All adults should be assessed at every healthcare visit for tobacco use, and those who use tobacco should be assisted and strongly advised to quit.Aspirin should be used infrequently in the routine primary prevention of ASCVD because of lack of net benefit.Statin therapy is first-line treatment for primary prevention of ASCVD in patients with elevated low-density lipoprotein cholesterol levels (≥190 mg/dL), those with diabetes mellitus, who are 40 to 75 years of age, and those determined to be at sufficient ASCVD risk after a clinician–patient risk discussion.Nonpharmacological interventions are recommended for all adults with elevated blood pressure or hypertension. For those requiring pharmacological therapy, the target blood pressure should generally be <130/80 mm Hg.PreambleSince 1980, the American College of Cardiology (ACC) and American Heart Association (AHA) have translated scientific evidence into clinical practice guidelines with recommendations to improve cardiovascular health. These guidelines, which are based on systematic methods to evaluate and classify evidence, provide a foundation for the delivery of quality cardiovascular care. The ACC and AHA sponsor the development and publication of clinical practice guidelines without commercial support, and members volunteer their time to the writing and review efforts.Clinical practice guidelines provide recommendations applicable to patients with or at risk of developing cardiovascular disease (CVD). The focus is on medical practice in the United States, but these guidelines are relevant to patients throughout the world. Although guidelines may be used to inform regulatory or payer decisions, the goals are to improve quality of care and align with patients’ interests. Guidelines are intended to define practices meeting the needs of patients in most but not all circumstances and should not replace clinical judgment.Recommendations for guideline-directed management and therapy, which encompasses clinical evaluation, diagnostic testing, and both pharmacological and procedural treatments, are effective only when adopted by both practitioners and patients. Adherence to recommendations can be enhanced by shared decision-making between clinicians and patients, with patient engagement in selecting interventions on the basis of individual values, preferences, and associated conditions and comorbidities.The ACC/AHA Task Force on Clinical Practice Guidelines strives to ensure that the guideline writing committee includes requisite expertise and is representative of the broader medical community by selecting experts from a broad array of backgrounds, representing different geographic regions, sexes, races, ethnicities, intellectual perspectives/biases, and scopes of clinical practice. The ACC and AHA have rigorous policies and methods to ensure that documents are developed without bias or improper influence. The complete policy on relationships with industry and other entities (RWI) can be found online.Beginning in 2017, numerous modifications to the guidelines have been and continue to be implemented to make guidelines shorter and enhance “user friendliness.” Guidelines are written and presented in a modular knowledge chunk format, in which each chunk includes a table of recommendations, a brief synopsis, recommendation-specific supportive text and, when appropriate, flow diagrams or additional tables. Hyperlinked references are provided for each modular knowledge chunk to facilitate quick access and review. More structured guidelines—including word limits (“targets”) and a web guideline supplement for useful but noncritical tables and figures—are 2 such changes. This Preamble is an abbreviated version, with the detailed version available online.Patrick T. O’Gara, MD, MACC, FAHAChair, ACC/AHA Task Force on Clinical Practice Guidelines1. IntroductionAlthough there has been substantial improvement in atherosclerotic cardiovascular disease (ASCVD) outcomes in recent decades, ASCVD remains the leading cause of morbidity and mortality globally.S1-1–S1-3 In the United States, it is also the leading cause of death for people of most racial/ethnic groups, with an estimated cost of >$200 billion annually in healthcare services, medications, and lost productivity. Much of this is attributable to suboptimal implementation of prevention strategies and uncontrolled ASCVD risk factors in many adults.S1-2Most Americans who have had a myocardial infarction (MI) had unfavorable levels of at least 1 cardiovascular risk factor before their ASCVD event.S1-4 In 2010, the AHA defined a new model of “ideal cardiovascular health,” referred to as Life’s Simple 7.S1-5 Clinicians will find the 2018 Journal of American College of Cardiology (JACC) Cardiovascular Health Promotion Series very helpful in approaching the various aspects of prevention with patients.S1-6 An increasing number of ideal cardiovascular health factors have been associated with a lower prevalence and incidence of ASCVD events, heart failure, atrial fibrillation, cancer, depression, and cognitive impairment.S1-7 Therefore, moving individuals toward ideal cardiovascular health is critically important for prevention of many important health conditions.The ACC/AHA Task Force on Clinical Practice Guidelines has commissioned this guideline to consolidate existing recommendations and various recent scientific statements, expert consensus documents, and clinical practice guidelines into a single guidance document focused on the primary prevention of ASCVD. However, this guideline also includes newly generated recommendations for aspirin use, exercise and physical activity, and tobacco use, in addition to recommendations related to team-based care, shared decision-making, and assessment of social determinants of health, to create a comprehensive yet targeted ACC/AHA guideline on the prevention of ASCVD. This guideline has been formatted in the modular chunk format to facilitate readability and future updating.Prevention strategies occur at the population level but must also engage individual adults to slow the development of ASCVD. The most important way to prevent ASCVD is to promote a healthy lifestyle throughout life. Prevention strategies must include a strong focus on lifestyle optimization (improvements in diet, physical activity, and avoidance of tobacco use and exposure to secondhand smoke) to minimize the risk of future ASCVD events.A comprehensive patient-centered approach that addresses all aspects of a patient’s lifestyle habits and estimated risk of a future ASCVD event is the first step in deciding on where there may be a need for pharmacotherapy. Even if a blood pressure (BP)–reducing medication, lipid-lowering medication, or diabetes medication is ultimately prescribed, lifestyle goals should be emphasized on a regular basis. Only when a person’s risk is sufficiently high should medications to reduce ASCVD risk be considered as part of a shared decision-making process for optimal treatment. In summary, clinicians and individuals should focus attention on living a healthy lifestyle by referring to these evidence-based recommendations to help prevent ASCVD.1.1. Methodology and Evidence ReviewThis guideline continues the ACC and AHA effort to design a comprehensive yet succinct compilation of practical guidance for the primary prevention of ASCVD and to promote optimal dissemination of information by using concise language and formatting. The recommendations listed in this guideline are evidence based and supported by an extensive evidence review. A search for literature derived from research involving human subjects, published in English, and indexed in Ovid MEDLINE, PubMed, Cochrane Library, National Institute for Health and Care Excellence (NICE), and other selected databases relevant to this guideline, was conducted between May and July 2018. For specific search terms used and years searched per section, please see Appendix 1.Randomized controlled trials (RCTs), systematic reviews of RCTs, meta-analyses, and large, United States–based, high-quality cohort studies, as well as observational studies and systematic reviews of observational studies, were evaluated for their content on the prevention of ASCVD outcomes related to the following 9 topic areas: risk assessment, diet, exercise/physical activity, obesity and weight loss, type 2 diabetes mellitus (T2DM), blood cholesterol, hypertension, smoking cessation, and aspirin use. Previous ACC/AHA guidelines, as well as US Preventive Services Task Force (USPSTF) reviews and other guidance relevant to this guideline, were also assessed. The final evidence tables included in the Online Data Supplement summarize the evidence used to formulate recommendations. References selected and published in this document are representative and not all-inclusive.Avalere Health, a healthcare advisory services firm contracted by ACC/AHA, served as the document manager for this guideline to facilitate its development process. As document manager, Avalere facilitated the deliberations of the writing committee and led the modified Delphi process for establishing the Class of Recommendation and the Level of Evidence. In parallel, an independent health data and epidemiology expert, Lee Ann Prebil, conducted a systematic evidence review for the key topic of exercise and physical activity and conducted targeted literature searches to support this document’s discussion of patient-centered approaches, including team-based care, shared decision-making, and assessment of social determinants of health. A targeted literature search was also conducted for this guideline’s cost and value considerations. These searches are available as downloadable Excel files.Recommendations and supportive text relevant to cardiovascular risk, blood cholesterol, and high BP were taken directly from 2 recently released ACC/AHA guidelines, the 2017 Hypertension Clinical Practice GuidelinesS1.1-1 and the 2018 Cholesterol Clinical Practice Guideline,S1.1-2 and were adapted for the present guideline, which aims to provide an overview of the primary prevention of ASCVD among adults. Recommendations that were adapted from previous publications are noted in the recommendation tables, and both the original published recommendation and the adapted version are provided in the guideline Web Supplement.The results of these evidence reviews were evaluated by the writing committee for incorporation into the present guideline. (See Table S1 in the Web Supplement for a list of relevant publications and statements used in support of the guideline’s recommendations.) Each topic area was assigned a primary writer, as well as a primary, and sometimes secondary, reviewer. These assignments were based on areas of particular expertise of writing committee members. All recommendations were fully reviewed and discussed among the full committee to allow for diverse perspectives and considerations for this guideline. Recommendations were then voted upon, with a modified Delphi process used to reach consensus.1.2. Organization of the Writing CommitteeThe writing committee consisted of clinicians, cardiologists, health services researchers, epidemiologists, internists, nurses, and a lay representative. The writing committee included representatives from the ACC and AHA. Appendix 2 of the present document lists writing committee members’ relevant RWI. For the purposes of full transparency, the writing committee members’ comprehensive disclosure information is available online.1.3. Document Review and ApprovalThis document was reviewed by 5 official reviewers nominated by the ACC and AHA (1 reviewer from the ACC/AHA Task Force for Practice Guidelines, 2 reviewers from the AHA, and 2 reviewers from the ACC); 3 reviewers on behalf of the American Association of Cardiovascular and Pulmonary Rehabilitation, the American Society for Nutrition, and the American Society of Preventive Medicine; and 23 individual content reviewers. Reviewers’ RWI information was distributed to the writing committee and is published in this document (Appendix 3). This document was approved for publication by the governing bodies of the ACC and AHA.1.4. Scope of the GuidelineThis guideline is intended to be a resource for the clinical and public health practice communities. It addresses the primary prevention of CVD in adults (≥18 years of age), focused on outcomes of ASCVD (ie, acute coronary syndromes, MI, stable or unstable angina, arterial revascularization, stroke, transient ischemic attack, or peripheral arterial disease of atherosclerotic origin), as well as heart failure and atrial fibrillation. The guideline presents recommendations to prevent CVD that are related to lifestyle factors (eg, diet and exercise or physical activity), other factors affecting CVD risk (eg, obesity, diabetes, blood cholesterol, high BP, smoking, aspirin use), patient-centered approaches (eg, team-based care, shared decision-making, assessment of social determinants of health), and considerations of the cost and value of primary prevention.1.5. Class of Recommendation and Level of EvidenceRecommendations are designated with both a Class of Recommendation (COR) and a Level of Evidence (LOE). The COR indicates the strength of recommendation, encompassing the estimated magnitude and certainty of benefit in proportion to risk. The LOE rates the quality of scientific evidence supporting the intervention on the basis of the type, quantity, and consistency of data from clinical trials and other sources (Table 1).S1.5-1Table 1. Applying Class of Recommendation and Level of Evidence to Clinical Strategies, Interventions, Treatments, or Diagnostic Testing in Patient Care (Updated August 2015)Table 1. Applying Class of Recommendation and Level of Evidence to Clinical Strategies, Interventions, Treatments, or Diagnostic Testing in Patient Care (Updated August 2015)1.6. AbbreviationsAbbreviationMeaning/PhraseASCVDatherosclerotic cardiovascular diseaseAUAgatston unitsBMIbody mass indexBPblood pressureCHDcoronary heart diseaseCKDchronic kidney diseaseCVDcardiovascular diseaseDASHDietary Approaches to Stop HypertensionDBPdiastolic blood pressureDMdiabetes mellitusENDSelectronic nicotine delivery systemsFDAUS Food and Drug AdministrationGLP-1Rglucagon-like peptide-1 receptorHbA1chemoglobin A1cHDL-Chigh-density lipoprotein cholesterolHbA1chemoglobin A1cLDL-Clow-density lipoprotein cholesterolMImyocardial infarctionPCEpooled cohort equationsRCTrandomized controlled trialSBPsystolic blood pressureSGLT-2sodium-glucose cotransporter 2T2DMtype 2 diabetes mellitusUSPSTFUS Preventive Services Task Force2. Overarching Recommendations for ASCVD Prevention Efforts2.1. Patient-Centered Approaches to Comprehensive ASCVD PreventionTable 2 outlines key considerations related to social determinants of health and ASCVD prevention.Table 2. Example Considerations for Addressing Social Determinants of Health to Help Prevent ASCVD EventsTopic/DomainExample ConsiderationsCardiovascular riskAdults should be routinely assessed for psychosocial stressors and provided with appropriate counseling.S2.1-26Health literacy should be assessed every 4 to 6 y to maximize recommendation effectiveness.S2.1-27DietIn addition to the prescription of diet modifications, body size perception, as well as social and cultural influences, should be assessed.S2.1-28,S2.1-29Potential barriers to adhering to a heart-healthy diet should be assessed, including food access and economic factors; these factors may be particularly relevant to persons from vulnerable populations, such as individuals residing in either inner-city or rural environments, those at socioeconomic disadvantage, and those of advanced age*.S2.1-30Exercise and physical activityIn addition to the prescription of exercise, neighborhood environment and access to facilities for physical activity should be assessed.S2.1-31–S2.1-33Obesity and weight lossLifestyle counseling for weight loss should include assessment of and interventional recommendations for psychosocial stressors, sleep hygiene, and other individualized barriers.S2.1-34–S2.1-36Weight maintenance should be promoted in patients with overweight/obesity who are unable to achieve recommended weight loss.Diabetes mellitusIn addition to the prescription of type 2 diabetes mellitus interventions, environmental and psychosocial factors, including depression, stress, self-efficacy, and social support, should be assessed to improve achievement of glycemic control and adherence to treatment.S2.1-37–S2.1-40High blood pressureShort sleep duration (<6 h) and poor-quality sleep are associated with high blood pressure and should be considered.S2.1-41 Because other lifestyle habits can impact blood pressure, access to a healthy, low-sodium diet and viable exercise options should also be considered.Tobacco treatmentSocial support is another potential determinant of tobacco use. Therefore, in adults who use tobacco, assistance and arrangement for individualized and group social support counseling are recommended.S2.1-42,S2.1-43*Advanced age generally refers to age ≥75 years.ASCVD indicates atherosclerotic cardiovascular disease.2.2. Assessment of Cardiovascular RiskAmong adults at borderline (5% to <7.5%) and intermediate (≥7.5% to <20%) risk, one may consider additional individual risk-enhancing clinical factors (Table 3) that can be used to revise the 10-year ASCVD risk estimate.S2.2-4 These factors may include having a family history of premature ASCVD,S2.2-5 chronic inflammatory disease [rheumatoid arthritis,S2.2-6 lupus,S2.2-7 or HIV infectionS2.2-12], South Asian ancestry,S2.2-13 a history of preeclampsiaS2.2-8 or preterm delivery,S2.2-9 early menopause,S2.2-10 erectile dysfunction,S2.2-11 chronic kidney disease (CKD), metabolic syndrome, persistently elevated inflammatory markers,S2.2-14 or elevated lipid biomarkers.S2.2-4 After these clinically available risk-enhancing factors have been considered, if there is still uncertainty about the reliability of the risk estimate for individuals in the borderline- or intermediate-risk categories, further testing to document subclinical coronary atherosclerosis is reasonable to more accurately reclassify the risk estimate upward or downward.S2.2-17–S2.2-19,S2.2-36Table 3. Risk-Enhancing Factors for Clinician–Patient Risk DiscussionRisk-Enhancing Factors Family history of premature ASCVD (males, age <55 y; females, age <65 y) Primary hypercholesterolemia (LDL-C 160–189 mg/dL [4.1–4.8 mmol/L]; non–HDL-C 190–219 mg/dL [4.9–5.6 mmol/L])* Metabolic syndrome (increased waist circumference [by ethnically appropriate cutpoints], elevated triglycerides [>150 mg/dL, nonfasting], elevated blood pressure, elevated glucose, and low HDL-C [<40 mg/dL in men; <50 mg/dL in women] are factors; a tally of 3 makes the diagnosis) Chronic kidney disease (eGFR 15–59 mL/min/1.73 m2 with or without albuminuria; not treated with dialysis or kidney transplantation) Chronic inflammatory conditions, such as psoriasis, RA, lupus, or HIV/AIDS History of premature menopause (before age 40 y) and history of pregnancy-associated conditions that increase later ASCVD risk, such as preeclampsia High-risk race/ethnicity (eg, South Asian ancestry) Lipids/biomarkers: associated with increased ASCVD risk Persistently elevated* primary hypertriglyceridemia (≥175 mg/dL, nonfasting); If measured: Elevated high-sensitivity C-reactive protein (≥2.0 mg/L) Elevated Lp(a): A relative indication for its measurement is family history of premature ASCVD. An Lp(a) ≥50 mg/dL or ≥125 nmol/L constitutes a risk-enhancing factor, especially at higher levels of Lp(a). Elevated apoB (≥130 mg/dL): A relative indication for its measurement would be triglyceride ≥200 mg/dL. A level ≥130 mg/dL corresponds to an LDL-C >160 mg/dL and constitutes a risk-enhancing factor ABI (<0.9)*Optimally, 3 determinations.ABI indicates ankle-brachial index; AIDS, acquired immunodeficiency syndrome; apoB, apolipoprotein B; ASCVD, atherosclerotic cardiovascular disease; eGFR, estimated glomerular filtration rate; HDL-C, high-density lipoprotein cholesterol; HIV, human immunodeficiency virus; LDL-C, low-density lipoprotein cholesterol; Lp(a), lipoprotein (a); and RA, rheumatoid arthritis.Reproduced with permission from Grundy et al.S2.2-4 Copyright © 2018, American Heart Association, Inc., and American College of Cardiology Foundation.3. Lifestyle Factors Affecting Cardiovascular Risk3.1. Nutrition and Diet3.2. Exercise and Physical ActivityOther activity states that comprise a 24-hour period for an average individual include sleep, light-intensity physical activity, and sedentary behavior (Figure 1). Sedentary behavior refers to waking behavior with an energy expenditure of ≤1.5 metabolic equivalents while in a sitting or reclining posture (Table 4).S3.2-12Table 4. Definitions and Examples of Different Intensities of Physical ActivityIntensityMETsExamplesSedentary behavior*1–1.5Sitting, reclining, or lying; watching televisionLight1.6–2.9Walking slowly, cooking, light houseworkModerate3.0–5.9Brisk walking (2.4–4 mph), biking (5–9 mph), ballroom dancing, active yoga, recreational swimmingVigorous≥6Jogging/running, biking (≥10 mph), singles tennis, swimming laps*Sedentary behavior is defined as any waking behavior characterized by an energy expenditure ≤1.5 METs while in a sitting, reclining, or lying posture. Standing is a sedentary activity in that it involves ≤1.5 METs, but it is not considered a component of sedentary behavior.MET indicates metabolic equivalent; mph, miles per hour.Download figureDownload PowerPointFigure 1. Hours per day spent in various states of activity. US adults spend >7 h/d on average in sedentary activities. Replacing sedentary time with other physical activity involves increasing either moderate- to vigorous-intensity physical activity or light-intensity physical activity. Data modified from Young et al.S3.2-124. Other Factors Affecting Cardiovascular Risk4.1. Adults With Overweight and Obesity4.2. Adults With Type 2 Diabetes MellitusSee Figure 2 for an algorithm for treatment of T2DM for primary prevention of cardiovascular disease.Download figureDownload PowerPointFigure 2. Treatment of t2dm for primary prevention of cardiovascular disease. CVD indicates cardiovascular disease; GLP-1R, glucagon-like peptide-1 receptor; HbA1c, hemoglobin A1c; SGLT-2, sodium-glucose cotransporter 2; and T2DM, type 2 diabetes mellitus.4.3. Adults With High Blood CholesterolRecommendations from the 2018 Cholesterol Clinical Practice GuidelinesS4.3-1 are included and adapted below.Primary ASCVD prevention requires attention to ASCVD risk factors beginning early in life (Figure 3). The benefit from statin therapy is related to both global risk and intensity of treatment,S4.3-2 and no RCTs of high-intensity statin therapy have been carried out in cohorts of patients exclusively with diabetes. On the basis of these considerations a

HomeCirculationVol. 140, No. 112019 ACC/AHA Guideline on the Primary Prevention of Cardiovascular Disease: A Report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines Free AccessReview ArticlePDF/EPUBAboutView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissionsDownload Articles + Supplements ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toSupplemental MaterialFree AccessReview ArticlePDF/EPUB2019 ACC/AHA Guideline on the Primary Prevention of Cardiovascular Disease: A Report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines Donna K. Arnett, PhD, MSPH, FAHA, Co-Chair, Roger S. Blumenthal, MD, FACC, FAHA, Co-Chair, Michelle A. Albert, MD, MPH, FAHA, Andrew B. Buroker, Esq, Zachary D. Goldberger, MD, MS, FACC, FAHA, Ellen J. Hahn, PhD, RN, Cheryl Dennison Himmelfarb, PhD, RN, ANP, FAHA, Amit Khera, MD, MSc, FACC, FAHA, Donald Lloyd-Jones, MD, SCM, FACC, FAHA, J. William McEvoy, MBBCh, MEd, MHS, Erin D. Michos, MD, MHS, FACC, FAHA, Michael D. Miedema, MD, MPH, Daniel Muñoz, MD, MPA, FACC, Sidney C. Smith Jr, MD, MACC, FAHA, Salim S. Virani, MD, PhD, FACC, FAHA, Kim A. Williams Sr, MD, MACC, FAHA, Joseph Yeboah, MD, MS, FACC, FAHA and Boback Ziaeian, MD, PhD, FACC, FAHA Donna K. ArnettDonna K. Arnett Search for more papers by this author , Roger S. BlumenthalRoger S. Blumenthal Search for more papers by this author , Michelle A. AlbertMichelle A. Albert Search for more papers by this author , Andrew B. BurokerAndrew B. Buroker Search for more papers by this author , Zachary D. GoldbergerZachary D. Goldberger Search for more papers by this author , Ellen J. HahnEllen J. Hahn Search for more papers by this author , Cheryl Dennison HimmelfarbCheryl Dennison Himmelfarb Search for more papers by this author , Amit KheraAmit Khera Search for more papers by this author , Donald Lloyd-JonesDonald Lloyd-Jones Search for more papers by this author , J. William McEvoyJ. William McEvoy Search for more papers by this author , Erin D. MichosErin D. Michos Search for more papers by this author , Michael D. MiedemaMichael D. Miedema Search for more papers by this author , Daniel MuñozDaniel Muñoz Search for more papers by this author , Sidney C. Smith JrSidney C. Smith Jr Search for more papers by this author , Salim S. ViraniSalim S. Virani Search for more papers by this author , Kim A. Williams SrKim A. Williams Sr Search for more papers by this author , Joseph YeboahJoseph Yeboah Search for more papers by this author and Boback ZiaeianBoback Ziaeian Search for more papers by this author Originally published17 Mar 2019https://doi.org/10.1161/CIR.0000000000000678Circulation. 2019;140:e596–e646is corrected byCorrection to: 2019 ACC/AHA Guideline on the Primary Prevention of Cardiovascular Disease: A Report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice GuidelinesCorrection to: 2019 ACC/AHA Guideline on the Primary Prevention of Cardiovascular Disease: A Report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice GuidelinesCorrection to: 2019 ACC/AHA Guideline on the Primary Prevention of Cardiovascular Disease: A Report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice GuidelinesOther version(s) of this articleYou are viewing the most recent version of this article. Previous versions: September 9, 2019: Previous Version of Record March 17, 2019: Ahead of Print Table of ContentsTop 10 Take-Home Messages for the Primary Prevention of Cardiovascular Disease e597Preamble e5971. Introduction e5981.1. Methodology and Evidence Review e5991.2. Organization of the Writing Committee e5991.3. Document Review and Approval e5991.4. Scope of the Guideline e5991.5. Class of Recommendation and Level of Evidence e6001.6. Abbreviations e6012. Overarching Recommendations for ASCVD Prevention Efforts e6012.1. Patient-Centered Approaches to Comprehensive ASCVD Prevention e6012.2. Assessment of Cardiovascular Risk e6023. Lifestyle Factors Affecting Cardiovascular Risk e6053.1. Nutrition and Diet e6053.2. Exercise and Physical Activity e6074. Other Factors Affecting Cardiovascular Risk e6094.1. Adults With Overweight and Obesity e6094.2. Adults With Type 2 Diabetes Mellitus e6104.3. Adults With High Blood Cholesterol e6124.4. Adults With High Blood Pressure or Hypertension e6164.5. Treatment of Tobacco Use e6184.6. Aspirin Use e6215. Cost and Value Considerations e6226. Conclusion e623Appendix 1: Search Criteria e636Appendix 2: Author Relationships With Industry and Other Entities (Relevant) e641Appendix 3: Reviewer Relationships With Industry and Other Entities (Comprehensive) e642References e624Top 10 Take-Home Messages for the Primary Prevention of Cardiovascular DiseaseThe most important way to prevent atherosclerotic vascular disease, heart failure, and atrial fibrillation is to promote a healthy lifestyle throughout life.A team-based care approach is an effective strategy for the prevention of cardiovascular disease. Clinicians should evaluate the social determinants of health that affect individuals to inform treatment decisions.Adults who are 40 to 75 years of age and are being evaluated for cardiovascular disease prevention should undergo 10-year atherosclerotic cardiovascular disease (ASCVD) risk estimation and have a clinician–patient risk discussion before starting on pharmacological therapy, such as antihypertensive therapy, a statin, or aspirin. In addition, assessing for other risk-enhancing factors can help guide decisions about preventive interventions in select individuals, as can coronary artery calcium scanning.All adults should consume a healthy diet that emphasizes the intake of vegetables, fruits, nuts, whole grains, lean vegetable or animal protein, and fish and minimizes the intake of trans fats, red meat and processed red meats, refined carbohydrates, and sweetened beverages. For adults with overweight and obesity, counseling and caloric restriction are recommended for achieving and maintaining weight loss.Adults should engage in at least 150 minutes per week of accumulated moderate-intensity physical activity or 75 minutes per week of vigorous-intensity physical activity.For adults with type 2 diabetes mellitus, lifestyle changes, such as improving dietary habits and achieving exercise recommendations, are crucial. If medication is indicated, metformin is first-line therapy, followed by consideration of a sodium-glucose cotransporter 2 inhibitor or a glucagon-like peptide-1 receptor agonist.All adults should be assessed at every healthcare visit for tobacco use, and those who use tobacco should be assisted and strongly advised to quit.Aspirin should be used infrequently in the routine primary prevention of ASCVD because of lack of net benefit.Statin therapy is first-line treatment for primary prevention of ASCVD in patients with elevated low-density lipoprotein cholesterol levels (≥190 mg/dL), those with diabetes mellitus, who are 40 to 75 years of age, and those determined to be at sufficient ASCVD risk after a clinician–patient risk discussion.Nonpharmacological interventions are recommended for all adults with elevated blood pressure or hypertension. For those requiring pharmacological therapy, the target blood pressure should generally be <130/80 mm Hg.PreambleSince 1980, the American College of Cardiology (ACC) and American Heart Association (AHA) have translated scientific evidence into clinical practice guidelines with recommendations to improve cardiovascular health. These guidelines, which are based on systematic methods to evaluate and classify evidence, provide a foundation for the delivery of quality cardiovascular care. The ACC and AHA sponsor the development and publication of clinical practice guidelines without commercial support, and members volunteer their time to the writing and review efforts.Clinical practice guidelines provide recommendations applicable to patients with or at risk of developing cardiovascular disease (CVD). The focus is on medical practice in the United States, but these guidelines are relevant to patients throughout the world. Although guidelines may be used to inform regulatory or payer decisions, the goals are to improve quality of care and align with patients’ interests. Guidelines are intended to define practices meeting the needs of patients in most but not all circumstances and should not replace clinical judgment.Recommendations for guideline-directed management and therapy, which encompasses clinical evaluation, diagnostic testing, and both pharmacological and procedural treatments, are effective only when adopted by both practitioners and patients. Adherence to recommendations can be enhanced by shared decision-making between clinicians and patients, with patient engagement in selecting interventions on the basis of individual values, preferences, and associated conditions and comorbidities.The ACC/AHA Task Force on Clinical Practice Guidelines strives to ensure that the guideline writing committee includes requisite expertise and is representative of the broader medical community by selecting experts from a broad array of backgrounds, representing different geographic regions, sexes, races, ethnicities, intellectual perspectives/biases, and scopes of clinical practice. The ACC and AHA have rigorous policies and methods to ensure that documents are developed without bias or improper influence. The complete policy on relationships with industry and other entities (RWI) can be found online.Beginning in 2017, numerous modifications to the guidelines have been and continue to be implemented to make guidelines shorter and enhance “user friendliness.” Guidelines are written and presented in a modular knowledge chunk format, in which each chunk includes a table of recommendations, a brief synopsis, recommendation-specific supportive text and, when appropriate, flow diagrams or additional tables. Hyperlinked references are provided for each modular knowledge chunk to facilitate quick access and review. More structured guidelines—including word limits (“targets”) and a web guideline supplement for useful but noncritical tables and figures—are 2 such changes. This Preamble is an abbreviated version, with the detailed version available online.Patrick T. O’Gara, MD, MACC, FAHAChair, ACC/AHA Task Force on Clinical Practice Guidelines1. IntroductionAlthough there has been substantial improvement in atherosclerotic cardiovascular disease (ASCVD) outcomes in recent decades, ASCVD remains the leading cause of morbidity and mortality globally.S1-1–S1-3 In the United States, it is also the leading cause of death for people of most racial/ethnic groups, with an estimated cost of >$200 billion annually in healthcare services, medications, and lost productivity. Much of this is attributable to suboptimal implementation of prevention strategies and uncontrolled ASCVD risk factors in many adults.S1-2Most Americans who have had a myocardial infarction (MI) had unfavorable levels of at least 1 cardiovascular risk factor before their ASCVD event.S1-4 In 2010, the AHA defined a new model of “ideal cardiovascular health,” referred to as Life’s Simple 7.S1-5 Clinicians will find the 2018 Journal of American College of Cardiology (JACC) Cardiovascular Health Promotion Series very helpful in approaching the various aspects of prevention with patients.S1-6 An increasing number of ideal cardiovascular health factors have been associated with a lower prevalence and incidence of ASCVD events, heart failure, atrial fibrillation, cancer, depression, and cognitive impairment.S1-7 Therefore, moving individuals toward ideal cardiovascular health is critically important for prevention of many important health conditions.The ACC/AHA Task Force on Clinical Practice Guidelines has commissioned this guideline to consolidate existing recommendations and various recent scientific statements, expert consensus documents, and clinical practice guidelines into a single guidance document focused on the primary prevention of ASCVD. However, this guideline also includes newly generated recommendations for aspirin use, exercise and physical activity, and tobacco use, in addition to recommendations related to team-based care, shared decision-making, and assessment of social determinants of health, to create a comprehensive yet targeted ACC/AHA guideline on the prevention of ASCVD. This guideline has been formatted in the modular chunk format to facilitate readability and future updating.Prevention strategies occur at the population level but must also engage individual adults to slow the development of ASCVD. The most important way to prevent ASCVD is to promote a healthy lifestyle throughout life. Prevention strategies must include a strong focus on lifestyle optimization (improvements in diet, physical activity, and avoidance of tobacco use and exposure to secondhand smoke) to minimize the risk of future ASCVD events.A comprehensive patient-centered approach that addresses all aspects of a patient’s lifestyle habits and estimated risk of a future ASCVD event is the first step in deciding on where there may be a need for pharmacotherapy. Even if a blood pressure (BP)–reducing medication, lipid-lowering medication, or diabetes medication is ultimately prescribed, lifestyle goals should be emphasized on a regular basis. Only when a person’s risk is sufficiently high should medications to reduce ASCVD risk be considered as part of a shared decision-making process for optimal treatment. In summary, clinicians and individuals should focus attention on living a healthy lifestyle by referring to these evidence-based recommendations to help prevent ASCVD.1.1. Methodology and Evidence ReviewThis guideline continues the ACC and AHA effort to design a comprehensive yet succinct compilation of practical guidance for the primary prevention of ASCVD and to promote optimal dissemination of information by using concise language and formatting. The recommendations listed in this guideline are evidence based and supported by an extensive evidence review. A search for literature derived from research involving human subjects, published in English, and indexed in Ovid MEDLINE, PubMed, Cochrane Library, National Institute for Health and Care Excellence (NICE), and other selected databases relevant to this guideline, was conducted between May and July 2018. For specific search terms used and years searched per section, please see Appendix 1.Randomized controlled trials (RCTs), systematic reviews of RCTs, meta-analyses, and large, United States–based, high-quality cohort studies, as well as observational studies and systematic reviews of observational studies, were evaluated for their content on the prevention of ASCVD outcomes related to the following 9 topic areas: risk assessment, diet, exercise/physical activity, obesity and weight loss, type 2 diabetes mellitus (T2DM), blood cholesterol, hypertension, smoking cessation, and aspirin use. Previous ACC/AHA guidelines, as well as US Preventive Services Task Force (USPSTF) reviews and other guidance relevant to this guideline, were also assessed. The final evidence tables included in the Online Data Supplement summarize the evidence used to formulate recommendations. References selected and published in this document are representative and not all-inclusive.Avalere Health, a healthcare advisory services firm contracted by ACC/AHA, served as the document manager for this guideline to facilitate its development process. As document manager, Avalere facilitated the deliberations of the Writing Committee and led the modified Delphi process for establishing the Class of Recommendation and the Level of Evidence. In parallel, an independent health data and epidemiology expert, Lee Ann Prebil, conducted a systematic evidence review for the key topic of exercise and physical activity and conducted targeted literature searches to support this document’s discussion of patient-centered approaches, including team-based care, shared decision-making, and assessment of social determinants of health. A targeted literature search was also conducted for this guideline’s cost and value considerations. These searches are available as downloadable Excel files.Recommendations and supportive text relevant to cardiovascular risk, blood cholesterol, and high BP were taken directly from 2 recently released ACC/AHA guidelines, the 2017 Hypertension Clinical Practice GuidelinesS1.1-1 and the 2018 Cholesterol Clinical Practice Guideline,S1.1-2 and were adapted for the present guideline, which aims to provide an overview of the primary prevention of ASCVD among adults. Recommendations that were adapted from previous publications are noted in the recommendation tables, and both the original published recommendation and the adapted version are provided in the guideline.The results of these evidence reviews were evaluated by the writing committee for incorporation into the present guideline. (See Table S1 in the Web Supplement for a list of relevant publications and statements used in support of the guideline’s recommendations.) Each topic area was assigned a primary writer, as well as a primary, and sometimes secondary, reviewer. These assignments were based on areas of particular expertise of writing committee members. All recommendations were fully reviewed and discussed among the full committee to allow for diverse perspectives and considerations for this guideline. Recommendations were then voted upon, with a modified Delphi process used to reach consensus.1.2. Organization of the Writing CommitteeThe writing committee consisted of clinicians, cardiologists, health services researchers, epidemiologists, internists, nurses, and a lay representative. The writing committee included representatives from the ACC and AHA. Appendix 2 of the present document lists writing committee members’ relevant RWI. For the purposes of full transparency, the writing committee members’ comprehensive disclosure information is available online.1.3. Document Review and ApprovalThis document was reviewed by 5 official reviewers nominated by the ACC and AHA (1 reviewer from the ACC/AHA Task Force for Practice Guidelines, 2 reviewers from the AHA, and 2 reviewers from the ACC); 3 reviewers on behalf of the American Association of Cardiovascular and Pulmonary Rehabilitation, the American Society for Nutrition, and the American Society of Preventive Medicine; and 23 individual content reviewers. Reviewers’ RWI information was distributed to the writing committee and is published in this document (Appendix 3). This document was approved for publication by the governing bodies of the ACC and AHA.1.4. Scope of the GuidelineThis guideline is intended to be a resource for the clinical and public health practice communities. It addresses the primary prevention of CVD in adults (≥18 years of age), focused on outcomes of ASCVD (ie, acute coronary syndromes, MI, stable or unstable angina, arterial revascularization, stroke, transient ischemic attack, or peripheral arterial disease of atherosclerotic origin), as well as heart failure and atrial fibrillation. The guideline presents recommendations to prevent CVD that are related to lifestyle factors (eg, diet and exercise or physical activity), other factors affecting CVD risk (eg, obesity, diabetes, blood cholesterol, high BP, smoking, aspirin use), patient-centered approaches (eg, team-based care, shared decision-making, assessment of social determinants of health), and considerations of the cost and value of primary prevention.1.5. Class of Recommendation and Level of EvidenceRecommendations are designated with both a Class of Recommendation (COR) and a Level of Evidence (LOE). The COR indicates the strength of recommendation, encompassing the estimated magnitude and certainty of benefit in proportion to risk. The LOE rates the quality of scientific evidence supporting the intervention on the basis of the type, quantity, and consistency of data from clinical trials and other sources (Table 1).S1.5-1Table 1. Applying Class of Recommendation and Level of Evidence to Clinical Strategies, Interventions, Treatments, or Diagnostic Testing in Patient Care (Updated August 2015)Table 1. Applying Class of Recommendation and Level of Evidence to Clinical Strategies, Interventions, Treatments, or Diagnostic Testing in Patient Care (Updated August 2015)1.6. AbbreviationsAbbreviationMeaning/PhraseASCVDatherosclerotic cardiovascular diseaseAUAgatston unitsBMIbody mass indexBPblood pressureCHDcoronary heart diseaseCKDchronic kidney diseaseCVDcardiovascular diseaseDASHDietary Approaches to Stop HypertensionDBPdiastolic blood pressureDMdiabetes mellitusENDSelectronic nicotine delivery systemsFDAUS Food and Drug AdministrationGLP-1Rglucagon-like peptide-1 receptorHbA1chemoglobin A1cHDL-Chigh-density lipoprotein cholesterolHbA1chemoglobin A1cLDL-Clow-density lipoprotein cholesterolMImyocardial infarctionPCEpooled cohort equationsRCTrandomized controlled trialSBPsystolic blood pressureSGLT-2sodium-glucose cotransporter 2T2DMtype 2 diabetes mellitusUSPSTFUS Preventive Services Task Force2. Overarching Recommendations for ASCVD Prevention Efforts2.1. Patient-Centered Approaches to Comprehensive ASCVD PreventionSynopsisThis 2019 ACC/AHA Guideline on the Primary Prevention of CVD aims to promote the delivery of patient-centered care, which the writing committee felt was foundational to the guidance provided throughout. These patient-centered recommendations emphasize the importance of team-based care delivery, shared decision-making, and the evaluation of social determinants of health in ASCVD prevention efforts. These recommendations apply to all aspects of clinical practice for the primary prevention of ASCVD.Recommendation-Specific Supportive TextTeam-based care makes use of multidisciplinary health professionals to improve the quality and maintenance of ASCVD prevention. It is a multifaceted approach that supports clinical decision-making (ie, treatment algorithms), collaboration among different clinicians, and patient and family member participation to facilitate the treatment goals of patients.S2.1-26 RCTs and systematic reviews with meta-analyses demonstrated greater reduction of ASCVD risk with team-based care than with usual care in patients with hypertension, diabetes, and hyperlipidemia.S2.1-1–S2.1-14 A team-based approach to ASCVD prevention may result in significant improvements in patient outcomesS2.1-27 and often meets patient needs better than standard care, especially in low-resource settings and among vulnerable populations. In a team-based care model that compared patients enrolled in a preventive cardiology clinic staffed by advanced practice providers with a propensity-matched cohort of patients enrolled in primary care clinics, a reduction in cardiovascular risk was demonstrated through effective risk stratification and preventive management.S2.1-28 Other successful interventions that have used team-based care include telehealth monitoring, follow-up support aids, and patient education.S2.1-27Decisions about primary prevention should be collaborative between a clinician and a patient. Shared decision-making occurs when practitioners engage patients in discussions about personalized ASCVD risk estimates and their implications for the perceived benefits of preventive strategies, including lifestyle habits, goals, and medical therapies. Collaborative decisions are more likely to address potential barriers to treatment options, compared with treatment and guidance offered without patient input.S2.1-15–S2.1-18Socioeconomic inequalities are strong determinants of CVD risk internationally.S2.1-21,S2.1-24 Therefore, the clinician should tailor advice to a patient’s socioeconomic and educational status, as well as cultural, work, and home environments.S2.1-23 The Centers for Medicare & Medicaid Services has developed a screening tool to assess 5 domains of non–health-related measures that affect health outcomes: housing instability, food insecurity, transportation difficulties, utility assistance needs, and interpersonal safety.S2.1-29 ASCVD prevention could benefit from such screening. ASCVD risk begins early in life, with heightened susceptibility tied to low socioeconomic status.S2.1-25 Examples of upstream social determinants of health that affect treatment adherence and ASCVD health outcomes include comorbid mental illness, lack of health literacy, exposure to adversity (eg, home/community violence, trauma exposures, safety concerns), financial strain, inadequate housing conditions, lack of food security (ie, access to affordable and nutritious food), and inadequate social support.S2.1-30 Systems of care should evaluate social determinants of health that affect care delivery for the primary prevention of ASCVD (eg, transportation barriers, the availability of health services).Important considerations related to socioeconomic disadvantage are not captured by existing CVD risk equations.S2.1-31 Addressing unmet social needs improves management of BP and lipids,S2.1-32 which highlights the importance of dietary counseling and encouraging physical activity.S2.1-19 More time may be required to address ASCVD prevention with adults of low health literacy or disadvantaged educational backgrounds.Differential cardiovascular outcomes persist by important sociodemographic characteristics that include but are not limited to age, sex, and race/ethnicity.S2.1-22,S2.1-33–S2.1-35 Failure to address the impact of social determinants of health impedes efficacy of proven prevention recommendations. Table 2 outlines key considerations related to social determinants of health and ASCVD prevention.Table 2. Example Considerations for Addressing Social Determinants of Health to Help Prevent ASCVD EventsTopic/DomainExample ConsiderationsCardiovascular riskAdults should be routinely assessed for psychosocial stressors and provided with appropriate counseling.S2.1-31Health literacy should be assessed every 4 to 6 y to maximize recommendation effectiveness.S2.1-36DietIn addition to the prescription of diet modifications, body size perception, as well as social and cultural influences, should be assessed.S2.1-37,S2.1-38Potential barriers to adhering to a heart-healthy diet should be assessed, including food access and economic factors; these factors may be particularly relevant to persons from vulnerable populations, such as individuals residing in either inner-city or rural environments, those at socioeconomic disadvantage, and those of advanced age*.S2.1-39Exercise and physical activityIn addition to the prescription of exercise, neighborhood environment and access to facilities for physical activity should be assessed.S2.1- 30,S2.1-40,S2.1-41Obesity and weight lossLifestyle counseling for weight loss should include assessment of and interventional recommendations for psychosocial stressors, sleep hygiene, and other individualized barriers.S2.1-42–S2.1-44Weight maintenance should be promoted in patients with overweight/obesity who are unable to achieve recommended weight loss.Diabetes mellitusIn addition to the prescription of type 2 diabetes mellitus interventions, environmental and psychosocial factors, including depression, stress, self-efficacy, and social support, should be assessed to improve achievement of glycemic control and adherence to treatment.S2.1-45–S2.1-48High blood pressureShort sleep duration (<6 h) and poor-quality sleep are associated with high blood pressure and should be considered.S2.1-49 Because other lifestyle habits can impact blood pressure, access to a healthy, low-sodium diet and viable exercise options should also be considered.Tobacco treatmentSocial support is another potential determinant of tobacco use. Therefore, in adults who use tobacco, assistance and arrangement for individualized and group social support counseling are recommended.S2.1-50,S2.1-51*Advanced age generally refers to age ≥75 years.ASCVD indicates atherosclerotic cardiovascular disease.2.2. Assessment of Cardiovascular RiskSynopsisAssessment of ASCVD risk remains the foundation of primary prevention. Although all individuals should be encouraged to follow a heart-healthy lifestyle, estimating an individual’s 10-year absolute ASCVD risk enables matching the intensity of preventive interventions to the patient’s absolute risk, to maximize anticipated benefit and minimize potential harm from overtreatment. The 10-year ASCVD risk estimate is used to guide decision-making for many preventive interventions, including lipid managementS2.2-4,S2.2-36 and BP management;S2.2-37 it should be the start of a conversation with the patient about risk-reducing strategies (the “clinician–patient discussion”) and not the sole decision factor for the initiation of pharmacotherapy.S2.2-4,S2.2-36,S2.2-38 All risk estimation tools have inherent limitations, and population-based risk scores must be interpreted in light of specific circumstances for individual patients. The PCE have been shown to overestimateS2.2-15,S2.2-39–S2.2-47 or underestimateS2.2-12,S2.2-48–S2.2-51 ASCVD risk for certain subgroups. Thus, after calculation of the PCE, it is reasonable to use additional risk-enhancing factors to guide decisions about preventive interventions for borderline- or intermediate-risk adults.S2.2-4–S2.2-14 However, the value of preventive therapy may remain uncertain for many individuals with borderline or intermediate estimated 10-year risk, and some patients may be reluctant to take medical therapy without clearer evidence of increased ASCVD risk. For these

Air pollution is a heterogeneous, complex mixture of gases, liquids, and particulate matter. Epidemiological studies have demonstrated a consistent increased risk for cardiovascular events in relation to both short- and long-term exposure to present-day concentrations of ambient particulate matter. Several plausible mechanistic pathways have been described, including enhanced coagulation/thrombosis, a propensity for arrhythmias, acute arterial vasoconstriction, systemic inflammatory responses, and the chronic promotion of atherosclerosis. The purpose of this statement is to provide healthcare professionals and regulatory agencies with a comprehensive review of the literature on air pollution and cardiovascular disease. In addition, the implications of these findings in relation to public health and regulatory policies are addressed. Practical recommendations for healthcare providers and their patients are outlined. In the final section, suggestions for future research are made to address a number of remaining scientific questions.

HomeCirculationVol. 100, No. 10Diabetes and Cardiovascular Disease Free AccessOtherPDF/EPUBAboutView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toFree AccessOtherPDF/EPUBDiabetes and Cardiovascular Disease A Statement for Healthcare Professionals From the American Heart Association Scott M. Grundy, Ivor J. Benjamin, Gregory L. Burke, Alan Chait, Robert H. Eckel, Barbara V. Howard, William Mitch, Sidney C. SmithJr and James R. Sowers Scott M. GrundyScott M. Grundy Search for more papers by this author , Ivor J. BenjaminIvor J. Benjamin Search for more papers by this author , Gregory L. BurkeGregory L. Burke Search for more papers by this author , Alan ChaitAlan Chait Search for more papers by this author , Robert H. EckelRobert H. Eckel Search for more papers by this author , Barbara V. HowardBarbara V. Howard Search for more papers by this author , William MitchWilliam Mitch Search for more papers by this author , Sidney C. SmithJrSidney C. SmithJr Search for more papers by this author and James R. SowersJames R. Sowers Search for more papers by this author Originally published7 Sep 1999https://doi.org/10.1161/01.CIR.100.10.1134Circulation. 1999;100:1134–1146is corrected byCorrectionThis statement examines the cardiovascular complications of diabetes mellitus and considers opportunities for their prevention. These complications include coronary heart disease (CHD), stroke, peripheral arterial disease, nephropathy, retinopathy, and possibly neuropathy and cardiomyopathy. Because of the aging of the population and an increasing prevalence of obesity and sedentary life habits in the United States, the prevalence of diabetes is increasing. Thus, diabetes must take its place alongside the other major risk factors as important causes of cardiovascular disease (CVD). In fact, from the point of view of cardiovascular medicine, it may be appropriate to say, “diabetes is a cardiovascular disease.”Clinical Presentations of Diabetes MellitusThe most prevalent form of diabetes mellitus is type 2 diabetes. This disorder typically makes its appearance later in life. The underlying metabolic causes of type 2 diabetes are the combination of impairment in insulin-mediated glucose disposal (insulin resistance) and defective secretion of insulin by pancreatic β-cells. Insulin resistance develops from obesity and physical inactivity, acting on a substrate of genetic susceptibility.12 Insulin secretion declines with advancing age,34 and this decline may be accelerated by genetic factors.56 Insulin resistance typically precedes the onset of type 2 diabetes and is commonly accompanied by other cardiovascular risk factors: dyslipidemia, hypertension, and prothrombotic factors.78 The common clustering of these risk factors in a single individual has been called the metabolic syndrome. Many patients with the metabolic syndrome manifest impaired fasting glucose (IFG)9 even when they do not have overt diabetes mellitus.10 The metabolic syndrome commonly precedes the development of type 2 diabetes by many years11 ; of great importance, the risk factors that constitute this syndrome contribute independently to CVD risk.Recently, new criteria have been accepted for the diagnosis of diabetes.9 The upper threshold of fasting plasma glucose for the diagnosis of diabetes has been lowered from ≥140 mg/dL to ≥126 mg/dL. The upper threshold for normoglycemia likewise has been reduced from <115 to <110 mg/dL. A fasting plasma glucose of 110 to 125 mg/dL is now designated IGF. These changes removed the need for oral glucose tolerance testing for diagnosis of diabetes; a diagnosis rests entirely on confirmed elevations of fasting plasma glucose. Furthermore, the terms insulin-dependent diabetes mellitus and non–insulin-dependent diabetes mellitus have been replaced by type 1 diabetes and type 2 diabetes, respectively.The other form of diabetes mellitus is type 1 diabetes, which follows immunologic destruction of pancreatic β-cells.12 Type 1 diabetes usually begins early in life and is often called juvenile diabetes. This form of diabetes frequently produces microvascular complications, nephropathy, and retinopathy,12 but it also predisposes to CHD.13 Because type 2 diabetes occurs much more commonly than type 1 diabetes, the present statement will emphasize type 2 diabetes. Nonetheless, type 1 diabetes will be integrated into the overall strategy of cardiovascular risk reduction.Scope of the ProblemAt least 10.3 million Americans carry a diagnosis of diabetes mellitus.14 Another 5.4 million are estimated to have undiagnosed diabetes.14 Approximately 90% of patients with diabetes have the type 2 variety.14 The onset of type 2 diabetes usually precedes clinical diagnosis by several years.14 An increasing prevalence of type 2 diabetes cannot be divorced from the rising prevalence of obesity and physical inactivity in our society. An estimated 97 million adults in the United States are overweight or obese.15 Furthermore, ≈75% of adult Americans have minimal physical activity or daily exercise.16 Both excess body fat and physical inactivity predispose to type 2 diabetes. Several ethnic groups are particularly susceptible to type 2 diabetes: Hispanics, blacks, Native Americans, and Asians (especially South Asians).17181920 The growing ethnic diversity, including these groups, contributes to the increasing prevalence of type 2 diabetes in the United States.Diabetes as a Major Risk FactorA large body of epidemiological and pathological data documents that diabetes is an independent risk factor for CVD in both men and women.212223 Women with diabetes seem to lose most of their inherent protection against developing CVD.2124 CVDs are listed as the cause of death in ≈65% of persons with diabetes.25 Diabetes acts as an independent risk factor for several forms of CVD. To make matters worse, when patients with diabetes develop clinical CVD, they sustain a worse prognosis for survival than do CVD patients without diabetes.262728 These considerations have convinced the Scientific Advisory and Coordinating Committee of the American Heart Association (AHA) that diabetes mellitus deserves to be designated a major risk factor for CVD. This formal designation commits the AHA to a greater emphasis on diabetes as a risk factor in its scientific and educational programs. This statement provides the scientific rationale for the decision to classify diabetes as a major risk factor for CVD.Diabetes and Specific CVDAtherosclerotic CHDBoth type 1 diabetes and type 2 diabetes are independent risk factors for CHD.212223 Moreover, myocardial ischemia due to coronary atherosclerosis commonly occurs without symptoms in patients with diabetes.29 As a result, multivessel atherosclerosis often is present before ischemic symptoms occur and before treatment is instituted. A delayed recognition of various forms of CHD undoubtedly worsens the prognosis for survival for many diabetic patients.Diabetic CardiomyopathyOne reason for the poor prognosis in patients with both diabetes and ischemic heart disease seems to be an enhanced myocardial dysfunction leading to accelerated heart failure (diabetic cardiomyopathy).3031323334353637 Thus, patients with diabetes are unusually prone to congestive heart failure. Several factors probably underlie diabetic cardiomyopathy: severe coronary atherosclerosis, prolonged hypertension, chronic hyperglycemia, microvascular disease, glycosylation of myocardial proteins, and autonomic neuropathy. Improved glycemic control, better control of hypertension, and prevention of atherosclerosis with cholesterol-lowering therapy may prevent or mitigate diabetic cardiomyopathy. An early clinical trial38 suggested that sulfonyl ureas used for control of hyperglycemia are cardiotoxic and may exacerbate diabetic cardiomyopathy. This side effect, however, was not confirmed in a recent large clinical trial.39StrokeMortality from stroke is increased almost 3-fold when patients with diabetes are matched to those without diabetes.40 The most common site of cerebrovascular disease in patients with diabetes is occlusion of small paramedial penetrating arteries.41 Diabetes also increases the likelihood of severe carotid atherosclerosis.4243 Patients with diabetes, moreover, are likely to suffer irreversible brain damage with carotid emboli that otherwise would produce only transient ischemic attacks in persons without diabetes. Approximately 13% of patients with diabetes >65 years old have had a stroke.44Renal DiseaseRenal disease is a common and often severe complication of diabetes.45 Approximately 35% of patients with type 1 diabetes of 18 years’ duration will have signs of diabetic renal involvement.46 Up to 35% of new patients beginning dialysis therapy have type 2 diabetes.47 End-stage renal disease (ESRD) appears to be especially common among Hispanics, blacks, and Native Americans with diabetes.4849505152 For patients with diabetes who are on renal dialysis, mortality rates probably exceed 20% per year.47 When diabetes is present, CVD is the leading cause of death among patients with ESRD.535455Covariate Risk FactorsProspective studies22232425262728293031323334353637383940 indicate that all of the major cardiovascular risk factors—cigarette smoking, hypertension, and high serum cholesterol—continue to act as independent contributors to CVD in patients with diabetes. As already mentioned, clustering of metabolic risk factors, called the metabolic syndrome, occurs commonly in type 2 diabetes.56 The onset of hyperglycemia in patients with the metabolic syndrome appears to accelerate atherogenesis, possibly by enhanced formation of glycosylated proteins and advanced glycation products5758 and/or by increasing endothelial dysfunction.59 These direct consequences of hyperglycemia probably contribute to the microvascular disease underlying nephropathy and retinopathy, and they may promote macrovascular disease as well.Predisposing Risk FactorsSeveral predisposing factors simultaneously affect the development of CVD and diabetes mellitus. Among these concomitant factors are obesity, physical inactivity, heredity, sex, and advancing age. The mechanisms whereby they predispose to chronic diseases are complex and often overlapping. To some extent, these predisposing factors exacerbate the major risk factors: dyslipidemia, hypertension, and glucose tolerance; and they may cause CVD and diabetes mellitus through other pathways as well. To a large extent, both CVD and diabetes must be prevented through control of the predisposing risk factors. Modification of life habits is at the heart of the public health strategy for prevention of CVD and diabetes mellitus. High priorities are the prevention (or treatment) of obesity and promotion of physical activity. Drug therapy nonetheless may be required to control the metabolic risk factors, particularly when they arise from genetic aberration and aging. Effective drugs are currently available for treatment of hypertension and dyslipidemia. Hypoglycemic agents also are available for treatment of type 2 diabetes, but new pharmacological strategies are under investigation for more effective treatment and prevention.Insulin Resistance and the Metabolic SyndromeMost patients with type 2 diabetes have insulin resistance. Indeed, insulin resistance seems to predispose to both CVD and diabetes.60 Research suggests that insulin resistance is a multisystem disorder that induces multiple metabolic alterations. Factors that contribute to insulin resistance are genetics,61 obesity,62 physical inactivity,63 and advancing age.64 Patients with insulin resistance often have abdominal obesity.65 Metabolic risk factors that occur commonly in patients with insulin resistance are atherogenic dyslipidemia, hypertension, glucose intolerance, and a prothrombotic state.60 Each of these risk factors can be reviewed briefly.Atherogenic DyslipidemiaAtherogenic dyslipidemia is characterized by 3 lipoprotein abnormalities: elevated very-low-density lipoproteins (VLDL), small LDL particles, and low high-density-lipoprotein (HDL) cholesterol (the lipid triad). The lipid triad occurs frequently in patients with premature CHD and appears to be an atherogenic lipoprotein phenotype independent of elevated LDL cholesterol.66676869 Most patients with atherogenic dyslipidemia are insulin resistant.697071 Atherogenic dyslipidemia in diabetic patients often is called diabetic dyslipidemia. Many patients with atherogenic dyslipidemia also have an elevated serum total apolipoprotein B.72 Growing evidence suggests that all of the components of the lipid triad are independently atherogenic. Together they represent a set of lipoprotein abnormalities besides elevated LDL cholesterol that promote atherosclerosis.HypertensionHypertension is a well-established major risk factor for CVD.22 It increases risk for both CHD and stroke and contributes to diabetic nephropathy.73 Several investigators7475 report a positive association between insulin resistance and hypertension; this finding suggests that elevated blood pressure deserves to be listed among the components of the metabolic syndrome. Hypertension nonetheless is a multifactorial disorder, and the mechanistic connections between insulin resistance and hypertension are largely conjectural; even so, evidence for a causal link is growing.76 When hypertension coexists with overt diabetes, which it commonly does, the risk for CVD, including nephropathy, is doubly increased.Elevated Plasma GlucoseFor several years after onset of insulin resistance, fasting and postprandial glucose levels typically are normal. During this period, pancreatic β-cells are able to increase insulin secretion in response to insulin resistance and thereby maintain normal plasma glucose levels. In some people, however, insulin secretion declines with aging, and elevated glucose concentrations appear. The first abnormality in plasma glucose in patients with insulin resistance is IFG (or impaired glucose tolerance).9 The presence of IFG usually accompanies long-standing insulin resistance. It is currently estimated that 13.4 million adults, 7.0% of the US population, have IFG.14 Many prospective studies7778 show that IFG (or impaired glucose tolerance) is a risk factor for CVD; the degree of independence as a risk factor, however, is uncertain, because IGF commonly coexists with other components of the metabolic syndrome.11 A patient with IFG nonetheless must be considered at risk for both CVD and type 2 diabetes. As already indicated, once categorical hyperglycemia develops, it counts as an independent risk factor for CVD.22Prothrombotic StateA newly recognized component of the metabolic syndrome is a prothrombotic state.76 Patients with insulin resistance frequently manifest several alterations in coagulation mechanisms that predispose them to arterial thrombosis. These alterations include increased fibrinogen levels,79 increased plasminogen activator inhibitor-1,80 and various platelet abnormalities.81LDL Cholesterol and Atherogenesis in Diabetic PatientsAn elevated concentration of serum LDL cholesterol is a major risk factor for CHD.82 In fact, some elevation of LDL cholesterol appears to be necessary for the initiation and progression of atherosclerosis. In populations having very low LDL cholesterol levels, clinical CHD is relatively rare, even when other risk factors—hypertension, cigarette smoking, and diabetes—are common.83 In contrast, severe elevations in LDL cholesterol can produce full-blown atherosclerosis and premature CHD in the complete absence of other risk factors.84The view has been expressed that most patients with diabetes do not have an elevated serum LDL cholesterol; if not, a high LDL serum cholesterol would not be a common risk factor in patients with diabetes. It is true that most patients who have diabetes do not have marked elevations of LDL cholesterol, but these patients nonetheless carry high enough levels to support the development of atherosclerosis.85 A role for LDL in hyperglycemic patients became apparent in recent clinical trials, eg, the Scandinavian Simvastatin Survival Study (4S),8687 the Cholesterol and Recurrent Events (CARE) trial,8889 and the Long-Term Intervention with Pravastatin in Ischemic Disease (LIPID).90 In all of these trials, aggressive LDL-lowering therapy reduced recurrent CHD events in patients with diabetes.Cigarette SmokingCigarette smoking is a leading risk factor for CVD. Patients with diabetes who are smokers are doubly at risk. Unfortunately, many patients continue to smoke despite having diabetes; for these patients, the benefits that can be derived from modifying other risk factors are mitigated.Diabetic NephropathyDiabetic nephropathy can be divided into 4 phases: microalbuminuria, macroalbuminuria, the nephrotic syndrome, and chronic renal failure.45 Microalbuminuria (urine albumin 30 to 300 mg/d or <300 mg/g creatinine) is the first clinical sign of diabetic damage to the kidney.9192 Not only is microalbuminuria a harbinger of progressive kidney damage, but its presence also reflects a higher risk for CVD.92939495 Macroalbuminuria (urine albumin >300 mg/d or >300 mg/g creatinine) usually denotes significant diabetic nephropathy and will be followed by a decline in glomerular filtration rate (GFR). The majority of patients with diabetes who have macroalbuminuria also have hypertension9697 ; in these patients, control of hypertension slows the decline in GFR.9899100 Some patients with diabetes develop the nephrotic syndrome (urine protein >3 g/d); diabetic dyslipidemia in such patients often is compounded by nephrotic dyslipidemia, most notably by higher cholesterol levels. The nephrotic syndrome usually heralds progressive renal insufficiency; thereafter, ESRD ensues and dialysis and/or transplantation become necessary to sustain life.Risk Assessment in the Diabetic PatientRisk assessment must take into account the major risk factors (cigarette smoking, elevated blood pressure, abnormal serum lipids and lipoproteins, and hyperglycemia) and predisposing risk factors (excess body weight and abdominal obesity, physical inactivity, and family history of CVD). Identification of risk factors is a major first step for developing a plan for risk reduction in persons with diabetes. Specific steps in the evaluation of the major risk factors in such persons are presented in Table 1. These steps include a thorough medical history, careful physical examination, and appropriate laboratory measurements. Specialized testing may be particularly useful, eg, 24-hour monitoring of ambulatory blood pressure by automated techniques. Lipoprotein analysis should draw a clear distinction between elevated LDL cholesterol concentrations and atherogenic dyslipidemia (or diabetic dyslipidemia) as manifested by elevated triglycerides and small LDL and low HDL cholesterol levels. Even borderline-high-risk LDL cholesterol levels (130 to 159 mg/dL) are of concern in patients with diabetes and call for aggressive intervention. The quality of glycemic control can best be assessed by periodic measurement of hemoglobin A1c. Furthermore, because hyperglycemia per se confers increased risk for CVD, the presence of other risk factors—smoking, hypertension, even borderline-high-risk LDL cholesterol, and atherogenic dyslipidemia—signifies enhanced risk and signals the need for more aggressive intervention on all risk factors.Risk assessment in the diabetic patient is not complete until predisposing risk factors—obesity, physical inactivity, and family history of premature CVD—have been evaluated (Table 2). Identification of predisposing risk factors will provide insight into the causation of the major risk factors. The finding of abdominal obesity, as evidenced by an increased waist circumference, usually indicates the presence of insulin resistance. A careful assessment of the status of the predisposing risk factor sets the stage for therapeutic modification of life habits. A genetic basis for risk, as revealed by a positive family history of CVD or diabetes, may point to the need for pharmacological control of risk factors. Moreover, a positive family history often uncovers family members who also need risk-factor intervention.Clinical EvaluationDetection of Clinical and Subclinical CVDProspective studies101 document an increased likelihood of sudden cardiac death and unrecognized myocardial infarctions in patients with diabetes. Moreover, acute ischemic syndromes, peripheral arterial disease, and advanced CVD complications occur more commonly in patients with diabetes than in those without.101 Because the typical cardiac symptoms often are masked in patients with diabetes, the diagnosis of myocardial infarction commonly is missed or delayed. Effective strategies for earlier detection of clinical CVD could reduce morbidity and mortality in patients with diabetes. In addition, detection of subclinical atherosclerosis and early clinical manifestation of CVD could lead to more effective primary prevention in some patients with diabetes.Table 3 outlines a general approach to the detection of clinical and subclinical CVD in the hyperglycemic patient. Stress testing for myocardial ischemia and dysfunction should be performed in accord with general American College of Cardiology (ACC)/AHA guidelines102 ; Table 3 lists further special considerations for exercise testing in patients with diabetes. Noninvasive evaluation of cardiac function in hyperglycemic patients suspected of having myocardial dysfunction may be a useful guide to cardiovascular management in some of these patients. Many patients with diabetes suffer from an autonomic dysfunction that impairs quality of life and predisposes to life-threatening cardiovascular complications. Finally, the finding of subclinical CVD signals the need for institution of more aggressive preventive measures.Evaluation of Renal StatusChronic renal failure is a major clinical outcome in patients with diabetes. It is more likely to develop in type 1 diabetes than in type 2 diabetes. However, the high prevalence of type 2 diabetes makes it a major cause of ESRD. The renal status of patients with diabetes therefore must be appropriately monitored so that effective intervention can be introduced early in the course of renal disease. Table 4 outlines the steps in evaluation. Testing for urine albumin and protein is the first step. Microalbuminuria is indicative of early diabetic nephropathy. In patients with type 1 diabetes, it is a harbinger of ongoing renal damage; in type 2 diabetes, it signifies enhanced risk for CVD. Macroalbuminuria and/or nephrotic-range proteinuria predicts a decline in renal function. Patients with macroalbuminuria should be referred to a nephrologist who can rule out another kidney disease and who can help to plan a strategy for preventing progression to ESRD. This strategy should include aggressive management of hypertension to blood pressure levels of <130/85 mm Hg. Although the serum creatinine is not a sensitive indicator of the degree of loss of GFR, a rising serum creatinine plotted as changes in the reciprocal of serum creatinine versus time provides a means of determining the rate of decline in renal function. Direct measurement of GFR is the most reliable estimate of the amount of residual kidney function but is more expensive and technically demanding.Cardiovascular Clinical ManagementMedical (Noninvasive) Management of Diabetic Patients With Clinical CVDCompelling evidence, including data from recent clinical trials, demonstrates that comprehensive medical intervention in patients with established atherosclerotic CVD has thefollowing benefits: it extends overall survival; improves quality of life; decreases the need for intervention procedures, such as angioplasty and coronary artery bypass graft surgery; and reduces the incidence of subsequent myocardial infarction.103 In many patients with CHD, aggressive risk reduction with medical therapy will delay or eliminate the need for revascularization procedures. Treatment of risk factors in patients with established CHD or other clinical atherosclerotic disease has been called secondary prevention. Although the number of patients with diabetes included in clinical trials has been limited, the available results suggest that these patients respond to secondary prevention interventions at least as well as those without diabetes.8687888990 Consequently, the general guidelines for noninvasive, medical management in secondary prevention can be applied when patients with diabetes have clinical atherosclerotic CVD. Table 5 summarizes the AHA/ACC guide103 to comprehensive risk reduction in patients with clinical coronary and other vascular disease, as modified for CVD patients with diabetes.A few general comments can be made about application of these guidelines to patients with diabetes. Because cigarette smoking remains a powerful risk factor in patients with diabetes, a major effort must be made to overcome the smoking habit. The AHA has recently published practical guidelines for assisting patients in smoking cessation.104 For lipid management, the primary goal of therapy is to reduce LDL-cholesterol levels to ≤100 mg/dL.103 This goal should be achieved by addition of drug therapy (when necessary) to maximal dietary therapy. Statins are first-line therapy to achieve an LDL cholesterol of ≤100 mg/dL. When triglycerides remain >200 mg/dL in patients receiving statin therapy, consideration should be given to adding a fibrate to achieve the secondary goal of lipid management, ie, a triglyceride <200 mg/dL. Although nicotinic acid effectively lowers triglycerides and raises HDL levels in patients with type 2 diabetes, its tendency to worsen hyperglycemia causes it to be relatively contraindicated. The goal of blood pressure control is to reduce blood pressure to <135/85 mm Hg in hypertensive patients105 ; this goal often will require antihypertensive drug therapy.Treatment of hyperglycemia is stepwise and typically dependent on duration of disease. To prevent microangiopathy, neuropathy, and perhaps macrovascular disease, a prudent therapeutic goal is to reduce the glycohemoglobin to ≤1% above the upper limit of normal.39106 Weight loss and increased exercise are first-line therapy for reducing hyperglycemia. If hyperglycemia persists, a sulfonylurea or metformin can be used next. The recent UK Prospective Diabetes Study39 revealed the safety and efficacy of sulfonylureas in control of hyperglycemia in diabetic patients. Metformin also proved efficacious, although an apparent increase in death rates on the combination of metformin and sulfonylureas calls for more study on the safety of this combination.107Another promising group of agents for treatment of type 2 diabetes includes the thiazolidenediones. These agents lower glucose levels by reducing insulin resistance. The first drug in this class to be approved for clinical use was troglitazone. This agent is approved for use in combination with insulin therapy to improve glycemic control. Unfortunately, troglitazone produces rare but severe liver toxicity108109110 ; the possibility of this adverse reaction requires close monitoring of patients. Nonetheless, despite its potential hepatotoxicity, troglitazone is currently being widely used to treat hyperglycemia. New drugs of the same class, rosiglitazone and pioglitazone, may have less potential hepatotoxicity. A different type of drug available for glucose control is acarbose; this agent partially blocks glucose absorption. In patients who fail to achieve glucose control and near-normal hemoglobin A1c levels by changes in life habits and oral hypoglycemic agents, insulin should be initiated.Other risk-reduction strategies in patients with diabetes deserve attention equal to that given glucose control. Patients with type 2 diabetes should increase physical activity and eliminate excess body weight; both may be facilitated with the help of professional guidance. Antiplatelet agents have become almost routine in patients with atherosclerotic CVD, and their use can be extended to patients with diabetes who have established atherosclerotic disease. β-Blockers reduce cardiovascular mortality after myocardial infarction. They may be particularly effective in patients with diabetes, who are at risk for symptomatic ischemic episodes secondary to increased sympathetic activity.111 β-Blockers are often mentioned as being contraindicated for patients with diabetes because of their blocking of hypoglycemic symptoms in the presence of a hypoglycemic regimen. Clinicians should be aware of this potential danger, although this side effect need not preclude use of β-blockers when CHD patients have diabetes. Angiotensin-converting enzyme (ACE) inhibitors are widely prescribed in the post–myocardial infarction period to favorably influence myocardial remodeling and fibrosis, and they should be continued indefinitely in all patients with reduced left ventricular ejection fraction or symptoms of heart failure. Unfortunately, limited data are available on use of estrogen replacement therapy in postmenopausal women with diabetes; a recent clinical trial calls into question its putative benefit in postmenopausal, nondiabetic women with established CHD.112Management of Diabetic NephropathyMore than one strategy has been shown to slow the progression of nephropathy in patients with diabetes. A general approach is outlined in Table 6. Specific interventions include control of hyperglycemia, treatment of hypertension (particularly by use of ACE inhibitors), sodium restriction, and dietary protein restriction. Treatment of hypertensi

HomeCirculationVol. 114, No. 7ACC/AHA/ESC 2006 Guidelines for the Management of Patients With Atrial Fibrillation Free AccessReview ArticlePDF/EPUBAboutView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toFree AccessReview ArticlePDF/EPUBACC/AHA/ESC 2006 Guidelines for the Management of Patients With Atrial FibrillationA Report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines and the European Society of Cardiology Committee for Practice Guidelines (Writing Committee to Revise the 2001 Guidelines for the Management of Patients With Atrial Fibrillation): Developed in Collaboration With the European Heart Rhythm Association and the Heart Rhythm Society Valentin Fuster, WRITING COMMITTEE:, MD, PhD, FACC, FAHA, FESC, Co-Chair, Lars E. Rydén, MD, PhD, FACC, FESC, FAHA, Co-Chair, David S. Cannom, MD, FACC, Harry J. Crijns, MD, FACC, FESC, Anne B. Curtis, MD, FACC, FAHA, Kenneth A. Ellenbogen, MD, FACC, Jonathan L. Halperin, MD, FACC, FAHA, Jean-Yves Le Heuzey, MD, FESC, G. Neal Kay, MD, FACC, James E. Lowe, MD, FACC, S. Bertil Olsson, MD, PhD, FESC, Eric N. Prystowsky, MD, FACC, Juan Luis Tamargo, MD, FESC, Samuel Wann, MD, FACC, FESC, ACC/AHA TASK FORCE MEMBERS Sidney C. SmithJr, MD, FACC, FAHA, FESC, Chair, Alice K. Jacobs, MD, FACC, FAHA, Vice-Chair, Cynthia D. Adams, MSN, APRN-BC, FAHA, Jeffery L. Anderson, MD, FACC, FAHA, Elliott M. Antman, MD, FACC, FAHA, Jonathan L. Halperin, MD, FACC, FAHA, Sharon Ann Hunt, MD, FACC, FAHA, Rick Nishimura, MD, FACC, FAHA, Joseph P. Ornato, MD, FACC, FAHA, Richard L. Page, MD, FACC, FAHA, Barbara Riegel, DNSc, RN, FAHA, ESC COMMITTEE FOR PRACTICE GUIDELINES Silvia G. Priori, MD, PhD, FESC, Chair, Jean-Jacques Blanc, MD, FESC, France, Andrzej Budaj, MD, FESC, Poland, A. John Camm, MD, FESC, FACC, FAHA, United Kingdom, Veronica Dean, France, Jaap W. Deckers, MD, FESC, The Netherlands, Catherine Despres, France, Kenneth Dickstein, MD, PhD, FESC, Norway, John Lekakis, MD, FESC, Greece, Keith McGregor, PhD, France, Marco Metra, MD, Italy, Joao Morais, MD, FESC, Portugal, Ady Osterspey, MD, Germany, Juan Luis Tamargo, MD, FESC, Spain and José Luis Zamorano, MD, FESC, Spain Valentin FusterValentin Fuster Search for more papers by this author , Lars E. RydénLars E. Rydén Search for more papers by this author , David S. CannomDavid S. Cannom Search for more papers by this author , Harry J. CrijnsHarry J. Crijns Search for more papers by this author , Anne B. CurtisAnne B. Curtis Search for more papers by this author , Kenneth A. EllenbogenKenneth A. Ellenbogen Search for more papers by this author , Jonathan L. HalperinJonathan L. Halperin Search for more papers by this author , Jean-Yves Le HeuzeyJean-Yves Le Heuzey Search for more papers by this author , G. Neal KayG. Neal Kay Search for more papers by this author , James E. LoweJames E. Lowe Search for more papers by this author , S. Bertil OlssonS. Bertil Olsson Search for more papers by this author , Eric N. PrystowskyEric N. Prystowsky Search for more papers by this author , Juan Luis TamargoJuan Luis Tamargo Search for more papers by this author , Samuel WannSamuel Wann Search for more papers by this author , ACC/AHA TASK FORCE MEMBERS Search for more papers by this author , Sidney C. SmithJrSidney C. SmithJr Search for more papers by this author , Alice K. JacobsAlice K. Jacobs Search for more papers by this author , Cynthia D. AdamsCynthia D. Adams Search for more papers by this author , Jeffery L. AndersonJeffery L. Anderson Search for more papers by this author , Elliott M. AntmanElliott M. Antman Search for more papers by this author , Jonathan L. HalperinJonathan L. Halperin Search for more papers by this author , Sharon Ann HuntSharon Ann Hunt Search for more papers by this author , Rick NishimuraRick Nishimura Search for more papers by this author , Joseph P. OrnatoJoseph P. Ornato Search for more papers by this author , Richard L. PageRichard L. Page Search for more papers by this author , Barbara RiegelBarbara Riegel Search for more papers by this author , ESC COMMITTEE FOR PRACTICE GUIDELINES Search for more papers by this author , Silvia G. PrioriSilvia G. Priori Search for more papers by this author , Jean-Jacques BlancJean-Jacques Blanc Search for more papers by this author , Andrzej BudajAndrzej Budaj Search for more papers by this author , A. John CammA. John Camm Search for more papers by this author , Veronica DeanVeronica Dean Search for more papers by this author , Jaap W. DeckersJaap W. Deckers Search for more papers by this author , Catherine DespresCatherine Despres Search for more papers by this author , Kenneth DicksteinKenneth Dickstein Search for more papers by this author , John LekakisJohn Lekakis Search for more papers by this author , Keith McGregorKeith McGregor Search for more papers by this author , Marco MetraMarco Metra Search for more papers by this author , Joao MoraisJoao Morais Search for more papers by this author , Ady OsterspeyAdy Osterspey Search for more papers by this author , Juan Luis TamargoJuan Luis Tamargo Search for more papers by this author and José Luis ZamoranoJosé Luis Zamorano Search for more papers by this author Originally published15 Aug 2006https://doi.org/10.1161/CIRCULATIONAHA.106.177292Circulation. 2006;114:e257–e354is corrected byCorrectionTABLE OF CONTENTSPreamble…e2601. Introduction…e261 1.1. Organization of Committee and Evidence Review…e261 1.2. Contents of These Guidelines…e261 1.3. Changes Since the Initial Publication of These Guidelines in 2001…e2632. Definition…e263 2.1. Atrial Fibrillation…e263 2.2. Related Arrhythmias…e2633. Classification…e2634. Epidemiology and Prognosis…e265 4.1. Prevalence…e266 4.2. Incidence…e266 4.3. Prognosis…e2675. Pathophysiological Mechanisms…e268 5.1. Atrial Factors…e268 5.1.1. Atrial Pathology as a Cause of Atrial Fibrillation…e268 5.1.1.1. Pathological Changes Caused by Atrial Fibrillation…e268 5.1.2. Mechanisms of Atrial Fibrillation…e269 5.1.2.1. Automatic Focus Theory…e269 5.1.2.2. Multiple-Wavelet Hypothesis…e269 5.1.3. Atrial Electrical Remodeling…e270 5.1.4. Counteracting Atrial Electrical Remodeling…e271 5.1.5. Other Factors Contributing to Atrial Fibrillation…e271 5.2. Atrioventricular Conduction…e272 5.2.1. General Aspects…e272 5.2.2. Atrioventricular Conduction in Patients With Preexcitation Syndromes…e272 5.3. Myocardial and Hemodynamic Consequences of Atrial Fibrillation…e272 5.4. Thromboembolism…e273 5.4.1. Pathophysiology of Thrombus Formation…e273 5.4.2. Clinical Implications…e2746. Causes, Associated Conditions, Clinical Manifestations, and Quality of Life…e274 6.1. Causes and Associated Conditions…e274 6.1.1. Reversible Causes of Atrial Fibrillation…e274 6.1.2. Atrial Fibrillation Without Associated Heart Disease…e274 6.1.3. Medical Conditions Associated With Atrial Fibrillation…e274 6.1.4. Atrial Fibrillation With Associated Heart Disease…e275 6.1.5. Familial (Genetic) Atrial Fibrillation…e275 6.1.6. Autonomic Influences in Atrial Fibrillation…e275 6.2. Clinical Manifestations…e275 6.3. Quality of Life…e2767. Clinical Evaluation…e276 7.1. Basic Evaluation of the Patient With Atrial Fibrillation…e276 7.1.1. Clinical History and Physical Examination…e276 7.1.2. Investigations…e276 7.2. Additional Investigation of Selected Patients With Atrial Fibrillation…e278 7.2.1. Electrocardiogram Monitoring and Exercise Testing…e278 7.2.2. Transesophageal Echocardiography…e278 7.2.3. Electrophysiological Study…e2788. Management…e278 8.1. Pharmacological and Nonpharmacological Therapeutic Options…e279 8.1.1. Pharmacological Therapy…e279 8.1.1.1. Drugs Modulating the Renin- Angiotensin-Aldosterone System…e279 8.1.1.2. HMG CoA-Reductase Inhibitors (Statins)…e280 8.1.2. Heart Rate Control Versus Rhythm Control…e280 8.1.2.1. Distinguishing Short-Term and Long-Term Treatment Goals…e280 8.1.2.2. Clinical Trials Comparing Rate Control and Rhythm Control…e280 8.1.2.3. Effect on Symptoms and Quality of Life…e280 8.1.2.4. Effects on Heart Failure…e281 8.1.2.5. Effects on Thromboembolic Complications…e281 8.1.2.6. Effects on Mortality and Hospitalization…e282 8.1.2.7. Implications of the Rhythm-Control Versus Rate-Control Studies…e282 8.1.3. Rate Control During Atrial Fibrillation…e282 8.1.3.1. Pharmacological Rate Control During Atrial Fibrillation…e283 8.1.3.1.1. Beta Blockers…e284 8.1.3.1.2. Nondihydropyridine Calcium Channel Antagonists…e285 8.1.3.1.3. Digoxin…e285 8.1.3.1.4. Antiarrhythmic Agents…e285 8.1.3.1.5. Combination Therapy…e285 8.1.3.1.6. Special Considerations in Patients With the Wolff- Parkinson-White (WPW) Syndrome…e286 8.1.3.2. Pharmacological Therapy to Control Heart Rate in Patients With Both Atrial Fibrillation and Atrial Flutter…e286 8.1.3.3. Regulation of Atrioventricular Nodal Conduction by Pacing…e286 8.1.3.4. AV Nodal Ablation…e286 8.1.4. Preventing Thromboembolism…e287 8.1.4.1. Risk Stratification…e288 8.1.4.1.1. Epidemiological Data…e288 8.1.4.1.2. Echocardiography and Risk Stratification…e289 8.1.4.1.3. Therapeutic Implications…e290 8.1.4.2. Antithrombotic Strategies for Prevention of Ischemic Stroke and Systemic Embolism…e292 8.1.4.2.1. Anticoagulation With Vitamin K Antagonist Agents…e292 8.1.4.2.2. Aspirin for Antithrombotic Therapy in Patients With Atrial Fibrillation…e294 8.1.4.2.3. Other Antiplatelet Agents for Antithrombotic Therapy in Patients With Atrial Fibrillation…e295 8.1.4.2.4. Combining Anticoagulant and Platelet-Inhibitor Therapy…e296 8.1.4.2.5. Emerging and Investigational Antithrombotic Agents…e297 8.1.4.2.6. Interruption of Anticoagulation for Diagnostic or Therapeutic Procedures…e298 8.1.4.3. Nonpharmacological Approaches to Prevention of Thromboembolism…e298 8.1.5. Cardioversion of Atrial Fibrillation…e298 8.1.5.1. Basis for Cardioversion of Atrial Fibrillation…e298 8.1.5.2. Methods of Cardioversion…e299 8.1.5.3. Pharmacological Cardioversion…e299 8.1.5.4. Agents With Proven Efficacy for Cardioversion of Atrial Fibrillation…e300 8.1.5.4.1. Amiodarone…e300 8.1.5.4.2. Dofetilide…e300 8.1.5.4.3. Flecainide…e300 8.1.5.4.4. Ibutilide…e302 8.1.5.4.5. Propafenone…e302 8.1.5.5. Less Effective or Incompletely Studied Agents for Cardioversion of Atrial Fibrillation…e303 8.1.5.5.1. Quinidine…e303 8.1.5.5.2. Procainamide…e303 8.1.5.5.3. Beta Blockers…e304 8.1.5.5.4. Nondihydropyridine Calcium Channel Antagonists (Verapamil and Diltiazem)…e304 8.1.5.5.5. Digoxin…e304 8.1.5.5.6. Disopyramide…e304 8.1.5.5.7. Sotalol…e304 8.1.6. Pharmacological Agents to Maintain Sinus Rhythm…e304 8.1.6.1. Agents With Proven Efficacy to Maintain Sinus Rhythm…e304 8.1.6.1.1. Amiodarone…e304 8.1.6.1.2. Beta Blockers…e305 8.1.6.1.3. Dofetilide…e305 8.1.6.1.4. Disopyramide…e306 8.1.6.1.5. Flecainide…e306 8.1.6.1.6. Propafenone…e306 8.1.6.1.7. Sotalol…e306 8.1.6.2. Drugs With Unproven Efficacy or No Longer Recommended…e307 8.1.6.2.1. Digoxin…e307 8.1.6.2.2. Procainamide…e307 8.1.6.2.3. Quinidine…e307 8.1.6.2.4. Verapamil and Diltiazem…e307 8.1.7. Out-of-Hospital Initiation of Antiarrhythmic Drugs in Patients With Atrial Fibrillation…e307 8.1.8. Drugs Under Development…e309 8.1.8.1. Atrioselective Agents…e310 8.1.8.2. Nonselective Ion Channel–Blocking Drugs…e310 8.2. Direct-Current Cardioversion of Atrial Fibrillation and Flutter…e310 8.2.1. Terminology…e310 8.2.2. Technical Aspects…e310 8.2.3. Procedural Aspects…e311 8.2.4. Direct-Current Cardioversion in Patients With Implanted Pacemakers and Defibrillators…e311 8.2.5. Risks and Complications of Direct-Current Cardioversion of Atrial Fibrillation…e312 8.2.6. Pharmacological Enhancement of Direct-Current Cardioversion…e312 8.2.6.1. Amiodarone…e313 8.2.6.2. Beta-Adrenergic Antagonists…e313 8.2.6.3. Nondihydropyridine Calcium Channel Antagonists…e313 8.2.6.4. Quinidine…e314 8.2.6.5. Type IC Antiarrhythmic Agents…e314 8.2.6.6. Type III Antiarrhythmic Agents…e314 8.2.7. Prevention of Thromboembolism in Patients With Atrial Fibrillation Undergoing Cardioversion…e314 8.3. Maintenance of Sinus Rhythm…e315 8.3.1. Pharmacological Therapy…e316 8.3.1.1. Goals of Treatment…e316 8.3.1.2. Endpoints in Antiarrhythmic Drug Studies…e316 8.3.1.3. Predictors of Recurrent AF…e317 8.3.2. General Approach to Antiarrhythmic Drug Therapy…e317 8.3.3. Selection of Antiarrhythmic Agents in Patients With Cardiac Diseases…e317 8.3.3.1. Heart Failure…e317 8.3.3.2. Coronary Artery Disease…e318 8.3.3.3. Hypertensive Heart Disease…e318 8.3.4. Nonpharmacological Therapy for Atrial Fibrillation…e319 8.3.4.1. Surgical Ablation…e319 8.3.4.2. Catheter Ablation…e319 8.3.4.2.1. Complications of Catheter- Based Ablation…e320 8.3.4.2.2. Future Directions in Catheter-Based Ablation Therapy for Atrial Fibrillation…e320 8.3.4.3. Suppression of Atrial Fibrillation Through Pacing…e320 8.3.4.4. Internal Atrial Defibrillators…e321 8.4. Special Considerations…e321 8.4.1. Postoperative AF…e321 8.4.1.1. Clinical and Pathophysiological Correlates…e322 8.4.1.2. Prevention of Postoperative AF…e322 8.4.1.3. Treatment of Postoperative AF…e323 8.4.2. Acute Myocardial Infarction…e323 8.4.3. Wolff-Parkinson White (WPW) Preexcitation Syndromes…e324 8.4.4. Hyperthyroidism…e325 8.4.5. Pregnancy…e325 8.4.6. Hypertrophic Cardiomyopathy…e326 8.4.7. Pulmonary Diseases…e327 8.5. Primary Prevention…e3279. Proposed Management Strategies…e327 9.1. Overview of Algorithms for Management of Patients With Atrial Fibrillation…e327 9.1.1. Newly Discovered Atrial Fibrillation…e328 9.1.2. Recurrent Paroxysmal Atrial Fibrillation…e328 9.1.3. Recurrent Persistent Atrial Fibrillation…e328 9.1.4. Permanent Atrial Fibrillation…e329APPENDIX I…e330APPENDIX II…e331APPENDIX III…e333References…e335PreambleIt is important that the medical profession play a significant role in critically evaluating the use of diagnostic procedures and therapies as they are introduced and tested in the detection, management, or prevention of disease states. Rigorous and expert analysis of the available data documenting absolute and relative benefits and risks of those procedures and therapies can produce helpful guidelines that improve the effectiveness of care, optimize patient outcomes, and favorably affect the overall cost of care by focusing resources on the most effective strategies.The American College of Cardiology Foundation (ACCF) and the American Heart Association (AHA) have jointly engaged in the production of such guidelines in the area of cardiovascular disease since 1980. The ACC/AHA Task Force on Practice Guidelines, whose charge is to develop, update, or revise practice guidelines for important cardiovascular diseases and procedures, directs this effort. The Task Force is pleased to have this guideline developed in conjunction with the European Society of Cardiology (ESC). Writing committees are charged with the task of performing an assessment of the evidence and acting as an independent group of authors to develop or update written recommendations for clinical practice.Experts in the subject under consideration have been selected from all 3 organizations to examine subject-specific data and write guidelines. The process includes additional representatives from other medical practitioner and specialty groups when appropriate. Writing committees are specifically charged to perform a formal literature review, weigh the strength of evidence for or against a particular treatment or procedure, and include estimates of expected health outcomes where data exist. Patient-specific modifiers, comorbidities, and issues of patient preference that might influence the choice of particular tests or therapies are considered as well as frequency of follow-up and cost-effectiveness. When available, information from studies on cost will be considered; however, review of data on efficacy and clinical outcomes will constitute the primary basis for preparing recommendations in these guidelines.The ACC/AHA Task Force on Practice Guidelines and the ESC Committee for Practice Guidelines make every effort to avoid any actual, potential, or perceived conflict of interest that might arise as a result of an outside relationship or personal interest of the writing committee. Specifically, all members of the Writing Committee and peer reviewers of the document are asked to provide disclosure statements of all such relationships that might be perceived as real or potential conflicts of interest. Writing committee members are also strongly encouraged to declare a previous relationship with industry that might be perceived as relevant to guideline development. If a writing committee member develops a new relationship with industry during their tenure, they are required to notify guideline staff in writing. The continued participation of the writing committee member will be reviewed. These statements are reviewed by the parent Task Force, reported orally to all members of the writing committee at each meeting, and updated and reviewed by the writing committee as changes occur. Please refer to the methodology manuals for further description of the policies used in guideline development, including relationships with industry, available online at the ACC, AHA, and ESC World Wide Web sites (http://www.acc.org/clinical/manual/manual_introltr.htm, http://circ.ahajournals.org/manual/, and http://www.escardio.org/knowledge/guidelines/Rules/). Please see Appendix I for author relationships with industry and Appendix II for peer reviewer relationships with industry that are pertinent to these guidelines.These practice guidelines are intended to assist healthcare providers in clinical decision making by describing a range of generally acceptable approaches for the diagnosis, management, and prevention of specific diseases and conditions. These guidelines attempt to define practices that meet the needs of most patients in most circumstances. These guideline recommendations reflect a consensus of expert opinion after a thorough review of the available, current scientific evidence and are intended to improve patient care. If these guidelines are used as the basis for regulatory/payer decisions, the ultimate goal is quality of care and serving the patient’s best interests. The ultimate judgment regarding care of a particular patient must be made by the healthcare provider and the patient in light of all of the circumstances presented by that patient. There are circumstances in which deviations from these guidelines are appropriate.The guidelines will be reviewed annually by the ACC/AHA Task Force on Practice Guidelines and the ESC Committee for Practice Guidelines and will be considered current unless they are updated, revised, or sunsetted and withdrawn from distribution. The executive summary and recommendations are published in the August 15, 2006, issues of the Journal of the American College of Cardiology and Circulation and the August 16, 2006, issue of the European Heart Journal. The full-text guidelines are published in the August 15, 2006, issues of the Journal of the American College of Cardiology and Circulation and the September 2006 issue of Europace, as well as posted on the ACC (www.acc.org), AHA (www.americanheart.org), and ESC (www.escardio.org) World Wide Web sites. Copies of the full-text guidelines and the executive summary are available from all 3 organizations.Sidney C. Smith Jr, MD, FACC, FAHA, FESC, Chair, ACC/AHA Task Force on Practice GuidelinesSilvia G. Priori, MD, PhD, FESC, Chair, ESC Committee for Practice Guidelines1. Introduction1.1. Organization of Committee and Evidence ReviewAtrial fibrillation (AF) is the most common sustained cardiac rhythm disturbance, increasing in prevalence with age. AF is often associated with structural heart disease, although a substantial proportion of patients with AF have no detectable heart disease. Hemodynamic impairment and thromboembolic events related to AF result in significant morbidity, mortality, and cost. Accordingly, the American College of Cardiology (ACC), the American Heart Association (AHA), and the European Society of Cardiology (ESC) created a committee to establish guidelines for optimum management of this frequent and complex arrhythmia.The committee was composed of members representing the ACC, AHA, and ESC, as well as the European Heart Rhythm Association (EHRA) and the Heart Rhythm Society (HRS). This document was reviewed by 2 official reviewers nominated by the ACC, 2 official reviewers nominated by the AHA, and 2 official reviewers nominated by the ESC, as well as by the ACCF Clinical Electrophysiology Committee, the AHA ECG and Arrhythmias Committee, the AHA Stroke Review Committee, EHRA, HRS, and numerous additional content reviewers nominated by the writing committee. The document was approved for publication by the governing bodies of the ACC, AHA, and ESC and officially endorsed by the EHRA and the HRS.The ACC/AHA/ESC Writing Committee to Revise the 2001 Guidelines for the Management of Patients With Atrial Fibrillation conducted a comprehensive review of the relevant literature from 2001 to 2006. Literature searches were conducted in the following databases: PubMed/MEDLINE and the Cochrane Library (including the Cochrane Database of Systematic Reviews and the Cochrane Controlled Trials Registry). Searches focused on English-language sources and studies in human subjects. Articles related to animal experimentation were cited when the information was important to understanding pathophysiological concepts pertinent to patient management and comparable data were not available from human studies. Major search terms included atrial fibrillation, age, atrial remodeling, atrioventricular conduction, atrioventricular node, cardioversion, classification, clinical trial, complications, concealed conduction, cost-effectiveness, defibrillator, demographics, epidemiology, experimental, heart failure (HF), hemodynamics, human, hyperthyroidism, hypothyroidism, meta-analysis, myocardial infarction, pharmacology, postoperative, pregnancy, pulmonary disease, quality of life, rate control, rhythm control, risks, sinus rhythm, symptoms, andtachycardia-mediated cardiomyopathy.The complete list of search terms is beyond the scope of this section.Classification of Recommendations and Level of Evidence are expressed in the ACC/AHA/ESC format as follows and described in Table 1. Recommendations are evidence based and derived primarily from published data. TABLE 1. Applying Classification of Recommendations and Level of Evidence†Size of Treatment Effect*Data available from clinical trials or registries about the usefulness/efficacy in different subpopulations, such as gender, age, history of diabetes, history of prior myocardial infarction, history of heart failure, and prior aspirin use. A recommendation with Level of Evidence B or C does not imply that the recommendation is weak. Many important clinical questions addressed in the guidelines do not lend themselves to clinical trials. Even though randomized trials are not available, there may be a very clear clinical consensus that a particular test or therapy is useful or effective.†In 2003, the ACC/AHA Task Force on Practice Guidelines developed a list of suggested phrases to use when writing recommendations. All guideline recommendations have been written in full sentences that express a complete thought, such that a recommendation, even if separated and presented apart from the rest of the document (including headings above sets of recommendations), would still convey the full intent of the recommendation. It is hoped that this will increase readers’ comprehension of the guidelines and will allow queries at the individual recommendation level.Estimate of Certainty (Precision) of Treatment EffectClass IClass IIaClass IIbClass IIIBenefit >>> RiskBenefit >> RiskBenefit ≥ RiskRisk ≥ BenefitAdditional studies with focused objectives neededAdditional studies with broad objectives needed; additional registry data would be helpfulNo additional studies neededProcedure/treatment SHOULD be performed/administeredIT IS REASONABLE to perform procedure/administer treatmentProcedure/treatment MAY BE CONSIDEREDProcedure/treatment should NOT be performed/administered SINCE IT IS NOT HELPFUL AND MAY BE HARMFULLevel A• Recommendation that procedure or treatment is useful/effective• Recommendation in favor of treatment or procedure being useful/effective• Recommendation’s usefulness/efficacy less well established• Recommendation that procedure or treatment is not useful/effective and may be harmfulMultiple (3 to 5) population risk strata evaluated*General consistency of direction and magnitude of effect• Sufficient evidence from multiple randomized trials or meta-analyses• Some conflicting evidence from multiple randomized trials or meta-analyses• Greater conflicting evidence from multiple randomized trials or meta-analyses• Sufficient evidence from multiple randomized trials or meta-analysesLevel B• Recommendation that procedure or treatment is useful/effective• Recommendation in favor of treatment or procedure being useful/effective• Recommendation’s usefulness/efficacy less well established• Recommendation that procedure or treatment is not useful/effective and may be harmfulLimited (2 to 3) population risk strata evaluated*• Limited evidence from single randomized trial or nonrandomized studies• Some conflicting evidence from single randomized trial or nonrandomized studies• Greater conflicting evidence from single randomized trial or nonrandomized studies• Limited evidence from single randomized trial or nonrandomized studiesLevel C• Recommendation that procedure or treatment is useful/effective• Recommendation in favor of treatment or procedure being useful/effective• Recommendation’s usefulness/efficacy less well established• Recommendation that procedure or treatment is not useful/effective and may be harmfulVery limited (1 to 2) population risk strata evaluated*• Only expert opinion, case studies, or standard-of-care• Only diverging expert opinion, case studies, or standard-of-care• Only diverging expert opinion, case studies, or standard-of-care• Only expert opinion, case studies, or standard-of-careClassification of RecommendationsClass I: Conditions for which there is evidence and/or general agreement that a given procedure/therapy is beneficial, useful, and effective.Class II: Conditions for which there is conflicting evidence and/or a divergence of opinion about the usefulness/efficacy of performing the procedure/therapy. ○ Class IIa: Weight of evidence/opinion is in favor of usefulness/efficacy. ○ Class IIb: Usefulness/efficacy is less well established by evidence/opinion.Class III: Conditions for which there is evidence and/or general agreement that a procedure/therapy is not useful or effective and in some cases may be harmful.Level of EvidenceThe weight of evidence was ranked from highest (A) to lowest (C), as follows:Level of Evidence A: Data derived from multiple randomized clinical trials or meta-analyses.Level of Evidence B: Data derived from a single randomized trial or nonrandomized studies.Level of Evidence C: Only consensus opinion of experts, case studies, or standard-of-care.1.2. Contents of These GuidelinesThese guidelines first present a comprehensive review of the latest information about the definition, classification, epidemiology, pathophysiological mechanisms, and clinical characteristics of AF. The management of this complex and potentially dangerous arrhythmia is then reviewed. This includes prevention of AF, control of heart rate, prevention of thromboembolism, and conversion to and maintenance of sinus rhythm. The treatment algorithms include pharmacological and nonpharmacological antiarrhythmic approaches, as well as antithrombotic strategies most appropriate for particular clinical conditions. Overall, this is a consensus document that attempts to reconcile evidence and opinion from both sides of the Atlantic Ocean. The pharmacological and nonpharmacological antiarrhythmic approaches may include some drugs and devices that do not have the approval of all government regulatory agencies. Additional information may be obtained from the package inserts when the drug or device has been approved for the stated indication.Because atrial flutter can precede or coexist with AF, special consideration is given to this arrhythmia in each section. There are important differences in the mechanisms of AF and atrial flutter, and the body of evidence av

T he initial Guide to the Primary Prevention of Cardiovas- cular Diseases was published in 1997 as an aid to healthcare professionals and their patients without established coronary artery disease or other atherosclerotic diseases. 1It was intended to complement the American Heart Association (AHA)/American College of Cardiology (ACC) Guidelines for Preventing Heart Attack and Death in Patients with Atherosclerotic Cardiovascular Disease (updated 2 ) and to provide the healthcare professional with a comprehensive approach to patients across a wide spectrum of risk.The imperative to prevent the first episode of coronary disease or stroke or the development of aortic aneurysm and peripheral arterial disease remains as strong as ever because of the still-high rate of first events that are fatal or disabling or require expensive intensive medical care.The evidence that most cardiovascular disease is preventable continues to grow.Results of long-term prospective studies consistently identify persons with low levels of risk factors as having lifelong low levels of heart disease and stroke. 3,4Moreover, these low levels of risk factors are related to healthy lifestyles.Data from the Nurses Health Study, 5 for example, suggest that in women, maintaining a desirable body weight, eating a healthy diet, exercising regularly, not smoking, and consuming a moderate amount of alcohol could account for an 84% reduction in risk, yet only 3% of the women studied were in that category.Clearly, the majority of the causes of cardiovascular disease are known and modifiable.This 2002 update of the Guide acknowledges a number of advances in the field of primary prevention since 1997.

the 2001 update of the American Heart Association (AHA)/American College of Cardiology (ACC) consensus statement on secondary prevention, 1 important evidence from clinical trials has emerged that further supports and broadens the merits of aggressive risk-reduction therapies for patients with established coronary and other atherosclerotic vascular disease, including peripheral arterial disease, atherosclerotic aortic disease, and carotid artery disease.This growing body of evidence confirms that aggressive comprehensive risk factor management improves survival, reduces recurrent events and the need for interventional procedures, and improves quality of life for these patients.Compelling evidence from recent clinical trials and revised practice guidelines provided the impetus for this update of the 2001 recommendations with evidence-based results (Table 1).Classification of Recommendations and Level of Evidence are expressed in ACC/AHA format, as detailed in Tables 2 and3.Recommendations made herein are based largely on major practice guidelines from the National Institutes of Health and ACC/AHA.In many cases, these practice guidelines were supplemented by research findings published after the publication of the primary reference(s).Thus, the development of the present statement involved a process of partial adaptation of other guideline statements and reports and supplemental literature searches. 2-32(For specific search criteria, see the Appendix.)The findings from additional lipid reduction trials [33][34][35][36][37] involving more than 50 000 patients resulted in new optional therapeutic targets, which were outlined in the 2004 update of the National Heart, Lung, and Blood Institute's Adult Treatment Panel (ATP) III report. 6hese changes defined optional lower target cholesterol levels for very high-risk coronary heart disease (CHD) patients, especially those with acute coronary syndromes, and expanded indications for drug treatment.Subsequent to the 2004 update of ATP III, 2 additional trials 8,9 demonstrated cardiovascular benefit for lipid lowering significantly below current cholesterol goal levels for those with chronic CHD.These new trials allow for alterations in guidelines, such that low-density lipoprotein cholesterol (LDL-C) should be Ͻ100 mg/dL for all patients with CHD and other clinical forms of atherosclerotic disease, but in addition, it is reasonable to treat to LDL-C Ͻ70 mg/dL in such patients.When

ClassI 1.The initial evaluation of the patient with suspected ACS should include a search for noncoronary causes that could explain the development of symptoms.(Level of Evidence: C)

HomeCirculationVol. 123, No. 11Effectiveness-Based Guidelines for the Prevention of Cardiovascular Disease in Women—2011 Update Free AccessResearch ArticlePDF/EPUBAboutView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissionsDownload Articles + Supplements ShareShare onFacebookTwitterLinked InMendeleyRedditDiggEmail Jump toSupplementary MaterialsFree AccessResearch ArticlePDF/EPUBEffectiveness-Based Guidelines for the Prevention of Cardiovascular Disease in Women—2011 UpdateA Guideline From the American Heart Association Lori Mosca, MD, MPH, PhD, FAHA, Chair, Emelia J. Benjamin, MD, ScM, FAHA, Kathy Berra, MSN, NP, Judy L. Bezanson, DSN, CNS, RN, Rowena J. Dolor, MD, MHS, Donald M. Lloyd-Jones, MD, ScM, L. Kristin Newby, MD, MHS, Ileana L. Piña, MD, MPH, FAHA, Véronique L. Roger, MD, MPH, Leslee J. Shaw, PhD, Dong Zhao, MD, PhD, Theresa M. Beckie, PhD, Cheryl Bushnell, MD, MHS, FAHA, Jeanine D'Armiento, MD, PhD, Penny M. Kris-Etherton, PhD, RD, Jing Fang, MD, MS, Theodore G. Ganiats, MD, Antoinette S. Gomes, MD, Clarisa R. Gracia, MD, MSCE, Constance K. Haan, MD, MS, Elizabeth A. Jackson, MD, MPH, Debra R. Judelson, MD, Ellie Kelepouris, MD, FAHA, Carl J. Lavie, MD, Anne Moore, APRN, Nancy A. Nussmeier, MD, FAHA, Elizabeth Ofili, MD, MPH, Suzanne Oparil, MD, FAHA, Pamela Ouyang, MBBS, Vivian W. Pinn, MD, Katherine Sherif, MD, Sidney C. SmithJr, MD, FAHA, George Sopko, MD, MPH, Nisha Chandra-Strobos, MD, Elaine M. Urbina, MD, MS, Viola Vaccarino, MD, PhD, FAHA and Nanette K. Wenger, MD, MACC, MACP, FAHA Lori MoscaLori Mosca The executive writing committee and expert panel members represent the following participating organizations and major cosponsors: the American Heart Association (L.M., E.J.B., K.B., J.L.B., R.J.D., D.M.L-J., L.K.N., I.L.P., V.L.R., L.J.S., D.Z., T.M.B., C.B., J.D., P.M.K-E., A.S.G., E.K., C.J.L., N.A.N., S.O., P.O., N.C-S., E.M.U., V.V., N.K.W.), Centers for Disease Control and Prevention* (J.F.), American Academy of Family Physicians (T.G.G.), American College of Obstetricians and Gynecologists (C.R.G.), Society of Thoracic Surgeons (C.K.H.), American College of Cardiology (E.A.J.), American Medical Women's Association (D.R.J.), National Association of Nurse Practitioners in Women's Health (A.M.), Association of Black Cardiologists (E.O.), National Institutes of Health Office of Research on Women's Health (V.W.P.), American College of Physicians† (K.S.), World Heart Federation (S.C.S.), and National Heart, Lung, and Blood Institute (G.S.). Search for more papers by this author , Emelia J. BenjaminEmelia J. Benjamin The executive writing committee and expert panel members represent the following participating organizations and major cosponsors: the American Heart Association (L.M., E.J.B., K.B., J.L.B., R.J.D., D.M.L-J., L.K.N., I.L.P., V.L.R., L.J.S., D.Z., T.M.B., C.B., J.D., P.M.K-E., A.S.G., E.K., C.J.L., N.A.N., S.O., P.O., N.C-S., E.M.U., V.V., N.K.W.), Centers for Disease Control and Prevention* (J.F.), American Academy of Family Physicians (T.G.G.), American College of Obstetricians and Gynecologists (C.R.G.), Society of Thoracic Surgeons (C.K.H.), American College of Cardiology (E.A.J.), American Medical Women's Association (D.R.J.), National Association of Nurse Practitioners in Women's Health (A.M.), Association of Black Cardiologists (E.O.), National Institutes of Health Office of Research on Women's Health (V.W.P.), American College of Physicians† (K.S.), World Heart Federation (S.C.S.), and National Heart, Lung, and Blood Institute (G.S.). Search for more papers by this author , Kathy BerraKathy Berra The executive writing committee and expert panel members represent the following participating organizations and major cosponsors: the American Heart Association (L.M., E.J.B., K.B., J.L.B., R.J.D., D.M.L-J., L.K.N., I.L.P., V.L.R., L.J.S., D.Z., T.M.B., C.B., J.D., P.M.K-E., A.S.G., E.K., C.J.L., N.A.N., S.O., P.O., N.C-S., E.M.U., V.V., N.K.W.), Centers for Disease Control and Prevention* (J.F.), American Academy of Family Physicians (T.G.G.), American College of Obstetricians and Gynecologists (C.R.G.), Society of Thoracic Surgeons (C.K.H.), American College of Cardiology (E.A.J.), American Medical Women's Association (D.R.J.), National Association of Nurse Practitioners in Women's Health (A.M.), Association of Black Cardiologists (E.O.), National Institutes of Health Office of Research on Women's Health (V.W.P.), American College of Physicians† (K.S.), World Heart Federation (S.C.S.), and National Heart, Lung, and Blood Institute (G.S.). Search for more papers by this author , Judy L. BezansonJudy L. Bezanson The executive writing committee and expert panel members represent the following participating organizations and major cosponsors: the American Heart Association (L.M., E.J.B., K.B., J.L.B., R.J.D., D.M.L-J., L.K.N., I.L.P., V.L.R., L.J.S., D.Z., T.M.B., C.B., J.D., P.M.K-E., A.S.G., E.K., C.J.L., N.A.N., S.O., P.O., N.C-S., E.M.U., V.V., N.K.W.), Centers for Disease Control and Prevention* (J.F.), American Academy of Family Physicians (T.G.G.), American College of Obstetricians and Gynecologists (C.R.G.), Society of Thoracic Surgeons (C.K.H.), American College of Cardiology (E.A.J.), American Medical Women's Association (D.R.J.), National Association of Nurse Practitioners in Women's Health (A.M.), Association of Black Cardiologists (E.O.), National Institutes of Health Office of Research on Women's Health (V.W.P.), American College of Physicians† (K.S.), World Heart Federation (S.C.S.), and National Heart, Lung, and Blood Institute (G.S.). Search for more papers by this author , Rowena J. DolorRowena J. Dolor The executive writing committee and expert panel members represent the following participating organizations and major cosponsors: the American Heart Association (L.M., E.J.B., K.B., J.L.B., R.J.D., D.M.L-J., L.K.N., I.L.P., V.L.R., L.J.S., D.Z., T.M.B., C.B., J.D., P.M.K-E., A.S.G., E.K., C.J.L., N.A.N., S.O., P.O., N.C-S., E.M.U., V.V., N.K.W.), Centers for Disease Control and Prevention* (J.F.), American Academy of Family Physicians (T.G.G.), American College of Obstetricians and Gynecologists (C.R.G.), Society of Thoracic Surgeons (C.K.H.), American College of Cardiology (E.A.J.), American Medical Women's Association (D.R.J.), National Association of Nurse Practitioners in Women's Health (A.M.), Association of Black Cardiologists (E.O.), National Institutes of Health Office of Research on Women's Health (V.W.P.), American College of Physicians† (K.S.), World Heart Federation (S.C.S.), and National Heart, Lung, and Blood Institute (G.S.). Search for more papers by this author , Donald M. Lloyd-JonesDonald M. Lloyd-Jones The executive writing committee and expert panel members represent the following participating organizations and major cosponsors: the American Heart Association (L.M., E.J.B., K.B., J.L.B., R.J.D., D.M.L-J., L.K.N., I.L.P., V.L.R., L.J.S., D.Z., T.M.B., C.B., J.D., P.M.K-E., A.S.G., E.K., C.J.L., N.A.N., S.O., P.O., N.C-S., E.M.U., V.V., N.K.W.), Centers for Disease Control and Prevention* (J.F.), American Academy of Family Physicians (T.G.G.), American College of Obstetricians and Gynecologists (C.R.G.), Society of Thoracic Surgeons (C.K.H.), American College of Cardiology (E.A.J.), American Medical Women's Association (D.R.J.), National Association of Nurse Practitioners in Women's Health (A.M.), Association of Black Cardiologists (E.O.), National Institutes of Health Office of Research on Women's Health (V.W.P.), American College of Physicians† (K.S.), World Heart Federation (S.C.S.), and National Heart, Lung, and Blood Institute (G.S.). Search for more papers by this author , L. Kristin NewbyL. Kristin Newby The executive writing committee and expert panel members represent the following participating organizations and major cosponsors: the American Heart Association (L.M., E.J.B., K.B., J.L.B., R.J.D., D.M.L-J., L.K.N., I.L.P., V.L.R., L.J.S., D.Z., T.M.B., C.B., J.D., P.M.K-E., A.S.G., E.K., C.J.L., N.A.N., S.O., P.O., N.C-S., E.M.U., V.V., N.K.W.), Centers for Disease Control and Prevention* (J.F.), American Academy of Family Physicians (T.G.G.), American College of Obstetricians and Gynecologists (C.R.G.), Society of Thoracic Surgeons (C.K.H.), American College of Cardiology (E.A.J.), American Medical Women's Association (D.R.J.), National Association of Nurse Practitioners in Women's Health (A.M.), Association of Black Cardiologists (E.O.), National Institutes of Health Office of Research on Women's Health (V.W.P.), American College of Physicians† (K.S.), World Heart Federation (S.C.S.), and National Heart, Lung, and Blood Institute (G.S.). Search for more papers by this author , Ileana L. PiñaIleana L. Piña The executive writing committee and expert panel members represent the following participating organizations and major cosponsors: the American Heart Association (L.M., E.J.B., K.B., J.L.B., R.J.D., D.M.L-J., L.K.N., I.L.P., V.L.R., L.J.S., D.Z., T.M.B., C.B., J.D., P.M.K-E., A.S.G., E.K., C.J.L., N.A.N., S.O., P.O., N.C-S., E.M.U., V.V., N.K.W.), Centers for Disease Control and Prevention* (J.F.), American Academy of Family Physicians (T.G.G.), American College of Obstetricians and Gynecologists (C.R.G.), Society of Thoracic Surgeons (C.K.H.), American College of Cardiology (E.A.J.), American Medical Women's Association (D.R.J.), National Association of Nurse Practitioners in Women's Health (A.M.), Association of Black Cardiologists (E.O.), National Institutes of Health Office of Research on Women's Health (V.W.P.), American College of Physicians† (K.S.), World Heart Federation (S.C.S.), and National Heart, Lung, and Blood Institute (G.S.). Search for more papers by this author , Véronique L. RogerVéronique L. Roger The executive writing committee and expert panel members represent the following participating organizations and major cosponsors: the American Heart Association (L.M., E.J.B., K.B., J.L.B., R.J.D., D.M.L-J., L.K.N., I.L.P., V.L.R., L.J.S., D.Z., T.M.B., C.B., J.D., P.M.K-E., A.S.G., E.K., C.J.L., N.A.N., S.O., P.O., N.C-S., E.M.U., V.V., N.K.W.), Centers for Disease Control and Prevention* (J.F.), American Academy of Family Physicians (T.G.G.), American College of Obstetricians and Gynecologists (C.R.G.), Society of Thoracic Surgeons (C.K.H.), American College of Cardiology (E.A.J.), American Medical Women's Association (D.R.J.), National Association of Nurse Practitioners in Women's Health (A.M.), Association of Black Cardiologists (E.O.), National Institutes of Health Office of Research on Women's Health (V.W.P.), American College of Physicians† (K.S.), World Heart Federation (S.C.S.), and National Heart, Lung, and Blood Institute (G.S.). Search for more papers by this author , Leslee J. ShawLeslee J. Shaw The executive writing committee and expert panel members represent the following participating organizations and major cosponsors: the American Heart Association (L.M., E.J.B., K.B., J.L.B., R.J.D., D.M.L-J., L.K.N., I.L.P., V.L.R., L.J.S., D.Z., T.M.B., C.B., J.D., P.M.K-E., A.S.G., E.K., C.J.L., N.A.N., S.O., P.O., N.C-S., E.M.U., V.V., N.K.W.), Centers for Disease Control and Prevention* (J.F.), American Academy of Family Physicians (T.G.G.), American College of Obstetricians and Gynecologists (C.R.G.), Society of Thoracic Surgeons (C.K.H.), American College of Cardiology (E.A.J.), American Medical Women's Association (D.R.J.), National Association of Nurse Practitioners in Women's Health (A.M.), Association of Black Cardiologists (E.O.), National Institutes of Health Office of Research on Women's Health (V.W.P.), American College of Physicians† (K.S.), World Heart Federation (S.C.S.), and National Heart, Lung, and Blood Institute (G.S.). Search for more papers by this author , Dong ZhaoDong Zhao The executive writing committee and expert panel members represent the following participating organizations and major cosponsors: the American Heart Association (L.M., E.J.B., K.B., J.L.B., R.J.D., D.M.L-J., L.K.N., I.L.P., V.L.R., L.J.S., D.Z., T.M.B., C.B., J.D., P.M.K-E., A.S.G., E.K., C.J.L., N.A.N., S.O., P.O., N.C-S., E.M.U., V.V., N.K.W.), Centers for Disease Control and Prevention* (J.F.), American Academy of Family Physicians (T.G.G.), American College of Obstetricians and Gynecologists (C.R.G.), Society of Thoracic Surgeons (C.K.H.), American College of Cardiology (E.A.J.), American Medical Women's Association (D.R.J.), National Association of Nurse Practitioners in Women's Health (A.M.), Association of Black Cardiologists (E.O.), National Institutes of Health Office of Research on Women's Health (V.W.P.), American College of Physicians† (K.S.), World Heart Federation (S.C.S.), and National Heart, Lung, and Blood Institute (G.S.). Search for more papers by this author , Theresa M. BeckieTheresa M. Beckie The executive writing committee and expert panel members represent the following participating organizations and major cosponsors: the American Heart Association (L.M., E.J.B., K.B., J.L.B., R.J.D., D.M.L-J., L.K.N., I.L.P., V.L.R., L.J.S., D.Z., T.M.B., C.B., J.D., P.M.K-E., A.S.G., E.K., C.J.L., N.A.N., S.O., P.O., N.C-S., E.M.U., V.V., N.K.W.), Centers for Disease Control and Prevention* (J.F.), American Academy of Family Physicians (T.G.G.), American College of Obstetricians and Gynecologists (C.R.G.), Society of Thoracic Surgeons (C.K.H.), American College of Cardiology (E.A.J.), American Medical Women's Association (D.R.J.), National Association of Nurse Practitioners in Women's Health (A.M.), Association of Black Cardiologists (E.O.), National Institutes of Health Office of Research on Women's Health (V.W.P.), American College of Physicians† (K.S.), World Heart Federation (S.C.S.), and National Heart, Lung, and Blood Institute (G.S.). Search for more papers by this author , Cheryl BushnellCheryl Bushnell The executive writing committee and expert panel members represent the following participating organizations and major cosponsors: the American Heart Association (L.M., E.J.B., K.B., J.L.B., R.J.D., D.M.L-J., L.K.N., I.L.P., V.L.R., L.J.S., D.Z., T.M.B., C.B., J.D., P.M.K-E., A.S.G., E.K., C.J.L., N.A.N., S.O., P.O., N.C-S., E.M.U., V.V., N.K.W.), Centers for Disease Control and Prevention* (J.F.), American Academy of Family Physicians (T.G.G.), American College of Obstetricians and Gynecologists (C.R.G.), Society of Thoracic Surgeons (C.K.H.), American College of Cardiology (E.A.J.), American Medical Women's Association (D.R.J.), National Association of Nurse Practitioners in Women's Health (A.M.), Association of Black Cardiologists (E.O.), National Institutes of Health Office of Research on Women's Health (V.W.P.), American College of Physicians† (K.S.), World Heart Federation (S.C.S.), and National Heart, Lung, and Blood Institute (G.S.). Search for more papers by this author , Jeanine D'ArmientoJeanine D'Armiento The executive writing committee and expert panel members represent the following participating organizations and major cosponsors: the American Heart Association (L.M., E.J.B., K.B., J.L.B., R.J.D., D.M.L-J., L.K.N., I.L.P., V.L.R., L.J.S., D.Z., T.M.B., C.B., J.D., P.M.K-E., A.S.G., E.K., C.J.L., N.A.N., S.O., P.O., N.C-S., E.M.U., V.V., N.K.W.), Centers for Disease Control and Prevention* (J.F.), American Academy of Family Physicians (T.G.G.), American College of Obstetricians and Gynecologists (C.R.G.), Society of Thoracic Surgeons (C.K.H.), American College of Cardiology (E.A.J.), American Medical Women's Association (D.R.J.), National Association of Nurse Practitioners in Women's Health (A.M.), Association of Black Cardiologists (E.O.), National Institutes of Health Office of Research on Women's Health (V.W.P.), American College of Physicians† (K.S.), World Heart Federation (S.C.S.), and National Heart, Lung, and Blood Institute (G.S.). Search for more papers by this author , Penny M. Kris-EthertonPenny M. Kris-Etherton The executive writing committee and expert panel members represent the following participating organizations and major cosponsors: the American Heart Association (L.M., E.J.B., K.B., J.L.B., R.J.D., D.M.L-J., L.K.N., I.L.P., V.L.R., L.J.S., D.Z., T.M.B., C.B., J.D., P.M.K-E., A.S.G., E.K., C.J.L., N.A.N., S.O., P.O., N.C-S., E.M.U., V.V., N.K.W.), Centers for Disease Control and Prevention* (J.F.), American Academy of Family Physicians (T.G.G.), American College of Obstetricians and Gynecologists (C.R.G.), Society of Thoracic Surgeons (C.K.H.), American College of Cardiology (E.A.J.), American Medical Women's Association (D.R.J.), National Association of Nurse Practitioners in Women's Health (A.M.), Association of Black Cardiologists (E.O.), National Institutes of Health Office of Research on Women's Health (V.W.P.), American College of Physicians† (K.S.), World Heart Federation (S.C.S.), and National Heart, Lung, and Blood Institute (G.S.). Search for more papers by this author , Jing FangJing Fang The executive writing committee and expert panel members represent the following participating organizations and major cosponsors: the American Heart Association (L.M., E.J.B., K.B., J.L.B., R.J.D., D.M.L-J., L.K.N., I.L.P., V.L.R., L.J.S., D.Z., T.M.B., C.B., J.D., P.M.K-E., A.S.G., E.K., C.J.L., N.A.N., S.O., P.O., N.C-S., E.M.U., V.V., N.K.W.), Centers for Disease Control and Prevention* (J.F.), American Academy of Family Physicians (T.G.G.), American College of Obstetricians and Gynecologists (C.R.G.), Society of Thoracic Surgeons (C.K.H.), American College of Cardiology (E.A.J.), American Medical Women's Association (D.R.J.), National Association of Nurse Practitioners in Women's Health (A.M.), Association of Black Cardiologists (E.O.), National Institutes of Health Office of Research on Women's Health (V.W.P.), American College of Physicians† (K.S.), World Heart Federation (S.C.S.), and National Heart, Lung, and Blood Institute (G.S.). Search for more papers by this author , Theodore G. GaniatsTheodore G. Ganiats The executive writing committee and expert panel members represent the following participating organizations and major cosponsors: the American Heart Association (L.M., E.J.B., K.B., J.L.B., R.J.D., D.M.L-J., L.K.N., I.L.P., V.L.R., L.J.S., D.Z., T.M.B., C.B., J.D., P.M.K-E., A.S.G., E.K., C.J.L., N.A.N., S.O., P.O., N.C-S., E.M.U., V.V., N.K.W.), Centers for Disease Control and Prevention* (J.F.), American Academy of Family Physicians (T.G.G.), American College of Obstetricians and Gynecologists (C.R.G.), Society of Thoracic Surgeons (C.K.H.), American College of Cardiology (E.A.J.), American Medical Women's Association (D.R.J.), National Association of Nurse Practitioners in Women's Health (A.M.), Association of Black Cardiologists (E.O.), National Institutes of Health Office of Research on Women's Health (V.W.P.), American College of Physicians† (K.S.), World Heart Federation (S.C.S.), and National Heart, Lung, and Blood Institute (G.S.). Search for more papers by this author , Antoinette S. GomesAntoinette S. Gomes The executive writing committee and expert panel members represent the following participating organizations and major cosponsors: the American Heart Association (L.M., E.J.B., K.B., J.L.B., R.J.D., D.M.L-J., L.K.N., I.L.P., V.L.R., L.J.S., D.Z., T.M.B., C.B., J.D., P.M.K-E., A.S.G., E.K., C.J.L., N.A.N., S.O., P.O., N.C-S., E.M.U., V.V., N.K.W.), Centers for Disease Control and Prevention* (J.F.), American Academy of Family Physicians (T.G.G.), American College of Obstetricians and Gynecologists (C.R.G.), Society of Thoracic Surgeons (C.K.H.), American College of Cardiology (E.A.J.), American Medical Women's Association (D.R.J.), National Association of Nurse Practitioners in Women's Health (A.M.), Association of Black Cardiologists (E.O.), National Institutes of Health Office of Research on Women's Health (V.W.P.), American College of Physicians† (K.S.), World Heart Federation (S.C.S.), and National Heart, Lung, and Blood Institute (G.S.). Search for more papers by this author , Clarisa R. GraciaClarisa R. Gracia The executive writing committee and expert panel members represent the following participating organizations and major cosponsors: the American Heart Association (L.M., E.J.B., K.B., J.L.B., R.J.D., D.M.L-J., L.K.N., I.L.P., V.L.R., L.J.S., D.Z., T.M.B., C.B., J.D., P.M.K-E., A.S.G., E.K., C.J.L., N.A.N., S.O., P.O., N.C-S., E.M.U., V.V., N.K.W.), Centers for Disease Control and Prevention* (J.F.), American Academy of Family Physicians (T.G.G.), American College of Obstetricians and Gynecologists (C.R.G.), Society of Thoracic Surgeons (C.K.H.), American College of Cardiology (E.A.J.), American Medical Women's Association (D.R.J.), National Association of Nurse Practitioners in Women's Health (A.M.), Association of Black Cardiologists (E.O.), National Institutes of Health Office of Research on Women's Health (V.W.P.), American College of Physicians† (K.S.), World Heart Federation (S.C.S.), and National Heart, Lung, and Blood Institute (G.S.). Search for more papers by this author , Constance K. HaanConstance K. Haan The executive writing committee and expert panel members represent the following participating organizations and major cosponsors: the American Heart Association (L.M., E.J.B., K.B., J.L.B., R.J.D., D.M.L-J., L.K.N., I.L.P., V.L.R., L.J.S., D.Z., T.M.B., C.B., J.D., P.M.K-E., A.S.G., E.K., C.J.L., N.A.N., S.O., P.O., N.C-S., E.M.U., V.V., N.K.W.), Centers for Disease Control and Prevention* (J.F.), American Academy of Family Physicians (T.G.G.), American College of Obstetricians and Gynecologists (C.R.G.), Society of Thoracic Surgeons (C.K.H.), American College of Cardiology (E.A.J.), American Medical Women's Association (D.R.J.), National Association of Nurse Practitioners in Women's Health (A.M.), Association of Black Cardiologists (E.O.), National Institutes of Health Office of Research on Women's Health (V.W.P.), American College of Physicians† (K.S.), World Heart Federation (S.C.S.), and National Heart, Lung, and Blood Institute (G.S.). Search for more papers by this author , Elizabeth A. JacksonElizabeth A. Jackson The executive writing committee and expert panel members represent the following participating organizations and major cosponsors: the American Heart Association (L.M., E.J.B., K.B., J.L.B., R.J.D., D.M.L-J., L.K.N., I.L.P., V.L.R., L.J.S., D.Z., T.M.B., C.B., J.D., P.M.K-E., A.S.G., E.K., C.J.L., N.A.N., S.O., P.O., N.C-S., E.M.U., V.V., N.K.W.), Centers for Disease Control and Prevention* (J.F.), American Academy of Family Physicians (T.G.G.), American College of Obstetricians and Gynecologists (C.R.G.), Society of Thoracic Surgeons (C.K.H.), American College of Cardiology (E.A.J.), American Medical Women's Association (D.R.J.), National Association of Nurse Practitioners in Women's Health (A.M.), Association of Black Cardiologists (E.O.), National Institutes of Health Office of Research on Women's Health (V.W.P.), American College of Physicians† (K.S.), World Heart Federation (S.C.S.), and National Heart, Lung, and Blood Institute (G.S.). Search for more papers by this author , Debra R. JudelsonDebra R. Judelson The executive writing committee and expert panel members represent the following participating organizations and major cosponsors: the American Heart Association (L.M., E.J.B., K.B., J.L.B., R.J.D., D.M.L-J., L.K.N., I.L.P., V.L.R., L.J.S., D.Z., T.M.B., C.B., J.D., P.M.K-E., A.S.G., E.K., C.J.L., N.A.N., S.O., P.O., N.C-S., E.M.U., V.V., N.K.W.), Centers for Disease Control and Prevention* (J.F.), American Academy of Family Physicians (T.G.G.), American College of Obstetricians and Gynecologists (C.R.G.), Society of Thoracic Surgeons (C.K.H.), American College of Cardiology (E.A.J.), American Medical Women's Association (D.R.J.), National Association of Nurse Practitioners in Women's Health (A.M.), Association of Black Cardiologists (E.O.), National Institutes of Health Office of Research on Women's Health (V.W.P.), American College of Physicians† (K.S.), World Heart Federation (S.C.S.), and National Heart, Lung, and Blood Institute (G.S.). Search for more papers by this author , Ellie KelepourisEllie Kelepouris The executive writing committee and expert panel members represent the following participating organizations and major cosponsors: the American Heart Association (L.M., E.J.B., K.B., J.L.B., R.J.D., D.M.L-J., L.K.N., I.L.P., V.L.R., L.J.S., D.Z., T.M.B., C.B., J.D., P.M.K-E., A.S.G., E.K., C.J.L., N.A.N., S.O., P.O., N.C-S., E.M.U., V.V., N.K.W.), Centers for Disease Control and Prevention* (J.F.), American Academy of Family Physicians (T.G.G.), American College of Obstetricians and Gynecologists (C.R.G.), Society of Thoracic Surgeons (C.K.H.), American College of Cardiology (E.A.J.), American Medical Women's Association (D.R.J.), National Association of Nurse Practitioners in Women's Health (A.M.), Association of Black Cardiologists (E.O.), National Institutes of Health Office of Research on Women's Health (V.W.P.), American College of Physicians† (K.S.), World Heart Federation (S.C.S.), and National Heart, Lung, and Blood Institute (G.S.). Search for more papers by this author , Carl J. LavieCarl J. Lavie The executive writing committee and expert panel members represent the following participating organizations and major cosponsors: the American Heart Association (L.M., E.J.B., K.B., J.L.B., R.J.D., D.M.L-J., L.K.N., I.L.P., V.L.R., L.J.S., D.Z., T.M.B., C.B., J.D., P.M.K-E., A.S.G., E.K., C.J.L., N.A.N., S.O., P.O., N.C-S., E.M.U., V.V., N.K.W.), Centers for Disease Control and Prevention* (J.F.), American Academy of Family Physicians (T.G.G.), American College of Obstetricians and Gynecologists (C.R.G.), Society of Thoracic Surgeons (C.K.H.), American College of Cardiology (E.A.J.), American Medical Women's Association (D.R.J.), National Association of Nurse Practitioners in Women's Health (A.M.), Association of Black Cardiologists (E.O.), National Institutes of Health Office of Research on Women's Health (V.W.P.), American College of Physicians† (K.S.), World Heart Federation (S.C.S.), and National Heart, Lung, and Blood Institute (G.S.). Search for more papers by this author , Anne MooreAnne Moore The executive writing committee and expert panel members represent the following participating organizations and major cosponsors: the American Heart Association (L.M., E.J.B., K.B., J.L.B., R.J.D., D.M.L-J., L.K.N., I.L.P., V.L.R., L.J.S., D.Z., T.M.B., C.B., J.D., P.M.K-E., A.S.G., E.K., C.J.L., N.A.N., S.O., P.O., N.C-S., E.M.U., V.V., N.K.W.), Centers for Disease Control and Prevention* (J.F.), American Academy of Family Physicians (T.G.G.), American College of Obstetricians and Gynecologists (C.R.G.), Society of Thoracic Surgeons (C.K.H.), American College of Cardiology (E.A.J.), American Medical Women's Association (D.R.J.), National Association of Nurse Practitioners in Women's Health (A.M.), Association of Black Cardiologists (E.O.), National Institutes of Health Office of Research on Women's Health (V.W.P.), American College of Physicians† (K.S.), World Heart Federation (S.C.S.), and National Heart, Lung, and Blood Institute (G.S.). Search for more papers by this author , Nancy A. NussmeierNancy A. Nussmeier The executive writing committee and expert panel members represent the following participating organizations and major cosponsors: the American Heart Association (L.M., E.J.B., K.B., J.L.B., R.J.D., D.M.L-J., L.K.N., I.L.P., V.L.R., L.J.S., D.Z., T.M.B., C.B., J.D., P.M.K-E., A.S.G., E.K., C.J.L., N.A.N., S.O., P.O., N.C-S., E.M.U., V.V., N.K.W.), Centers for Disease Control and Prevention* (J.F.), American Academy of Family Physicians (T.G.G.), American College of Obstetricians and Gynecologists (C.R.G.), Society of Thoracic Surgeons (C.K.H.), American College of Cardiology (E.A.J.), American Medical Women's Association (D.R.J.), National Association of Nurse Practitioners in Women's Health (A.M.), Association of Black Cardiologists (E.O.), National Institutes of Health Office of Research on Women's Health (V.W.P.), American College of Physicians† (K.S.), World Heart Federation (S.C.S.), and National Heart, Lung, and Blood Institute (G.S.). Search for more papers by this author , Elizabeth OfiliElizabeth Ofili The executive writing committee and expert panel members represent the following participating organizations and major cosponsors: the American Heart Association (L.M., E.J.B., K.B., J.L.B., R.J.D., D.M.L-J., L.K.N., I.L.P., V.L.R., L.J.S., D.Z., T.M.B., C.B., J.D., P.M.K-E., A.S.G., E.K., C.J.L., N.A.N., S.O., P.O., N.C-S., E.M.U., V.V., N.K.W.), Centers for Disease Control and Prevention* (J.F.), American Academy of Family Physicians (T.G.G.), American College of Obstetricians and Gynecologists (C.R.G.), Society of Thoracic Surgeons (C.K.H.), American College of Cardiology (E.A.J.), American Medical Women's Association (D.R.J.), National Association of Nurse Practitioners in Women's Health (A.M.), Association of Black Cardiologists (E.O.), National Institutes of Health Office of Research on Women's Health (V.W.P.), American College of Physicians† (K.S.), World Heart Federation (S.C.S.), and National Heart, Lung, and Blood Institute (G.S.). Search for more papers by this author , Suzanne OparilSuzanne Oparil The executive writing committee and expert panel members represent the following participating organizations and major cosponsors: the American Heart Association (L.M., E.J.B., K.B., J.L.B., R.J.D., D.M.L-J., L.K.N., I.L.P., V.L.R., L.J.S., D.Z., T.M.B., C.B., J.D., P.M.K-E., A.S.G., E.K., C.J.L., N.A.N., S.O., P.O., N.C-S., E.M.U., V.V., N.K.W.), Centers for Disease Control and Prevention* (J.F.), American Academy of Family Physicians (T.G.G.), American College of Obstetricians and Gynecologist

Heart Association (AHA) Task Force on Practice Guidelines regularly reviews existing guidelines to determine when an update or full revision is needed.This process gives priority to areas where major changes in text, and particularly recommendations, are mentioned on the basis of new understanding or evidence.Minor

It is important that the medical profession play a significant role in critically evaluating the use of diagnostic procedures and therapies as they are introduced and tested in the detection, management, or prevention of disease states.Rigorous and expert analysis of the available data documenting relative benefits and risks of those procedures and therapies can produce helpful guidelines that improve the effectiveness of care, optimize patient outcomes, and favorably affect the overall cost of care by focusing resources on the most effective strategies.The American College of Cardiology (ACC) and the American Heart Association (AHA) have jointly engaged in the production of such guidelines in the area of cardiovascular disease since 1980.This effort is directed by the ACC/AHA Task Force on Practice Guidelines, whose charge is to develop and revise practice guidelines for important cardiovascular diseases and procedures.Experts in the subject under consideration are selected from both organizations and charged with examining subject-specific data and writing or updating these guidelines.The process includes additional representatives from other medical practitioner and specialty groups where appropriate.Writing groups are specifically charged to perform a formal literature review, weigh the strength of evidence for or against a particular treatment or procedure, and include estimates of expected health outcomes where data exist.Patient-specific modifiers, comorbidities, and issues of patient preference that might influence the choice of particular tests or therapies are considered, as are frequency of follow-up and cost-effectiveness.When available, information from studies on cost will be considered; however, review of data on efficacy and clinical out-e156

HomeCirculationVol. 129, No. 25_suppl_22013 AHA/ACC Guideline on Lifestyle Management to Reduce Cardiovascular Risk Open AccessResearch ArticlePDF/EPUBAboutView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissionsDownload Articles + Supplements ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toSupplemental MaterialOpen AccessResearch ArticlePDF/EPUB2013 AHA/ACC Guideline on Lifestyle Management to Reduce Cardiovascular RiskA Report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines Robert H. Eckel, MD, FAHA, John M. Jakicic, PhD, Jamy D. Ard, MD, Janet M. de Jesus, MS, RD, Nancy Houston Miller, RN, BSN, FAHA, Van S. Hubbard, MD, PhD, I-Min Lee, MD, ScD, Alice H. Lichtenstein, DSc, FAHA, Catherine M. Loria, PhD, FAHA, Barbara E. Millen, DrPH, RD, FADA, Cathy A. Nonas, MS, RD, Frank M. Sacks, MD, FAHA, Sidney C. SmithJr, MD, FACC, FAHA, Laura P. Svetkey, MD, MHS, Thomas A. Wadden, PhD and Susan Z. Yanovski, MD Robert H. EckelRobert H. Eckel Search for more papers by this author , John M. JakicicJohn M. Jakicic Search for more papers by this author , Jamy D. ArdJamy D. Ard Search for more papers by this author , Janet M. de JesusJanet M. de Jesus *Ex-Officio Members. Search for more papers by this author , Nancy Houston MillerNancy Houston Miller Search for more papers by this author , Van S. HubbardVan S. Hubbard *Ex-Officio Members. Search for more papers by this author , I-Min LeeI-Min Lee Search for more papers by this author , Alice H. LichtensteinAlice H. Lichtenstein Search for more papers by this author , Catherine M. LoriaCatherine M. Loria *Ex-Officio Members. Search for more papers by this author , Barbara E. MillenBarbara E. Millen Search for more papers by this author , Cathy A. NonasCathy A. Nonas Search for more papers by this author , Frank M. SacksFrank M. Sacks Search for more papers by this author , Sidney C. SmithJrSidney C. SmithJr Search for more papers by this author , Laura P. SvetkeyLaura P. Svetkey Search for more papers by this author , Thomas A. WaddenThomas A. Wadden Search for more papers by this author and Susan Z. YanovskiSusan Z. Yanovski *Ex-Officio Members. Search for more papers by this author Originally published12 Nov 2013https://doi.org/10.1161/01.cir.0000437740.48606.d1Circulation. 2014;129:S76–S99is corrected byCorrectionCorrectionOther version(s) of this articleYou are viewing the most recent version of this article. Previous versions: January 1, 2013: Previous Version 1 Table of ContentsPreamble and Transition to ACC/AHA Guidelines toReduce Cardiovascular Risk S771.1. Scope of Guideline S781.2. Methodology and Evidence Review S781.2.1. Scope of the Evidence Review S781.2.2. CQ-Based Approach S811.3. Organization of Work Group S811.4. Document Reviews and Approval S812. Lifestyle Management Recommendations S833. CQ1—Dietary Patterns and Macronutrients: BP and Lipids S833.1. Introduction/Rationale S833.2. Selection of Inclusion/Exclusion Criteria S833.3. Literature Search Yield S833.3.1. Dietary Pattern/Macronutrient Composition Evidence S833.4. CQ1 Evidence Statements S833.4.1. Dietary Patterns S833.4.1.1. MED Pattern S833.4.1.2. DASH Dietary Pattern S833.4.1.3. DASH Variations S843.4.2. Dietary Fat and Cholesterol S843.5. Diet Recommendations for LDL-C Lowering S844. CQ2—Sodium and Potassium: BP and CVD Outcomes S854.1. Introduction and Rationale S854.2. Selection of Inclusion/Exclusion Criteria S864.3. Literature Search Yield S874.4. CQ2 Evidence Statements S874.4.1. Sodium and BP S874.5. Diet Recommendations for BP Lowering S875. CQ3—Physical Activity: Lipids and BP S895.1. Introduction/Rationale S895.2. Selection of Inclusion/Exclusion Criteria S895.3. Literature Search Yield S905.4. CQ3 Evidence Statements S905.4.1. Physical Activity and Lipids S905.4.2. Physical Activity and BP S905.4.2.1. Aerobic Exercise Training and BP S905.4.2.2. Resistance Exercise Training and BP S905.4.2.3. Combination of Aerobic and Resistance Exercise Training and BP S915.5. Physical Activity Recommendations S915.6. Heart-Healthy Nutrition and Physical Activity Behaviors S916. Gaps in Evidence and Future Research Needs S916.1. Diet S916.2. Physical Activity S92References S93Appendix 1. Author Relationships With Industry and Other Entities (Relevant) S96Appendix 2. Expert Reviewer Relationships With Industry and Other Entities S99Appendix 3. Abbreviations S99Preamble and Transition to ACC/AHA Guidelines to Reduce Cardiovascular RiskThe goals of the American College of Cardiology (ACC) and the American Heart Association (AHA) are to prevent cardiovascular diseases (CVDs); improve the management of people who have these diseases through professional education and research; and develop guidelines, standards, and policies that promote optimal patient care and cardiovascular health. Toward these objectives, the ACC and AHA have collaborated with the National Heart, Lung, and Blood Institute (NHLBI) and stakeholder and professional organizations to develop clinical practice guidelines for assessment of cardiovascular risk, lifestyle modifications to reduce cardiovascular risk, management of blood cholesterol in adults, and management of overweight and obesity in adults.In 2008, the NHLBI initiated these guidelines by sponsoring rigorous systematic evidence reviews for each topic by expert panels convened to develop critical questions (CQs), interpret the evidence, and craft recommendations. In response to the 2011 report from the Institute of Medicine on the development of trustworthy clinical guidelines,1 the NHLBI Advisory Council recommended that the NHLBI focus specifically on reviewing the highest-quality evidence and partner with other organizations to develop recommendations.2,3 Accordingly, in June 2013 the NHLBI initiated collaboration with the ACC and AHA to work with other organizations to complete and publish the 4 guidelines noted above and make them available to the widest possible constituency. Recognizing that the Expert Panels/Work Groups did not consider evidence beyond 2011 (except as specified in the methodology), the ACC, AHA, and collaborating societies plan to begin updating these guidelines starting in 2014.The joint ACC/AHA Task Force on Practice Guidelines (Task Force) appointed a subcommittee to shepherd this transition, communicate the rationale and expectations to the writing panels and partnering organizations, and expeditiously publish the documents. The ACC/AHA and partner organizations recruited a limited number of expert reviewers for fiduciary examination of content, recognizing that each document had undergone extensive peer review by representatives of the NHLBI Advisory Council, key federal agencies, and scientific experts. Each writing panel responded to comments from these reviewers. Clarifications were incorporated where appropriate, but there were no substantive changes because the bulk of the content was undisputed.Although the Task Force led the final development of these prevention guidelines, they differ from other ACC/AHA guidelines. First, as opposed to an extensive compendium of clinical information, these documents are significantly more limited in scope and focus on selected CQs on each topic, based on the highest-quality evidence available. Recommendations were derived from randomized trials, meta-analyses, and observational studies evaluated for quality and were not formulated when sufficient evidence was not available. Second, the text accompanying each recommendation is succinct, summarizing the evidence for each question. The Full Panel/Work Group Reports include more detailed information about the evidence statements (ESs) that serve as the basis for recommendations. Third, the format of the recommendations differs from other ACC/AHA guidelines. Each recommendation has been mapped from the NHLBI grading format to the ACC/AHA Classification of Recommendation/Level of Evidence (COR/LOE) construct (Table 1) and is expressed in both formats. Because of the inherent differences in grading systems and the clinical questions driving the recommendations, alignment between the NHLBI and ACC/AHA formats is in some cases imperfect. Explanations of these variations are noted in the recommendation tables, where applicable.Table 1. Applying Classification of Recommendation and Level of EvidenceTable 1. Applying Classification of Recommendation and Level of EvidenceIn consultation with NHLBI, the policies adopted by the writing panels to manage relationships of authors with industry and other entities (RWI) are outlined in the methods section of each panel report. These policies were in effect when this effort began in 2008 and throughout the writing process and voting on recommendations, until the process was transferred to ACC/AHA in 2013. In the interest of transparency, the ACC/AHA requested that panel authors resubmit RWI disclosures as of July 2013. Relationships relevant to this guideline are disclosed in Appendix 1. None of the ACC/AHA expert reviewers had relevant RWI (Appendix 2). See Appendix 3 for a list of abbreviations used in the guideline.Systematic evidence reports and accompanying summary tables were developed by the expert panels and NHLBI. The guideline was reviewed by the ACC/AHA Task Force and approved by the ACC Board of Trustees and the AHA Science Advisory and Coordinating Committee. In addition, ACC/AHA sought endorsement from other stakeholders, including professional organizations. It is the hope of the writing panels, stakeholders, professional organizations, NHLBI, and Task Force that the guidelines will garner the widest possible readership for the benefit of patients, providers, and the public health.These guidelines are meant to define practices that meet the needs of patients in most circumstances and are not a replacement for clinical judgment. The ultimate decision about care of a particular patient must be made by the healthcare provider and patient in light of the circumstances presented by that patient. As a result, situations might arise in which deviations from these guidelines may be appropriate. These considerations notwithstanding, in caring for most patients, clinicians can employ the recommendations confidently to reduce the risks of atherosclerotic CVD events.See Tables 2 and 3 for an explanation of the NHLBI recommendation grading methodology.Table 2. NHLBI Grading of the Strength of RecommendationsGradeStrength of Recommendation*AStrong recommendationThere is high certainty based on evidence that the net benefit† is substantial.BModerate recommendationThere is moderate certainty based on evidence that the net benefit is moderate to substantial, or there is high certaintythat the net benefit is moderate.CWeak recommendationThere is at least moderate certainty based on evidence that there is a small net benefit.DRecommendation againstThere is at least moderate certainty based on evidence that there is no net benefit or that risks/harms outweigh benefits.EExpert opinion (“There is insufficient evidence or evidence is unclear or conflicting, but this is what the Work Group recommends.”)Net benefit is unclear. Balance of benefits and harms cannot be determined because of no evidence, insufficient evidence, unclear evidence, or conflicting evidence, but the Work Group thought it was important to provide clinical guidance and make a recommendation. Further research is recommended in this area.NNo recommendation for or against (“There is insufficient evidence or evidence is unclear or conflicting.”)Net benefit is unclear. Balance of benefits and harms cannot be determined because of no evidence, insufficient evidence, unclear evidence, or conflicting evidence, and the Work Group thought no recommendation should be made. Further research is recommended in this area.*In most cases, the strength of the recommendation should be closely aligned with the quality of the evidence; however, under some circumstances, there may be valid reasons for making recommendations that are not closely aligned with the quality of the evidence (eg, strong recommendation when the evidence quality is moderate, such as smoking cessation to reduce cardiovascular disease risk or ordering an ECG as part of the initial diagnostic work-up for a patient presenting with possible MI). Those situations should be limited and the rationale explained clearly by the Work Group.†Net benefit is defined as benefits minus risks/harms of the service/intervention.ECG indicates electrocardiogram; MI, myocardial infarction; and NHLBI, National Heart, Lung, and Blood Institute.Table 3 NHLBI Quality Rating of the Strength of EvidenceType of EvidenceQuality Rating*Well-designed, well-executed† RCT that adequately represent populations to which the results are applied and directly assess effects on health outcomes.Meta-analyses of such studies.Highly certain about the estimate of effect. Further research is unlikely to change our confidence in the estimate of effect.HighRCT with minor limitations‡ affecting confidence in, or applicability of, the results.Well-designed, well-executed nonrandomized controlled studies§ and well-designed, well-executed observational studies‖.Meta-analyses of such studies.Moderately certain about the estimate of effect. Further research may have an impact on our confidence in the estimate of effect and may change the estimate.ModerateRCT with major limitations.Nonrandomized controlled studies and observational studies with major limitations affecting confidence in, or applicability of, the results.Uncontrolled clinical observations without an appropriate comparison group (eg, case series, case reports).Physiological studies in humans.Meta-analyses of such studies.Low certainty about the estimate of effect. Further research is likely to have an impact on our confidence in the estimate of effect and is likely to change the estimate.Low*In some cases, other evidence, such as large all-or-none case series (eg, jumping from airplanes or tall structures), can represent high- or moderate-quality evidence. In such cases, the rationale for the evidence rating exception should be explained by the Work Group and clearly justified.†“Well-designed, well-executed” refers to studies that directly address the question; use adequate randomization, blinding, and allocation concealment; are adequately powered; use intention-to-treat analyses; and have high follow-up rates.‡Limitations include concerns with the design and execution of a study that result in decreased confidence in the true estimate of the effect. Examples of such limitations include but are not limited to: inadequate randomization, lack of blinding of study participants or outcome assessors, inadequate power, outcomes of interest that are not prespecified for the primary outcomes, low follow-up rates, and findings based on subgroup analyses. Whether the limitations are considered minor or major is based on the number and severity of flaws in design or execution. Rules for determining whether the limitations are considered minor or major and how they will affect rating of the individual studies will be developed collaboratively with the methodology team.§Nonrandomized controlled studies refer to intervention studies where assignment to intervention and comparison groups is not random (eg, quasi-experimental study design).‖Observational studies include prospective and retrospective cohort, case-control, and cross-sectional studies.NHLBI indicates National Heart, Lung, and Blood Institute; and RCT, randomized controlled trials.1.1. Scope of GuidelineSee Table 4 for the Lifestyle Expert Work Group's CQs.Table 4. Critical QuestionsCritical Questions:CQ1.Among adults*, what is the effect of dietary patterns and/or macronutrient composition on CVD risk factors, when compared with no treatment or with other types of interventions?CQ2.Among adults, what is the effect of dietary intake of sodium and potassium on CVD risk factors and outcomes, when compared with no treatment or with other types of interventions?CQ3.Among adults, what is the effect of physical activity on BP and lipids when compared with no treatment or with other types of interventions?*Those ≥18 years of age and <80 years of age.BP indicates blood pressure; CQ, critical question; and CVD, cardiovascular disease.A healthy lifestyle is important in the prevention of CVD, the leading cause of morbidity and mortality worldwide. The intent of the Lifestyle Work Group (Work Group) was to evaluate evidence that particular dietary patterns, nutrient intake, and levels and types of physical activity can play a major role in CVD prevention and treatment through effects on modifiable CVD risk factors (ie, blood pressure [BP] and lipids). These ESs and recommendations may be used as appropriate in the management of hypercholesterolemia and hypertension. The target audience of the report is primary care providers.This guideline is based on the Full Work Group Report, which is provided as an online-only data supplement to the guideline. The Full Work Group Report supplement contains background and additional material related to content, methodology, evidence synthesis, rationale, and references and is supported by the NHLBI Systematic Evidence Review, which can be found at http://www.nhlbi.nih.gov/guidelines/cvd_adult/lifestyle/.Diet and physical activity interventions of interest to the Work Group that were not included in this report because of time and resource limitations were the following: calcium, magnesium, alcohol, cardiorespiratory fitness, single behavioral intervention or multicomponent lifestyle interventions, the addition of lifestyle intervention to pharmacotherapy, and smoking. Outcomes of interest not covered in this evidence review were the following risk factors: diabetes mellitus (diabetes)- and obesity-related measurements, incident diabetes metabolic syndrome, high-sensitivity C-reactive protein, and other inflammatory markers. The Work Group was interested in reviewing the evidence for CVD outcomes in all of the CQs; however, the evidence for mortality and CVD outcomes was reviewed only in CQ2.1.2. Methodology and Evidence Review1.2.1. Scope of the Evidence ReviewTo formulate the nutrition recommendations, the Work Group used randomized controlled trials (RCTs), observational studies, meta-analyses, and systematic reviews of studies carried out in adults (≥18 years of age) with or without established coronary heart disease/CVD and with or without risk factors for coronary heart disease/CVD, who were of normal weight, overweight, or obese. The evidence review date range was 1998 to 2009. To capture historical data or more recent evidence, date ranges were changed for subquestions in some instances. The evidence date ranges are described clearly in each CQ section. The Work Group assessed the impact of both dietary patterns and macronutrient composition on plasma low-density lipoprotein cholesterol (LDL-C), high-density lipoprotein cholesterol (HDL-C), and triglycerides and on systolic BP and diastolic BP over a minimum RCT intervention period of 1 month in studies performed in any geographic location and research setting.Overall, the Work Group emphasized dietary patterns rather than individual dietary components. Patterns were characterized by habitual or prescribed combinations of daily food intake. Dietary patterns offer the opportunity to characterize the overall composition and quality of the eating behaviors of a population (eg, Mediterranean-style dietary [MED] pattern). Eating patterns consist of various combinations of foods that may differ in macronutrient, vitamin, and mineral compositions. The macronutrients saturated, trans, monounsaturated, and polyunsaturated fatty acids are particularly relevant for their effects on plasma lipids and lipoproteins. Dietary sodium and potassium are particularly relevant for their effects on BP. Epidemiological research has examined the dietary patterns of populations and identified associations between various patterns and CVD risk factors and outcomes. Intervention studies have tested a priori hypotheses involving prescribed dietary patterns specifically formulated on the basis of these data (eg, Dietary Approaches to Stop Hypertension [DASH] or MED patterns). Population-based prospective cohort studies and RCTs suggest that there are healthier overall dietary patterns (foods and/or their constituent macronutrient, vitamin, and mineral combinations) that are associated with lower risk of chronic diseases, including CVD and risk factors such as type 2 diabetes and hypertension. We reviewed data exclusively on dietary intake rather than nutritional supplements provided in pharmaceutical preparations (eg, potassium pills), because nutritional supplements may not have similar effects and are not considered “lifestyle” interventions.The Work Group focused on CVD risk factors to provide a free-standing Lifestyle document and to inform the Blood Cholesterol guideline4 and the hypertension panel. It also recognized that RCTs examining the effects on hard outcomes (myocardial infarction, stroke, heart failure, and CVD-related death) are difficult if not impossible to conduct for several reasons (eg, long-term adherence to dietary changes). However, the Work Group also supplemented this evidence on risk factors with observational data on hard outcomes for sodium. The Work Group prioritized topics for the evidence review and was unable to review the evidence on hard outcomes for dietary patterns or physical activity.For physical activity, substantial epidemiological evidence links higher levels of aerobic physical activity to lower rates of CVD and other chronic diseases, such as type 2 diabetes. Evidence indicates a dose-dependent inverse relationship between levels of physical activity and rates of CVD. The proposed mechanisms mediating the relationship between physical activity and decreased CVD rates include beneficial effects on lipids, lipoproteins, BP, and type 2 diabetes. The search for evidence related to physical activity and CVD included only systematic reviews and meta-analyses of RCTs or individual controlled clinical trials in adults (≥18 years of age) that were published from 2001 to 2011. For this CQ, the intervention was defined as physical activity interventions of any type.Weight loss and maintenance are crucial for prevention and control of CVD risk factors. The Obesity Expert Panel simultaneously performed a systematic review of the evidence for weight management and CVD risk factors and outcomes.5 The primary intent of the Work Group's systematic review was to focus on the effects of diet and physical activity on CVD risk factors independent of effects on weight. Therefore, studies in which the primary outcome was weight loss or in which treatment was associated with >3% change in weight were excluded from the present review. However, the Work Group expects that recommendations from both evidence reviews will apply to many patients.Because of limited resources and time, the Work Group could not review every study pertaining to lifestyle and CVD risk factors and outcomes. Priority was given to strong study design and a contemporaneous timeframe (1998 to 2009). However, there were instances in which the evidence review was extended beyond that timeframe. Landmark evidence on the effect of fatty acids on lipids was included back to 1990. The sodium evidence review included evidence through April 2012, and the physical activity meta-analysis review was extended to May 2011. Given the expertise of Work Group members and their familiarity with the literature in this field, the Work Group is confident that a broader review would not substantially change our conclusions or recommendations.The results of the Work Group systematic review are the 10 lifestyle recommendations (8 dietary and 2 physical activity recommendations) (Table 5). Because the Work Group was convened to inform the development of clinical guidelines, and because most data meeting our criteria for review were derived from studies of high-risk populations, these recommendations are directed at patients with CVD risk factors (ie, abnormal lipids and/or prehypertension and hypertension). The majority of adults in the United States currently have ≥1 of these risk factors (33.5% with elevated LDL-C; 27.3%, hypertension; 31%, prehypertension; and 11.3%, diabetes), with risk factors increasing with age.6 The Work Group encourages heart-healthy nutrition and physical activity behaviors for all adults (Section 5.6) (Table 17).Table 5. Summary of Recommendations for Lifestyle ManagementTable 5. Summary of Recommendations for Lifestyle ManagementFor both BP and lipids, most studies of diet and/or physical activity exclude people taking antihypertensive or lipid-lowering medications. Although there is no direct evidence, it is reasonable to expect that the beneficial effects of these lifestyle recommendations apply to those taking such medications and that following these recommendations can potentially lead to better BP and lipid control in those taking medications and/or reduced medication needs. The recommendations apply to adults <80 years of age with and without CVD.1.2.2. CQ-Based ApproachThe Work Group developed an initial set of questions based on their expertise and a brief literature review to identify topics of the greatest relevance and impact for the target audience of the guideline: primary care providers Because of time and resource limitations, the Work Group prioritized the 3 CQs in Table 4.The body of this report is organized by CQ. For each CQ:The rationale for its selection is provided, and methods are described.The ESs are presented, which include a rating for quality, a rationale that supports each item of evidence, and a statement. A detailed description of methods is provided in the NHLBI Lifestyle Systematic Evidence Review Report (http://www.nhlbi.nih.gov/guidelines/cvd_adult/lifestyle/). The Full Work Group Report supplement presents documentation for search strategies and results from the search of the published literature.Recommendations include recommendation strength, accompanied by a summary of how the recommendation derives from the evidence and a discussion of issues considered by the Work Group in formulating the recommendation. The ACC/AHA COR/LOE ratings have also been added.The ESs and recommendations are presented by CQ and grouped by topic:CQ1 presents evidence on dietary patterns and macronutrients and their effect on BP and lipids. The dietary recommendations for LDL-C lowering are described at the end of CQ1.CQ2 presents the evidence on the effect of dietary sodium and potassium intake on BP and CVD outcomes. The dietary recommendations for BP lowering are located at the end of CQ2.Finally, CQ3 presents evidence on the effect of physical activity on lipids and BP and physical activity recommendations for BP and lipid lowering. The physical activity recommendations for BP and lipid lowering are located at the end of CQ3.It should be recognized that formulating recommendations derived from evidence reviews in response to CQs has some advantages as well as limitations. Because of its desire to adhere to the highest quality of evidence, the Work Group was restricted to using evidence that met inclusion/exclusion and quality criteria established by the Work Group in partnership with the methodologists. When the phrase “there is insufficient evidence” is used, the reader must distinguish between “insufficient” evidence where no studies meeting inclusion/exclusion and quality criteria were found to answer a CQ and “insufficient” evidence where RCTs or observational studies were conducted but the available data do not provide sufficient information to formulate a recommendation. This perspective is important because clinicians could see fewer recommendations derived from expert opinion. Given this perspective, the clinical and research community can identify research questions that need to be answered in the future to refine recommendations when updates to the guideline are written (Section 6).1.3. Organization of Work GroupThe Work Group was composed of 12 members and 4 ex-officio members, including physicians and experts in BP, blood cholesterol, obesity, and lifestyle management. The authors came from the primary care, nursing, pharmacology, nutrition, exercise, behavioral science, and epidemiology disciplines and also included senior scientific staff from NHLBI and the National Institutes of Health.1.4. Document Reviews and ApprovalA formal peer review process initially was completed under the auspices of the NHLBI and included 6 expert reviewers and representatives of federal agencies. This document was also reviewed by 4 expert reviewers nominated by the ACC and the AHA when the management of the guideline transitioned to the ACC/AHA. The ACC and AHA reviewers’ RWI information is published in this document (Appendix 2).This document was approved for publication by the governing bodies of the ACC and AHA and endorsed by the American Association of Cardiovascular and Pulmonary Rehabilitation, American Pharmacists Association, American Society for Nutrition, American Society for Preventive Cardiology, American Society of Hypertension, Association of Black Cardiologists, National Lipid Association, Preventive Cardiovascular Nurses Association, and WomenHeart: The National Coalition for Women With Heart Disease.2. Lifestyle Management RecommendationsSee Table 5 for the Summary of Lifestyle Recommendations.3. CQ1—Dietary Patterns and Macronutrients: BP and LipidsSee Table 6 for the CQ for BP and lipids with dietary patterns and macronutrients.Table 6. CQ for Dietary Patterns and Macronutrients: BP and

HomeCirculationVol. 124, No. 22AHA/ACCF Secondary Prevention and Risk Reduction Therapy for Patients With Coronary and Other Atherosclerotic Vascular Disease: 2011 Update Free AccessResearch ArticlePDF/EPUBAboutView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toFree AccessResearch ArticlePDF/EPUBAHA/ACCF Secondary Prevention and Risk Reduction Therapy for Patients With Coronary and Other Atherosclerotic Vascular Disease: 2011 UpdateA Guideline From the American Heart Association and American College of Cardiology Foundation Sidney C. SmithJr, MD, FAHA, FACC, Chair, Emelia J. Benjamin, MD, ScM, FAHA, FACC, Robert O. Bonow, MD, FAHA, FACC, Lynne T. Braun, PhD, ANP, FAHA, Mark A. Creager, MD, FAHA, FACC, Barry A. Franklin, PhD, FAHA, Raymond J. Gibbons, MD, FAHA, FACC, Scott M. Grundy, MD, PhD, FAHA, Loren F. Hiratzka, MD, FAHA, FACC, Daniel W. Jones, MD, FAHA, Donald M. Lloyd-Jones, MD, ScM, FAHA, FACC, Margo Minissian, ACNP, AACC, FAHA, Lori Mosca, MD, PhD, MPH, FAHA, Eric D. Peterson, MD, MPH, FAHA, FACC, Ralph L. Sacco, MD, MS, FAHA, John Spertus, MD, MPH, FAHA, FACC, James H. Stein, MD, FAHA, FACC and Kathryn A. Taubert, PhD, FAHA Sidney C. SmithJrSidney C. SmithJr Search for more papers by this author , Emelia J. BenjaminEmelia J. Benjamin Search for more papers by this author , Robert O. BonowRobert O. Bonow Search for more papers by this author , Lynne T. BraunLynne T. Braun Search for more papers by this author , Mark A. CreagerMark A. Creager Search for more papers by this author , Barry A. FranklinBarry A. Franklin Search for more papers by this author , Raymond J. GibbonsRaymond J. Gibbons Search for more papers by this author , Scott M. GrundyScott M. Grundy Search for more papers by this author , Loren F. HiratzkaLoren F. Hiratzka Search for more papers by this author , Daniel W. JonesDaniel W. Jones Search for more papers by this author , Donald M. Lloyd-JonesDonald M. Lloyd-Jones Search for more papers by this author , Margo MinissianMargo Minissian Search for more papers by this author , Lori MoscaLori Mosca Search for more papers by this author , Eric D. PetersonEric D. Peterson Search for more papers by this author , Ralph L. SaccoRalph L. Sacco Search for more papers by this author , John SpertusJohn Spertus Search for more papers by this author , James H. SteinJames H. Stein Search for more papers by this author and Kathryn A. TaubertKathryn A. Taubert Search for more papers by this author Originally published3 Nov 2011https://doi.org/10.1161/CIR.0b013e318235eb4dCirculation. 2011;124:2458–2473is corrected byCorrectionOther version(s) of this articleYou are viewing the most recent version of this article. Previous versions: January 1, 2011: Previous Version 1 Since the 2006 update of the American Heart Association (AHA)/American College of Cardiology Foundation (ACCF) guidelines on secondary prevention,1 important evidence from clinical trials has emerged that further supports and broadens the merits of intensive risk-reduction therapies for patients with established coronary and other atherosclerotic vascular disease, including peripheral artery disease, atherosclerotic aortic disease, and carotid artery disease. In reviewing this evidence and its clinical impact, the writing group believed it would be more appropriate to expand the title of this guideline to “Secondary Prevention and Risk Reduction Therapy for Patients With Coronary and Other Atherosclerotic Vascular Disease.” Indeed, the growing body of evidence confirms that in patients with atherosclerotic vascular disease, comprehensive risk factor management reduces risk as assessed by a variety of outcomes, including improved survival, reduced recurrent events, the need for revascularization procedures, and improved quality of life. It is important not only that the healthcare provider implement these recommendations in appropriate patients but also that healthcare systems support this implementation to maximize the benefit to the patient.Compelling evidence-based results from recent clinical trials and revised practice guidelines provide the impetus for this update of the 2006 recommendations with evidence-based results2–165 (Table 1). Classification of recommendations and level of evidence are expressed in ACCF/AHA format, as detailed in Table 2. Recommendations made herein are largely based on major practice guidelines from the National Institutes of Health and updated ACCF/AHA practice guidelines, as well as on results from recent clinical trials. Thus, the development of the present guideline involved a process of partial adaptation of other guideline statements and reports and supplemental literature searches. The recommendations listed in this document are, whenever possible, evidence based. Writing group members performed these relevant supplemental literature searches with key search phrases including but not limited to tobacco/smoking/smoking cessation; blood pressure control/hypertension; cholesterol/hypercholesterolemia/lipids/lipoproteins/dyslipidemia; physical activity/exercise/exercise training; weight management/overweight/obesity; type 2 diabetes mellitus management; antiplatelet agents/anticoagulants; renin/angiotensin/aldosterone system blockers; β-blockers; influenza vaccination; clinical depression/depression screening; and cardiac/cardiovascular rehabilitation. Additional searches cross-referenced these topics with the subtopics of clinical trials, secondary prevention, atherosclerosis, and coronary/cerebral/peripheral artery disease. These searches were limited to studies, reviews, and other evidence conducted in human subjects and published in English. In addition, the writing group reviewed documents related to the subject matter previously published by the AHA, the ACCF, and the National Institutes of Health.Table 1. AHA/ACCF Secondary Prevention and Risk Reduction Therapy for Patients With Coronary and Other Atherosclerotic Vascular Disease: 2011 Update: Intervention Recommendations With Class of Recommendation and Level of EvidenceArea for InterventionRecommendationsSmoking Goal: Complete cessation. No exposure to environmental tobacco smokeClass IPatients should be asked about tobacco use status at every office visit.2,3,4,5,7) (Level of Evidence: B)Every tobacco user should be advised at every visit to quit.4,5,7,9(Level of Evidence: A)The tobacco user's willingness to quit should be assessed at every visit. (Level of Evidence: C)Patients should be assisted by counseling and by development of a plan for quitting that may include pharmacotherapy and/or referral to a smoking cessation program.4–9(Level of Evidence: A)Arrangement for follow up is recommended. (Level of Evidence: C)All patients should be advised at every office visit to avoid exposure to environmental tobacco smoke at work, home, and public places.10,11(Level of Evidence: B)Blood pressure controlGoal: <140/90 mm HgNote: The writing committee did not think that the 2006 recommendations for blood pressure control (below) should be modified at this time. The writing committee anticipates that the recommendations will be reviewed when the updated JNC guidelines are released.Class I1. All patients should be counseled regarding the need for lifestyle modification: weight control; increased physical activity; alcohol moderation; sodium reduction; and emphasis on increased consumption of fresh fruits, vegetables, and low-fat dairy products.12–16(Level of Evidence: B)2. Patients with blood pressure ≥140/90 mm Hg should be treated, as tolerated, with blood pressure medication, treating initially with β-blockers and/or ACE inhibitors, with addition of other drugs as needed to achieve goal blood pressure.12,17,18(Level of Evidence: A)Lipid managementGoal: Treatment with statin therapy; use statin therapy to achieve an LDL-C of <100 mg/dL; for very high risk* patients an LDL-C <70 mg/dL is reasonable; if triglycerides are ≥200 mg/dL, non–HDL-C† should be <130 mg/dL, whereas non–HDL-C <100 mg/dL for very high risk patients is reasonableNote: The writing committee anticipates that the recommendations will be reviewed when the updated ATP guidelines are released.Class I1. A lipid profile in all patients should be established, and for hospitalized patients, lipid-lowering therapy as recommended below should be initiated before discharge.20(Level of Evidence: B)2. Lifestyle modifications including daily physical activity and weight management are strongly recommended for all patients.19,29(Level of Evidence: B)3. Dietary therapy for all patients should include reduced intake of saturated fats (to <7% of total calories), transfatty acids (to <1% of total calories), and cholesterol (to <200 mg/d).21–24,29(Level of Evidence: B)4. In addition to therapeutic lifestyle changes, statin therapy should be prescribed in the absence of contraindications or documented adverse effects.25–29(Level of Evidence: A)5. An adequate dose of statin should be used that reduces LDL-C to <100 mg/dL AND achieves at least a 30% lowering of LDL-C.25–29(Level of Evidence: C)6. Patients who have triglycerides ≥200 mg/dL should be treated with statins to lower non–HDL-C to <130 mg/dL.25–27,30(Level of Evidence: B)7. Patients who have triglycerides >500 mg/dL should be started on fibrate therapy in addition to statin therapy to prevent acute pancreatitis. (Level of Evidence: C)Class IIa1. If treatment with a statin (including trials of higher-dose statins and higher-potency statins) does not achieve the goal selected for a patient, intensification of LDL-C–lowering drug therapy with a bile acid sequestrant‡` or niacin§` is reasonable.31–33(Level of Evidence: B)2. For patients who do not tolerate statins, LDL-C–lowering therapy with bile acid sequestrants‡` and/or niacin§` is reasonable.35,36(Level of Evidence: B)3. It is reasonable to treat very high-risk patients* with statin therapy to lower LDL-C to <70 mg/dL.26–28,37,38,166(Level of Evidence: C)4. In patients who are at very high risk* and who have triglycerides ≥200 mg/dL, a non–HDL-C goal of <100 mg/dL is reasonable.25–27,30(Level of Evidence: B)Lipid management cont'dClass IIb1. The use of ezetimibe may be considered for patients who do not tolerate or achieve target LDL-C with statins, bile acid sequestrants,‡` and/or niacin.§` (Level of Evidence: C)2. For patients who continue to have an elevated non–HDL-C while on adequate statin therapy, niacin§` or fibrate∥` therapy32,41,41(Level of Evidence: B) or fish oil (Level of Evidence: C) may be reasonable.3. For all patients, it may be reasonable to recommend omega-3 fatty acids from fish¶` or fish oil capsules (1 g/d) for cardiovascular disease risk reduction.44–46(Level of Evidence: B)Physical activityClass I Goal: At least 30 minutes, 7 days per week (minimum 5 days per week)1. For all patients, the clinician should encourage 30 to 60 minutes of moderate-intensity aerobic activity, such as brisk walking, at least 5 days and preferably 7 days per week, supplemented by an increase in daily lifestyle activities (eg, walking breaks at work, gardening, household work) to improve cardiorespiratory fitness and move patients out of the least fit, least active high-risk cohort (bottom 20%).54,58,58(Level of Evidence: B)2. For all patients, risk assessment with a physical activity history and/or an exercise test is recommended to guide prognosis and prescription.47–52,58(Level of Evidence: B)3. The clinician should counsel patients to report and be evaluated for symptoms related to exercise. (Level of Evidence: C)Class IIa1. It is reasonable for the clinician to recommend complementary resistance training at least 2 days per week.59(Level of Evidence: C)Weight managementGoals: Body mass index: 18.5 to 24.9 kg/m2Waist circumference: women <35 inches (<89 cm), men <40 inches (<102 cm)Class I1. Body mass index and/or waist circumference should be assessed at every visit, and the clinician should consistently encourage weight maintenance/reduction through an appropriate balance of lifestyle physical activity, structured exercise, caloric intake, and formal behavioral programs when indicated to maintain/achieve a body mass index between 18.5 and 24.9 kg/m2.60–62,65–70(Level of Evidence: B)2. If waist circumference (measured horizontally at the iliac crest) is ≥35 inches (≥89 cm) in women and ≥40 inches (≥102 cm) in men, therapeutic lifestyle interventions should be intensified and focused on weight management.66–70(Level of Evidence: B)3. The initial goal of weight loss therapy should be to reduce body weight by approximately 5% to 10% from baseline. With success, further weight loss can be attempted if indicated. (Level of Evidence: C)Type 2 diabetes mellitus managementNote: Recommendations below are for prevention of cardiovascular complications.Class I1. Care for diabetes should be coordinated with the patient's primary care physician and/or endocrinologist. (Level of Evidence: C)2. Lifestyle modifications including daily physical activity, weight management, blood pressure control, and lipid management are recommended for all patients with diabetes.19,22–24,29,56,58,59,62,66,74,162 (Level of Evidence: B)Class IIa1. Metformin is an effective first-line pharmacotherapy and can be useful if not contraindicated.74–76(Level of Evidence: A)2. It is reasonable to individualize the intensity of blood sugar–lowering interventions based on the individual patient's risk of hypoglycemia during treatment. (Level of Evidence: C)Class IIb1. Initiation of pharmacotherapy interventions to achieve target HbA1c may be reasonable.71,72,74–80 (Level of Evidence: A)2. A target HbA1c of ≤7% may be considered. (Level of Evidence: C)3. Less stringent HbA1c goals may be considered for patients with a history of severe hypoglycemia, limited life expectancy, advanced microvascular or macrovascular complications, or extensive comorbidities, or those in whom the goal is difficult to attain despite intensive therapeutic interventions. (Level of Evidence: C)Antiplatelet agents/anticoagulantsClass I1. Aspirin 75–162 mg daily is recommended in all patients with coronary artery disease unless contraindicated.64,81,82,116(Level of Evidence: A)Clopidogrel 75 mg daily is recommended as an alternative for patients who are intolerant of or allergic to aspirin.117(Level of Evidence: B)2. A P2Y12 receptor antagonist in combination with aspirin is indicated in patients after ACS or PCI with stent placement.83–85(Level of Evidence: A)For patients receiving a bare-metal stent or drug-eluting stent during PCI for ACS, clopidogrel 75 mg daily, prasugrel 10 mg daily, or ticagrelor 90 mg twice daily should be given for at least 12 months.84,86,113,114(Level of Evidence: A)Antiplatelet agents/anticoagulants cont'd3. For patients undergoing coronary artery bypass grafting, aspirin should be started within 6 hours after surgery to reduce saphenous vein graft closure. Dosing regimens ranging from 100 to 325 mg daily for 1 year appear to be efficacious.87–90(Level of Evidence: A)4. In patients with extracranial carotid or vertebral atherosclerosis who have had ischemic stroke or TIA, treatment with aspirin alone (75–325 mg daily), clopidogrel alone (75 mg daily), or the combination of aspirin plus extended-release dipyridamole (25 mg and 200 mg twice daily, respectively) should be started and continued.91,116,116(Level of Evidence: A)5. For patients with symptomatic atherosclerotic peripheral artery disease of the lower extremity, antiplatelet therapy with aspirin (75–325 mg daily) or clopidogrel (75 mg daily) should be started and continued.92,107,116,117(Level of Evidence: A)6. Antiplatelet therapy is recommended in preference to anticoagulant therapy with warfarin or other vitamin K antagonists to treat patients with atherosclerosis.93,94,105,110(Level of Evidence: A)If there is a compelling indication for anticoagulant therapy, such as atrial fibrillation, prosthetic heart valve, left ventricular thrombus, or concomitant venous thromboembolic disease, warfarin should be administered.95,99–102(Level of Evidence: A) (NOTE: Patients receiving low dose aspirin for atherosclerosis should continue to receive it.)For patients requiring warfarin, therapy should be administered to achieve the recommended INR for the specific condition.81,96,110(Level of Evidence: B)Use of warfarin in conjunction with aspirin and/or clopidogrel is associated with increased risk of bleeding and should be monitored closely.97,110,110(Level of Evidence: A)Class IIa1. If the risk of morbidity from bleeding outweighs the anticipated benefit afforded by thienopyridine therapy after stent implantation, earlier discontinuation (eg, <12 months) is reasonable. (Level of Evidence: C) (Note: the risk for serious cardiovascular events because of early discontinuation of thienopyridines is greater for patients with drug-eluting stents than those with bare-metal stents.)2. After PCI, it is reasonable to use 81 mg of aspirin per day in preference to higher maintenance doses.84,85,118–122(Level of Evidence: B)3. For patients undergoing coronary artery bypass grafting, clopidogrel (75 mg daily) is a reasonable alternative in patients who are intolerant of or allergic to aspirin. (Level of Evidence: C)Class IIb1. The benefits of aspirin in patients with asymptomatic peripheral artery disease of the lower extremities are not well established.108,109(Level of Evidence: B)2. Combination therapy with both aspirin 75 to 162 mg daily and clopidogrel 75 mg daily may be considered in patients with stable coronary artery disease.112(Level of Evidence: B)Renin-angiotensin-aldosterone system blockers ACE inhibitorsClass I1. ACE inhibitors should be started and continued indefinitely in all patients with left ventricular ejection fraction ≤40% and in those with hypertension, diabetes, or chronic kidney disease, unless contraindicated.124,125(Level of Evidence: A)Class IIa1. It is reasonable to use ACE inhibitors in all other patients.126(Level of Evidence: B) ARBsClass I1. The use of ARBs is recommended in patients who have heart failure or who have had a myocardial infarction with left ventricular ejection fraction ≤40% and who are ACE-inhibitor intolerant.130–132(Level of Evidence: A)Class IIa1. It is reasonable to use ARBs in other patients who are ACE-inhibitor intolerant.133(Level of Evidence: B)Class IIb1. The use of ARBs in combination with an ACE inhibitor is not well established in those with systolic heart failure.132,134(Level of Evidence: A) Aldosterone blockadeClass I1. Use of aldosterone blockade in post–myocardial infarction patients without significant renal dysfunction#`or hyperkalemia** is recommended in patients who are already receiving therapeutic doses of an ACE inhibitor and β-blocker, who have a left ventricular ejection fraction ≤40%, and who have either diabetes or heart failure.136,137(Level of Evidence: A)β-BlockersClass I1. β-Blocker therapy should be used in all patients with left ventricular systolic dysfunction (ejection fraction ≤40%) with heart failure or prior myocardial infarction, unless contraindicated. (Use should be limited to carvedilol, metoprolol succinate, or bisoprolol, which have been shown to reduce mortality.)138,141,141(Level of Evidence: A)2. β-Blocker therapy should be started and continued for 3 years in all patients with normal left ventricular function who have had myocardial infarction or ACS.139,143,143(Level of Evidence: B)Class IIa1. It is reasonable to continue β-blockers beyond 3 years as chronic therapy in all patients with normal left ventricular function who have had myocardial infarction or ACS.139,143,143(Level of Evidence: B)2. It is reasonable to give β-blocker therapy in patients with left ventricular systolic dysfunction (ejection fraction ≤40%) without heart failure or prior myocardial infarction. (Level of Evidence: C)Class IIb1. β-Blockers may be considered as chronic therapy for all other patients with coronary or other vascular disease. (Level of Evidence: C)Influenza vaccinationClass I1. Patients with cardiovascular disease should have an annual influenza vaccination.144–147(Level of Evidence: B)DepressionClass IIa1. For patients with recent coronary artery bypass graft surgery or myocardial infarction, it is reasonable to screen for depression if patients have access to case management, in collaboration with their primary care physician and a mental health specialist.148–152(Level of Evidence: B)Class IIb1. Treatment of depression has not been shown to improve cardiovascular disease outcomes but may be reasonable for its other clinical benefits.(Level of Evidence: C)Cardiac rehabilitationClass I1. All eligible patients with ACS or whose status is immediately post coronary artery bypass surgery or post-PCI should be referred to a comprehensive outpatient cardiovascular rehabilitation program either prior to hospital discharge or during the first follow-up office visit.55,154,161,163(Level of Evidence: A)2. All eligible outpatients with the diagnosis of ACS, coronary artery bypass surgery or PCI (Level of Evidence: A),55,154,155,161 chronic angina (Level of Evidence: B),161,163 and/or peripheral artery disease (Level of Evidence: A)(158,164 within the past year should be referred to a comprehensive outpatient cardiovascular rehabilitation program.3. A home-based cardiac rehabilitation program can be substituted for a supervised, center-based program for low-risk patients.153,160,160(Level of Evidence: A)Class IIa1. A comprehensive exercise-based outpatient cardiac rehabilitation program can be safe and beneficial for clinically stable outpatients with a history of heart failure.159,159a–159c(Level of Evidence: B)JNC indicates the report of the National Heart, Lung, and Blood Institute's Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure guidelines; ACE, angiotensin-converting enzyme; ATP, Adult Treatment Panel; LDL-C, low-density lipoprotein cholesterol; HDL-C, high-density lipoprotein cholesterol; HbA1c, hemoglobin A1c; ACS, acute coronary syndrome; PCI, percutaneous coronary intervention; TIA, transient ischemic attack; INR, international normalized ratio; and ARB, angiotensin receptor blocker.*Presence of established CVD plus (1) multiple major risk factors (especially diabetes), (2) severe and poorly controlled risk factors (especially continued cigarette smoking), (3) multiple risk factors of the metabolic syndrome (especially high triglycerides ≥200 mg/dL plus non–HDL-C ≥130 mg/dL with low HDL-C <40 mg/dL), and (4) patients with ACSs.†Non–HDL-C=total cholesterol minus HDL-C.‡The use of bile acid sequestrants is relatively contraindicated when triglycerides are ≥200 mg/dL and is contraindicated when triglycerides are ≥500 mg/dL.§Dietary supplement niacin must not be used as a substitute for prescription niacin.∥The combination of high-dose statin plus fibrate (especially gemfibrozil) can increase risk for severe myopathy. Statin doses should be kept relatively low with this combination.¶Pregnant and lactating women should limit their intake of fish to minimize exposure to methylmercury.#Estimated creatinine clearance should be >30 mL/min.**Potassium should be <5.0 mEq/L.Table 2. Applying Classification of Recommendation and Level of EvidenceTable 2. Applying Classification of Recommendation and Level of EvidenceA recommendation with Level of Evidence B or C does not imply that the recommendation is weak. Many important clinical questions addressed in the guidelines do not lend themselves to clinical trials. Although randomized trials are unavailable, there may be a very clear clinical consensus that a particular test or therapy is useful or effective.*Data available from clinical trials or registries about the usefulness/efficacy in different subpopulations, such as sex, age, history of diabetes, history of prior myocardial infarction, history of heart failure, and prior aspirin use.†For comparative effectiveness recommendations (Class I and IIa; Level of Evidence A and B only), studies that support the use of comparator verbs should involve direct comparisons of the treatments or strategies being evaluated.With regard to lipids and dyslipidemias, the lipid reduction trials published between 2002 and 200618,25,166–168 included >50 000 patients and resulted in new optional therapeutic targets, which were outlined in the 2004 update of the National Heart, Lung, and Blood Institute's Adult Treatment Panel (ATP) III report.169 These changes defined optional lower target cholesterol levels for very high-risk coronary heart disease (CHD) patients, especially those with acute coronary syndromes, and expanded indications for drug treatment. Subsequent to the 2004 update of ATP III, 2 additional trials26,27 demonstrated cardiovascular benefit for lipid lowering significantly below current cholesterol goal levels for those with chronic coronary heart disease. These trials allowed for alterations in the 2006 guideline, such that low-density lipoprotein cholesterol (LDL-C) should be <100 mg/dL for all patients with CHD and other clinical forms of atherosclerotic disease, but in addition, it is reasonable to treat to LDL-C <70 mg/dL in patients at highest risk. The benefits of lipid-lowering therapy are in proportion to the reduction in LDL-C, and when LDL-C is above 100 mg/dL, an adequate dose of statin therapy should be used to achieve at least a 30% lowering of LDL-C. When the <70 mg/dL target is chosen, it may be prudent to increase statin therapy in a graded fashion to determine a patient's response and tolerance. Furthermore, if it is not possible to attain LDL-C <70 mg/dL because of a high baseline LDL-C, it generally is possible to achieve LDL-C reductions of >50% with either statins or LDL-C–lowering drug combinations. For patients with triglyceride levels ≥200 mg/dL, non–high-density lipoprotein cholesterol values should be used as a guide to therapy. Although no studies have directly tested treatment to target strategies, the target LDL-C and non–HDL-C levels are derived from several randomized controlled trials where the LDL-C levels achieved for patients showing benefit are used to suggest targets. Thus, references for the studies from which targets are derived are listed and targets are considered as level of evidence C. Importantly, this guideline statement for patients with atherosclerotic disease does not modify the recommendations of the 2004 ATP III update for patients without atherosclerotic disease who have diabetes mellitus or multiple risk factors and a 10-year risk level for CHD >20%. In the latter 2 types of high-risk patients, the recommended LDL-C goal of <100 mg/dL has not changed. Finally, to avoid any misunderstanding about cholesterol management in general, it must be emphasized that a reasonable cholesterol level of <70 mg/dL does not apply to other types of lower-risk individuals who do not have CHD or other forms of atherosclerotic disease; in such cases, recommendations contained in the 2004 ATP III update still pertain. The writing group agreed that no further changes be made in the recommendations for treatment of dyslipidemia pending the expected publication of the National Heart, Lung, and Blood Institute's updated ATP guidelines in 2012. Similar recommendations were made for the treatment of hypertension by the writing group pending the publication of the updated report of the National Heart, Lung, and Blood Institute's Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure guidelines, expected in the spring of 2012.Trials involving other secondary prevention therapies also have influenced major practice guidelines used to formulate the recommendations in the present update. Thus, specific recommendations for clopidogrel use in post–acute coronary syndrome or post–percutaneous coronary intervention stented patients were included in the 2006 update, and recommendations regarding prasugrel and ticagrelor are added to this guideline on the basis of the results of the TRITON-TIMI 38 trial (Trial to Assess Improvement in Therapeutic Outcomes by Optimizing Platelet Inhibition With Prasugrel–Thrombolysis in Myocardial Infarction) and PLATO (Study of Platelet Inhibition and Patient Outcomes). The present update continues to recommend lower-dose aspirin for chronic therapy. The results of additional studies have further confirmed the benefit of aldosterone antagonist therapy among patients with impaired left ventricular function. The results of several trials involving angiotensin-converting enzyme inhibitor therapy among patients at relatively low risk with stable coronary disease and normal left ventricular function influenced the current recommendations.32 Finally, the recommendations for β-blocker therapy have been clarified to reflect the fact that evidence supporting their efficacy is greatest among patients with recent myocardial infarction (<3 years) and/or left ventricular systolic dysfunction (left ventricular ejection fraction ≤40%). For those patients without these Class I indications, β-blocker therapy is optional (Class IIa or IIb).The writing group confirms the recommendation introduced in 2006 for this guideline with regard to influenza vaccination. According to the US Centers for Disease Control and Prevention, vaccination with inactivated influenza vaccine is recommended for individuals who have chronic disorders of the cardiovascular system because they are at increased risk for complications from influenza.147 Additionally, the writing group added new sections on depression and on cardiovascular rehabilitation.The writing group continues to emphasize the importance of giv

### Preamble A primary challenge in the development of clinical practice guidelines is keeping pace with the stream of new data on which recommendations are based. In an effort to respond promptly to new evidence, the American College of Cardiology Foundation/American Heart Association (ACCF/AHA)

Heart failure (HF) is a major public health problem in the United States. Nearly 5 million patients in this country have HF, and nearly 500,000 patients are diagnosed with HF for the first time each year. The disorder is the underlying reason for 12 to 15 million office visits and 6.5 million hospital days each year (1). During the last 10 years, the annual number of hospitalizations has increased from approximately 550,000 to nearly 900,000 for HF as a primary diagnosis and from 1.7 to 2.6 million for HF as a primary or secondary diagnosis (2). Nearly 300,000 patients die of HF as a primary or contributory cause each year, and the number of deaths has increased steadily despite advances in treatment. HFs primarily a disease of the elderly (3). Approximately 6% to 10% of people older than 65 years have HF (4), and approximately 80% of patients hospitalized with HF are more than 65 years old (2). HF is the most common Medicare diagnosis-related group, and more Medicare dollars are spent for the diagnosis and treatment of HF than for any other diagnosis (5). The total inpatient and outpatient costs for HF in 1991 were approximately $38.1 billion, which was approximately 5.4% of the healthcare budget that year (1). In the United States, approximately $500 million annually is spent on drugs for the treatment of HF. The American College of Cardiology (ACC) and the American Heart Association (AHA) first published guidelines for the evaluation and management of HF in 1995 (6). Since that time, a great deal of progress has been made in the development of both pharmacological and nonpharmacological approaches to treatment for this common, costly, disabling, and generally fatal disorder. For this reason, the 2 organizations believed that the time was right to reassess and update these …

It is important that the medical profession plays a significant role in critically evaluating the use of diagnostic procedures and therapies as they are introduced and tested in the detection, management, or prevention of disease states. Rigorous and expert analysis of the available data documenting

HomeCirculationVol. 126, No. 252012 ACCF/AHA/ACP/AATS/PCNA/SCAI/STS Guideline for the Diagnosis and Management of Patients With Stable Ischemic Heart Disease: Executive Summary Free AccessResearch ArticlePDF/EPUBAboutView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissionsDownload Articles + Supplements ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toSupplementary MaterialsFree AccessResearch ArticlePDF/EPUB2012 ACCF/AHA/ACP/AATS/PCNA/SCAI/STS Guideline for the Diagnosis and Management of Patients With Stable Ischemic Heart Disease: Executive SummaryA Report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines, and the American College of Physicians, American Association for Thoracic Surgery, Preventive Cardiovascular Nurses Association, Society for Cardiovascular Angiography and Interventions, and Society of Thoracic Surgeons Stephan D. Fihn, MD, MPH, Julius M. Gardin, MD, Jonathan Abrams, MD, Kathleen Berra, MSN, ANP, James C. Blankenship, MD, Apostolos P. Dallas, MD, Pamela S. Douglas, MD, JoAnne M. Foody, MD, Thomas C. Gerber, MD, PhD, Alan L. Hinderliter, MD, Spencer B. KingIII, MD, Paul D. Kligfield, MD, Harlan M. Krumholz, MD, Raymond Y.K. Kwong, MD, Michael J. Lim, MD, Jane A. Linderbaum, MS, CNP-BC, Michael J. Mack, MD, Mark A. Munger, PharmD, Richard L. Prager, MD, Joseph F. Sabik, MD, Leslee J. Shaw, PhD, Joanna D. Sikkema, MSN, ANP-BC, Craig R. SmithJr, MD, Sidney C. SmithJr, MD, John A. Spertus, MD, MPH and Sankey V. Williams, MD Stephan D. FihnStephan D. Fihn †ACP Representative. Search for more papers by this author , Julius M. GardinJulius M. Gardin *Writing committee members are required to recuse themselves from voting on sections to which their specific relationship could apply; see Appendix 1 for detailed information. Search for more papers by this author , Jonathan AbramsJonathan Abrams ‡ACCF/AHA Representative. Search for more papers by this author , Kathleen BerraKathleen Berra *Writing committee members are required to recuse themselves from voting on sections to which their specific relationship could apply; see Appendix 1 for detailed information. Search for more papers by this author , James C. BlankenshipJames C. Blankenship *Writing committee members are required to recuse themselves from voting on sections to which their specific relationship could apply; see Appendix 1 for detailed information. Search for more papers by this author , Apostolos P. DallasApostolos P. Dallas *Writing committee members are required to recuse themselves from voting on sections to which their specific relationship could apply; see Appendix 1 for detailed information. Search for more papers by this author , Pamela S. DouglasPamela S. Douglas *Writing committee members are required to recuse themselves from voting on sections to which their specific relationship could apply; see Appendix 1 for detailed information. Search for more papers by this author , JoAnne M. FoodyJoAnne M. Foody *Writing committee members are required to recuse themselves from voting on sections to which their specific relationship could apply; see Appendix 1 for detailed information. Search for more papers by this author , Thomas C. GerberThomas C. Gerber ‡ACCF/AHA Representative. Search for more papers by this author , Alan L. HinderliterAlan L. Hinderliter ‡ACCF/AHA Representative. Search for more papers by this author , Spencer B. KingIIISpencer B. KingIII *Writing committee members are required to recuse themselves from voting on sections to which their specific relationship could apply; see Appendix 1 for detailed information. Search for more papers by this author , Paul D. KligfieldPaul D. Kligfield ‡ACCF/AHA Representative. Search for more papers by this author , Harlan M. KrumholzHarlan M. Krumholz ‡ACCF/AHA Representative. Search for more papers by this author , Raymond Y.K. KwongRaymond Y.K. Kwong ‡ACCF/AHA Representative. Search for more papers by this author , Michael J. LimMichael J. Lim *Writing committee members are required to recuse themselves from voting on sections to which their specific relationship could apply; see Appendix 1 for detailed information. Search for more papers by this author , Jane A. LinderbaumJane A. Linderbaum ¶Critical care nursing expertise. Search for more papers by this author , Michael J. MackMichael J. Mack *Writing committee members are required to recuse themselves from voting on sections to which their specific relationship could apply; see Appendix 1 for detailed information. Search for more papers by this author , Mark A. MungerMark A. Munger *Writing committee members are required to recuse themselves from voting on sections to which their specific relationship could apply; see Appendix 1 for detailed information. Search for more papers by this author , Richard L. PragerRichard L. Prager #STS Representative. Search for more papers by this author , Joseph F. SabikJoseph F. Sabik *Writing committee members are required to recuse themselves from voting on sections to which their specific relationship could apply; see Appendix 1 for detailed information. Search for more papers by this author , Leslee J. ShawLeslee J. Shaw *Writing committee members are required to recuse themselves from voting on sections to which their specific relationship could apply; see Appendix 1 for detailed information. Search for more papers by this author , Joanna D. SikkemaJoanna D. Sikkema *Writing committee members are required to recuse themselves from voting on sections to which their specific relationship could apply; see Appendix 1 for detailed information. Search for more papers by this author , Craig R. SmithJrCraig R. SmithJr **AATS Representative. Search for more papers by this author , Sidney C. SmithJrSidney C. SmithJr *Writing committee members are required to recuse themselves from voting on sections to which their specific relationship could apply; see Appendix 1 for detailed information. Search for more papers by this author , John A. SpertusJohn A. Spertus *Writing committee members are required to recuse themselves from voting on sections to which their specific relationship could apply; see Appendix 1 for detailed information. Search for more papers by this author and Sankey V. WilliamsSankey V. Williams *Writing committee members are required to recuse themselves from voting on sections to which their specific relationship could apply; see Appendix 1 for detailed information. Search for more papers by this author Originally published19 Nov 2012https://doi.org/10.1161/CIR.0b013e3182776f83Circulation. 2012;126:3097–3137is corrected byCorrectionsOther version(s) of this articleYou are viewing the most recent version of this article. Previous versions: January 1, 2012: Previous Version 1 Table of ContentsPreamble. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .30991. Introduction. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .31011.1. Methodology and Evidence Overview. . . . . . .31011.2. Organization of the Writing Committee. . . . . .31011.3. Document Review and Approval. . . . . . . . . . .31011.4. Scope of the Guideline. . . . . . . . . . . . . . . . . . .31021.5. General Approach and Overlap With Other Guidelines or Statements. . . . . . . . . . . . . . . . .31031.6. Magnitude of the Problem. . . . . . . . . . . . . . . .31031.7. Organization of the Guideline. . . . . . . . . . . . . .31041.8. Vital Importance of Involvement by an Informed Patient: Recommendation. . . . . . . . .31042. Diagnosis of SIHD: Recommendations. . . . . . . . . .31042.1. Clinical Evaluation of Patients With Chest Pain. . .31042.1.1. Clinical Evaluation in the Initial Diagnosis of SIHD in Patients With Chest Pain. . . . . . . . . . . . . . . . . . .31042.1.2. Electrocardiography. . . . . . . . . . . . . . . .31062.1.2.1. Resting Electrocardiography to Assess Risk. . . . . . . . . . . . . . .31062.1.3. Stress Testing and Advanced Imaging for Initial Diagnosis in Patients With Suspected SIHD Who Require Noninvasive Testing. . . . . . . . .31062.1.3.1. Able to Exercise. . . . . . . . . . . .31062.1.3.2. Unable to Exercise. . . . . . . . . .31072.1.3.3. Other. . . . . . . . . . . . . . . . . . . .31083. Risk Assessment: Recommendations. . . . . . . . . . . .31083.1. Advanced Testing: Resting and Stress Noninvasive Testing. . . . . . . . . . . . . . . . . . . . .31083.1.1. Resting Imaging to Assess Cardiac Structure and Function. . . . . . . . . . . . . .31083.1.2. Stress Testing and Advanced Imaging in Patients With Known SIHD Who Require Noninvasive Testing for Risk Assessment. . . . . . . . . . . . . . . . . .31093.1.2.1. Risk Assessment in Patients Able to Exercise. . . . . . . . . . . .31093.1.2.2. Risk Assessment in Patients Unable to Exercise. . . . . . . . . .31103.1.2.3. Risk Assessment Regardless of Patients' Ability to Exercise. . .31113.2. Coronary Angiography. . . . . . . . . . . . . . . . . . .31123.2.1. Coronary Angiography as an Initial Testing Strategy to Assess Risk. . . . . . .31123.2.2. Coronary Angiography to Assess Risk After Initial Workup With Noninvasive Testing. . . . . . . . . . . . . . . .31124. Treatment: Recommendations. . . . . . . . . . . . . . . . .31124.1. Patient Education. . . . . . . . . . . . . . . . . . . . . . .31124.2. Guideline-Directed Medical Therapy. . . . . . . .31134.2.1. Risk Factor Modification. . . . . . . . . . . .31134.2.1.1. Lipid Management. . . . . . . . . .31134.2.1.2. Blood Pressure Management. . .31134.2.1.3. Diabetes Management. . . . . . . .31134.2.1.4. Physical Activity. . . . . . . . . . .31134.2.1.5. Weight Management. . . . . . . . .31134.2.1.6. Smoking Cessation Counseling. . .31144.2.1.7. Management of Psychological Factors. . . . . . . .31144.2.1.8. Alcohol Consumption. . . . . . . .31144.2.1.9. Avoiding Exposure to Air Pollution. . . . . . . . . . . . . . .31144.2.2. Additional Medical Therapy to Prevent MI and Death. . . . . . . . . . . . . . . . . . . . .31144.2.2.1. Antiplatelet Therapy. . . . . . . . .31144.2.2.2. Beta-Blocker Therapy. . . . . . . .31144.2.2.3. Renin-Angiotensin-Aldosterone Blocker Therapy. .31144.2.2.4. Influenza Vaccination. . . . . . . .31144.2.2.5. Additional Therapy to Reduce Risk of MI and Death. . . . . . . .31154.2.3. Medical Therapy for Relief of Symptoms. .31154.2.3.1. Use of Anti-Ischemic Medications. . . . . . . . . . . . . . .31154.2.4. Alternative Therapies for Relief of Symptoms in Patients With Refractory Angina. . . . . . . . . . . . . . . . .31155. CAD Revascularization: Recommendations. . . . . . .31155.1. Heart Team Approach to Revascularization Decisions. . . . . . . . . . . . . . . . . . . . . . . . . . . . .31155.2. Revascularization to Improve Survival. . . . . . .31155.3. Revascularization to Improve Symptoms. . . . .31185.4. Dual Antiplatelet Therapy Compliance and Stent Thrombosis. . . . . . . . . . . . . . . . . . . . . . .31195.5. Hybrid Coronary Revascularization. . . . . . . . .31196. Patient Follow-Up: Monitoring of Symptoms and Antianginal Therapy: Recommendations. . . . . . . . .31196.1. Clinical Evaluation, Echocardiography During Routine, Periodic Follow-Up. . . . . . . . . . . . . .31196.2. Noninvasive Testing in Known SIHD. . . . . . .31196.2.1. Follow-Up Noninvasive Testing in Patients With Known SIHD: New, Recurrent or Worsening Symptoms, Not Consistent With Unstable Angina. . . . . . . . . . . . . . . . . .31196.2.1.1. Patients Able to Exercise. . . . .31196.2.1.2. Patients Unable to Exercise. . .31206.2.1.3. Irrespective of Ability to Exercise. . . . . . . . . . . . . . . . . .31206.2.2. Noninvasive Testing in Known SIHD—Asymptomatic (or Stable Symptoms). . . . . . . . . . . . . .3121Appendix 1. Author Relationships With Industry and Other Entities (Relevant). . . . . . . . . . . . .3133Appendix 2. Reviewer Relationships With Industry and Other Entities (Relevant). . . . . . . . .3135Anderson Jeffrey L., MD, FACC, FAHAPreambleThe medical profession should play a central role in evaluating the evidence related to drugs, devices, and procedures for the detection, management, and prevention of disease. When properly applied, expert analysis of available data on the benefits and risks of these therapies and procedures can improve the quality of care, optimize patient outcomes, and favorably affect costs by focusing resources on the most effective strategies. An organized and directed approach to a thorough review of evidence has resulted in the production of clinical practice guidelines that assist physicians in selecting the best management strategy for an individual patient. Moreover, clinical practice guidelines can provide a foundation for other applications, such as performance measures, appropriate use criteria, and both quality improvement and clinical decision support tools.The American College of Cardiology Foundation (ACCF) and the American Heart Association (AHA) have jointly produced guidelines in the area of cardiovascular disease since 1980. The ACCF/AHA Task Force on Practice Guidelines (Task Force), charged with developing, updating, and revising practice guidelines for cardiovascular diseases and procedures, directs and oversees this effort. Writing committees are charged with regularly reviewing and evaluating all available evidence to develop balanced, patient-centric recommendations for clinical practice.Experts in the subject under consideration are selected by the ACCF and AHA to examine subject-specific data and write guidelines in partnership with representatives from other medical organizations and specialty groups. Writing committees are asked to perform a literature review; weigh the strength of evidence for or against particular tests, treatments, or procedures; and include estimates of expected outcomes where such data exist. Patient-specific modifiers, comorbidities, and issues of patient preference that may influence the choice of tests or therapies are considered. When available, information from studies on cost is considered, but data on efficacy and outcomes onstitute the primary basis for the recommendations contained herein.In analyzing the data and developing recommendations and supporting text, the writing committee uses evidence-based methodologies developed by the Task Force.1 The Class of Recommendation (COR) is an estimate of the size of the treatment effect, with consideration given to risks versus benefits in addition to evidence and/or agreement that a given treatment or procedure is or is not useful/effective or in some situations may cause harm. The Level of Evidence (LOE) is an estimate of the certainty or precision of the treatment effect. The writing committee reviews and ranks evidence supporting each recommendation, with the weight of evidence ranked as LOE A, B, or C according to specific definitions that are included in Table 1. Studies are identified as observational, retrospective, prospective, or randomized as appropriate. For certain conditions for which inadequate data are available, recommendations are based on expert consensus and clinical experience and are ranked as LOE C. When recommendations at LOE C are supported by historical clinical data, appropriate references (including clinical reviews) are cited if available. For issues for which sparse data are available, a survey of current practice among the clinicians on the writing committee is the basis for LOE C recommendations, and no references are cited. The schema for COR and LOE is summarized in Table 1, which also provides suggested phrases for writing recommendations within each COR. A new addition to this methodology is separation of the Class III recommendations to delineate whether the recommendation is determined to be of “no benefit” or is associated with “harm” to the patient. In addition, in view of the increasing number of comparative effectiveness studies, comparator verbs and suggested phrases for writing recommendations for the comparative effectiveness of one treatment or strategy versus another have been added for COR I and IIa, LOE A or B only.Table 1. Applying Classification of Recommendations and Level of EvidenceTable 1. Applying Classification of Recommendations and Level of EvidenceA recommendation with Level of Evidence B or C does not imply that the recommendation is weak. Many important clinical questions addressed in the guidelines do not lend themselves to clinical trials. Although randomized trials are unavailable, there may be a very clear clinical consensus that a particular test or therapy is useful or effective.*Data available from clinical trials or registries about the usefulness/efficacy in different subpopulations, such as sex, age, history of diabetes, history of prior myocardial infarction, history of heart failure, and prior aspirin use. †For comparative effectiveness recommendations (Class I and Ila; Level of Evidence A and B only), studies that support the use of comparator verbs should involve direct comparisons of the treatments or strategies being evaluated.In view of the advances in medical therapy across the spectrum of cardiovascular diseases, the Task Force has designated the term guideline-directed medical therapy (GDMT) to represent optimal medical therapy as defined by ACCF/AHA guideline-recommended therapies (primarily Class I). This new term, GDMT, will be used herein and throughout all future guidelines.Because the ACCF/AHA practice guidelines address patient populations (and healthcare providers) residing in North America, drugs that are not currently available in North America are discussed in the text without a specific COR. For studies performed in large numbers of subjects outside North America, each writing committee reviews the potential influence of different practice patterns and patient populations on the treatment effect and relevance to the ACCF/AHA target population to determine whether the findings should inform a specific recommendation.The ACCF/AHA practice guidelines are intended to assist healthcare providers in clinical decision making by describing a range of generally acceptable approaches to the diagnosis, management, and prevention of specific diseases or conditions. The guidelines attempt to define practices that meet the needs of most patients in most circumstances. The ultimate judgment about care of a particular patient must be made by the healthcare provider and patient in light of all the circumstances presented by that patient. As a result, situations may arise in which deviations from these guidelines might be appropriate. Clinical decision making should involve consideration of the quality and availability of expertise in the area where care is provided. When these guidelines are used as the basis for regulatory or payer decisions, the goal should be improvement in quality of care. The Task Force recognizes that situations arise in which additional data are needed to inform patient care more effectively; these areas will be identified within each respective guideline when appropriate.Prescribed courses of treatment in accordance with these recommendations are effective only if followed. Because lack of patient understanding and adherence may adversely affect outcomes, physicians and other healthcare providers should make every effort to engage the patient's active participation in prescribed medical regimens and lifestyles. In addition, patients should be informed of the risks, benefits, and alternatives to a particular treatment and should be involved in shared decision making whenever feasible, particularly for COR IIa and IIb, for which the benefit-to-risk ratio may be lower.The Task Force makes every effort to avoid actual, potential, or perceived conflicts of interest that may arise as a result of industry relationships or personal interests among the members of the writing committee. All writing committee members and peer reviewers of this guideline were required to disclose all such current healthcare-related relationships, as well as those existing 24 months (from 2005) before initiation of the writing effort. The writing committee chair may not have any relevant relationships with industry or other entities (RWI); however, RWI are permitted for the vice chair position. In December 2009, the ACCF and AHA implemented a new policy that requires a minimum of 50% of the writing committee have no relevant RWI; in addition, the disclosure term was changed to 12 months before writing committee initiation. The present guideline was developed during the transition in RWI policy and occurred over an extended period of time. In the interest of transparency, we provide full information on RWI existing over the entire period of guideline development, including delineation of relationships that expired more than 24 months before the guideline was finalized. This information is included in Appendix 1. These statements are reviewed by the Task Force and all members during each conference call and meeting of the writing committee and are updated as changes occur. All guideline recommendations require a confidential vote by the writing committee and must be approved by a consensus of the voting members. Members who recused themselves from voting are indicated in the list of writing committee members, and section recusals are noted in Appendix 1. Authors' and peer reviewers' RWI pertinent to this guideline are disclosed in Appendixes 1 and 2, respectively. Comprehensive disclosure information for the Task Force is also available online at http://www.cardiosource.org/ACC/About-ACC/Who-We-Are/Leadership/Guidelines-and-Documents-Task-Forces.aspx. The work of the writing committee is supported exclusively by the ACCF, AHA, American College of Physicians (ACP), American Association for Thoracic Surgery (AATS), Preventive Cardiovascular Nurses Association (PCNA), Society for Cardiovascular Angiography and Interventions (SCAI), and Society of Thoracic Surgeons (STS), without commercial support. Writing committee members volunteered their time for this activity.The recommendations in this guideline are considered current until they are superseded by a focused update or the full-text guideline is revised. The reader is encouraged to consult the full-text guideline2 for additional guidance and details about stable ischemic heart disease since the Executive Summary contains only the recommendations. Guidelines are official policy of both the ACCF and AHA.Jeffrey L. Anderson, MD, FACC, FAHA Chair, ACCF/AHA Task Force on Practice Guidelines1. Introduction1.1. Methodology and Evidence OverviewThe recommendations listed in this document are, whenever possible, evidence based. An extensive evidence review was conducted as the document was compiled through December 2008. Repeated literature searches were performed by the guideline development staff and writing committee members as new issues were considered. When available, current and credible meta-analyses were used instead of conducting a systematic review of all primary literature. New clinical trials published in peer-reviewed journals and articles through December 2011 were also reviewed and incorporated when relevant. Furthermore, because of the extended development time period for this guideline, peer review comments indicated that the sections focused on imaging technologies required additional updating, which occurred during 2011. Therefore, the evidence review for the imaging sections includes published literature through December 2011.Searches were limited to studies, reviews, and other evidence in human subjects and published in English. Key search words included, but were not limited to: accuracy, angina, asymptomatic patients, cardiac magnetic resonance (CMR), cardiac rehabilitation, chest pain, chronic angina, chronic coronary occlusions, chronic ischemic heart disease (IHD), chronic total occlusion, connective tissue disease, coronary artery bypass graft (CABG) versus medical therapy, coronary artery disease (CAD) and exercise, coronary calcium scanning, cardiac/coronary computed tomography angiography (CCTA), CMR angiography, CMR imaging, coronary stenosis, death, depression, detection of CAD in symptomatic patients, diabetes, diagnosis, dobutamine stress echocardiography, echocardiography, elderly, electrocardiogram (ECG) and chronic stable angina, emergency department, ethnic, exercise, exercise stress testing, follow-up testing, gender, glycemic control, hypertension, intravascular ultrasound, fractional flow reserve, invasive coronary angiography, kidney disease, low-density lipoprotein lowering, magnetic resonance imaging (MRI), medication adherence, minority groups, mortality, myocardial infarction (MI), noninvasive testing and mortality, nuclear myocardial perfusion, nutrition, obesity, outcomes, patient follow-up, patient education, prognosis, proximal left anterior descending (LAD) disease, physical activity, reoperation, risk stratification, smoking, stable ischemic heart disease (SIHD), stable angina and reoperation, stable angina and revascularization, stress echocardiography, radionuclide stress testing, stenting versus CABG, unprotected left main, weight reduction, and women.1.2. Organization of the Writing CommitteeThe writing committee was composed of physicians, cardiovascular interventionalists, surgeons, general internists, imagers, nurses, and pharmacists. The writing committee included representatives from the ACP, AATS, PCNA, SCAI, and STS.1.3. Document Review and ApprovalThis document was reviewed by 2 external reviewers nominated by both the ACCF and the AHA; 2 reviewers nominated by the ACP, AATS, PCNA, SCAI, and STS; and 19 content reviewers, including representatives from the ACCF Imaging Council, ACCF Interventional Scientific Council, and the AHA Council on Clinical Cardiology. All reviewer RWI information was collected and distributed to the writing committee and is published in this document (Appendix 2). Because extensive peer review comments resulted in substantial revision, the guideline was subjected to a second peer review by all official and organizational reviewers. Lastly, the imaging sections were also peer reviewed separately, after an update to that evidence base.This document was approved for publication by the governing bodies of the ACCF, AHA, ACP, AATS, PCNA, SCAI, and STS.1.4. Scope of the GuidelineThese guidelines are intended to apply to adult patients with stable known or suspected IHD, including new-onset chest pain (ie, low-risk unstable angina [UA]), or to adult patients with stable pain syndromes (Figure 1). Patients who have “ischemic equivalents,” such as dyspnea or arm pain with exertion, are included in the latter group. Many patients with IHD can become asymptomatic with appropriate therapy. Accordingly, the follow-up sections of this guideline pertain to patients who were previously symptomatic, including those who have undergone percutaneous coronary intervention (PCI) or CABG.Download figureDownload PowerPointFigure 1. Spectrum of IHD. Guidelines relevant to the spectrum of IHD are in parentheses. CABG indicates oronary artery bypass graft; CV, cardiovascular; ECG, electrocardiogram; IHD, ischemic heart disease; PCI, percutaneous coronary intervention; SCD, sudden cardiac death; SIHD, stable ischemic heart disease; STEMI, ST-elevation myocardial infarction; UA, unstable angina; UA/NSTEMI, unstable angina/non–ST-elevation myocardial infarction; and VA, ventricular arrhythmia.This guideline also addresses the initial diagnostic approach to patients who present with symptoms that suggest IHD, such as anginal-type chest pain, but who are not known to have IHD. In this circumstance, it is essential that the practitioner ascertain whether such symptoms represent the initial clinical recognition of chronic stable angina, reflecting gradual progression of obstructive CAD or an increase in supply/demand mismatch precipitated by a change in activity or concurrent illness (such as anemia or infection), or whether they represent an acute coronary syndrome (ACS), most likely due to an unstable plaque causing acute thrombosis. For patients with newly diagnosed stable angina, this guideline should be used. For patients with acute MI, the reader is referred to the ACCF/AHA guidelines for the management of patients with ST-elevation MI,3,4 and for patients with UA, the reader is referred to the “ACCF/AHA Guidelines for the Management of Patients With Unstable Angina/Non–ST-Elevation Myocardial Infarction.”5,5a There are, however, patients with UA who can be categorized as low risk and are addressed in this guideline (Table 2).Table 2. Short-Term Risk of Death or Nonfatal MI in Patients With UA/NSTEMIFeatureHigh RiskIntermediate RiskLow RiskAt least 1 of the following features must be present:No high-risk features are present, but patient must have 1 of the following:No high- or intermediate-risk features are present, but patient may have any of the following:HistoryAccelerating tempo of ischemic symptoms in preceding 48 hPrior MI, peripheral or cerebrovascular disease, or CABGPrior aspirin useN/ACharacteristics of painProlonged ongoing (>20 min) rest painProlonged (>20 min) rest angina, now resolved, with moderate or high likelihood of CADRest angina (>20 min) or relieved with rest or sublingual NTGNocturnal anginaNew-onset or progressive CCS Class III or IV angina in previous 2 wk without prolonged (>20 min) rest pain but with intermediate or high likelihood of CADIncreased angina frequency, severity, or durationAngina provoked at a lower thresholdNew-onset angina with onset 2 wk to 2 mo before presentationClinical findingsPulmonary edema, most likely due to ischemiaNew or worsening mitral regurgitation murmurS3 or new/worsening ralesHypote

HomeStrokeVol. 52, No. 72021 Guideline for the Prevention of Stroke in Patients With Stroke and Transient Ischemic Attack: A Guideline From the American Heart Association/American Stroke Association Free AccessReview ArticlePDF/EPUBAboutView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyRedditDiggEmail Jump toSupplementary MaterialsFree AccessReview ArticlePDF/EPUB2021 Guideline for the Prevention of Stroke in Patients With Stroke and Transient Ischemic Attack: A Guideline From the American Heart Association/American Stroke Association Dawn O. Kleindorfer, MD, FAHA, Chair Amytis Towfighi, MD, FAHA, Vice Chair Seemant Chaturvedi, MD, FAHA Kevin M. Cockroft, MD, MSc, FAHA Jose Gutierrez, MD, MPH Debbie Lombardi-Hill, BS, FAHA Hooman Kamel, MD Walter N. Kernan, MD Steven J. Kittner, MD, MPH, FAHA Enrique C. Leira, MD, MS, FAHA Olive Lennon, PhD James F. Meschia, MD, FAHA Thanh N. Nguyen, MD, FAHA Peter M. Pollak, MD Pasquale Santangeli, MD, PhD Anjail Z. Sharrief, MD, MPH, FAHA Sidney C. Smith Jr, MD, FAHA Tanya N. Turan, MD, MS, FAHA Linda S. WilliamsMD, FAHA Dawn O. KleindorferDawn O. Kleindorfer , Amytis TowfighiAmytis Towfighi , Seemant ChaturvediSeemant Chaturvedi , Kevin M. CockroftKevin M. Cockroft , Jose GutierrezJose Gutierrez , Debbie Lombardi-HillDebbie Lombardi-Hill , Hooman KamelHooman Kamel , Walter N. KernanWalter N. Kernan , Steven J. KittnerSteven J. Kittner , Enrique C. LeiraEnrique C. Leira , Olive LennonOlive Lennon , James F. MeschiaJames F. Meschia , Thanh N. NguyenThanh N. Nguyen , Peter M. PollakPeter M. Pollak , Pasquale SantangeliPasquale Santangeli , Anjail Z. SharriefAnjail Z. Sharrief , Sidney C. Smith JrSidney C. Smith Jr , Tanya N. TuranTanya N. Turan , and Linda S. WilliamsLinda S. Williams Originally published24 May 2021https://doi.org/10.1161/STR.0000000000000375Stroke. 2021;52:e364–e467is corrected byCorrection to: 2021 Guideline for the Prevention of Stroke in Patients With Stroke and Transient Ischemic Attack: A Guideline From the American Heart Association/American Stroke AssociationTOP 10 Take-Home Messages for the Secondary Stroke Prevention GuidelineSpecific recommendations for prevention strategies often depend on the ischemic stroke/transient ischemic attack subtype. Therefore, new in this guideline is a section describing recommendations for the diagnostic workup after ischemic stroke, to define ischemic stroke etiology (when possible), and to identify targets for treatment in order to reduce the risk of recurrent ischemic stroke. Recommendations are now grouped by etiologic subtype.Management of vascular risk factors remains extremely important in secondary stroke prevention, including (but not limited to) diabetes, smoking cessation, lipids, and especially hypertension. Intensive medical management, often performed by multidisciplinary teams, is usually best, with goals of therapy tailored to the individual patient.Lifestyle factors, including healthy diet and physical activity, are important for preventing a second stroke. Low-salt and Mediterranean diets are recommended for stroke risk reduction. Patients with stroke are especially at risk for sedentary and prolonged sitting behaviors, and they should be encouraged to perform physical activity in a supervised and safe manner.Changing patient behaviors such as diet, exercise, and medication compliance requires more than just simple advice or a brochure from their physician. Programs that use theoretical models of behavior change, proven techniques, and multidisciplinary support are needed.Antithrombotic therapy, including antiplatelet or anticoagulant agents, is recommended for nearly all patients without contraindications. With very few exceptions, the combination of antiplatelets and anticoagulation is typically not indicated for secondary stroke prevention. Dual antiplatelet therapy is not recommended long term, and short term, dual antiplatelet therapy is recommended only in very specific patients, including those with early arriving minor stroke and high-risk transient ischemic attack or severe symptomatic intracranial stenosis.Atrial fibrillation remains a common and high-risk condition for second ischemic stroke. Anticoagulation is usually recommended if the patient has no contraindications. Heart rhythm monitoring for occult atrial fibrillation is usually recommended if no other cause of stroke is discovered.Extracranial carotid artery disease is an important and treatable cause of stroke. Patients with severe stenosis ipsilateral to a nondisabling stroke or transient ischemic attack who are candidates for intervention should have the stenosis fixed, likely relatively early after their ischemic stroke. The choice between carotid endarterectomy and carotid artery stenting should be driven by specific patient comorbidities and features of their vascular anatomy.Patients with severe intracranial stenosis in the vascular territory of ischemic stroke or transient ischemic attack should not receive angioplasty and stenting as a first-line therapy for preventing recurrence. Aggressive medical management of risk factors and short-term dual antiplatelet therapy are preferred.There have been several studies evaluating secondary stroke prevention of patent foramen ovale closure since the previous guideline in 2014. It is now considered reasonable to percutaneously close patent foramen ovale in patients who meet each of the following criteria: age 18–60 years, nonlacunar stroke, no other identified cause, and high risk patent foramen ovale features.Patients with embolic stroke of uncertain source should not be treated empirically with anticoagulants or ticagrelor because it was found to be of no benefit.PreambleSince 1990, the American Heart Association (AHA)/American Stroke Association (ASA)* have translated scientific evidence into clinical practice guidelines with recommendations to improve cerebrovascular health. These guidelines, which are based on systematic methods to evaluate and classify evidence, provide a foundation for the delivery of quality cerebrovascular care. The AHA/ASA sponsor the development and publication of clinical practice guidelines without commercial support, and members volunteer their time to the writing and review efforts.Clinical practice guidelines for stroke provide recommendations applicable to patients with or at risk of developing cerebrovascular disease. The focus is on medical practice in the United States, but many aspects are relevant to patients throughout the world. Although it must be acknowledged that guidelines may be used to inform regulatory or payer decisions, the core intent is to improve quality of care and to align with patients’ interests. Guidelines are intended to define practices meeting the needs of patients in most, but not all, circumstances and should not replace clinical judgment; furthermore, the recommendations set forth should be considered in the context of individual patient values, preferences, and associated conditions.The AHA/ASA strive to ensure that guideline writing groups contain requisite expertise and are representative of the broader medical community by selecting experts from a broad array of backgrounds, representing different sexes, races, ethnicities, intellectual perspectives, geographic regions, and scopes of clinical practice and by inviting organizations and professional societies with related interests and expertise to participate as endorsers. The AHA/ASA have rigorous policies and methods for development of guidelines that limit bias and prevent improper influence. The complete policy on relationships with industry and other entities can be found at https://professional.heart.org/-/media/phd-files/guidelines-and-statements/policies-devolopment/aha-asa-disclosure-rwi-policy-5118.pdf?la=en.Beginning in 2017, numerous modifications to the guidelines have been implemented to make guidelines shorter and to enhance “user friendliness.” Guidelines are written and presented in a modular knowledge chunk format, in which each chunk includes a table of recommendations, a brief synopsis, recommendation-specific supportive text, and, when appropriate, flow diagrams or additional tables. Hyperlinked references are provided for each modular knowledge chunk to facilitate quick access and review. Other modifications to the guidelines include the addition of Knowledge Gaps and Future Research segments in some sections and a web guideline supplement (Data Supplement) for useful but noncritical tables and figures.Sepideh Amin-Hanjani, MD, FAHAImmediate Past Chair, AHA Stroke Council Scientific Statement Oversight CommitteeJoseph P. Broderick, MD, FAHAChair, AHA Stroke Council Scientific Statement Oversight Committee1. INTRODUCTIONEach year, ≈795 000 individuals in the United States experience a stroke, of which 87% (690 000) are ischemic and 185 000 are recurrent.1 Approximately 240 000 individuals experience a transient ischemic attack (TIA) each year.2 The risk of recurrent stroke or TIA is high but can be mitigated with appropriate secondary stroke prevention. In fact, cohort studies have shown a reduction in recurrent stroke and TIA rates in recent years as secondary stroke prevention strategies have improved.3,4 A meta-analysis of randomized controlled trials (RCTs) of secondary stroke prevention therapies published from 1960 to 2009 showed a reduction in annual stroke recurrence from 8.7% in the 1960s to 5.0% in the 2000s, with the reduction driven largely by improved blood pressure (BP) control and use of antiplatelet therapy.5 The changes may have been influenced by changes in diagnostic criteria and differing sensitivities of diagnostic tests over the years.The overwhelming majority of strokes can be prevented through BP control, a healthy diet, regular physical activity, and smoking cessation. In fact, 5 factors—BP, diet, physical inactivity, smoking, and abdominal obesity—accounted for 82% and 90% of the population-attributable risk (PAR) for ischemic and hemorrhagic stroke in the INTERSTROKE study (Global and regional effects of potentially modifiable risk factors associated with acute stroke in 32 countries).5a Similarly, the Global Burden of Disease Study showed that 90.5% (95% uncertainty interval, 88.5–92.2) of the global burden of stroke was attributable to modifiable risk factors.6 A modeling study showed that targeting multiple risk factors has additive benefits for secondary prevention; specifically, aspirin, statin, and antihypertensive medications, combined with diet modification and exercise, can result in an 80% cumulative risk reduction in recurrent vascular events.7 Although the benefits of a healthy lifestyle and vascular risk factor control are well documented,8,9 risk factors remain poorly controlled among stroke survivors.10–141.1. Methodology and Evidence ReviewThis guideline provides a comprehensive yet succinct compilation of practical guidance for the secondary prevention of ischemic stroke or TIA (ie, prevention of ischemic stroke or TIA in individuals with a history of stroke or TIA). We aim to promote optimal dissemination of information by using concise language and formatting. The recommendations listed in this guideline are, whenever possible, evidence based and supported by an extensive evidence review. A search for literature derived from research involving human subjects, published in English, and indexed in MEDLINE, PubMed, Cochrane Library, and other selected databases relevant to this guideline was conducted between July 2019 and February 2020. Additional trials published between February and June 2020 that affected the guideline recommendations were also included. For specific search terms used, please see the Data Supplement, which also contains the final evidence tables that summarize the evidence used by the guideline writing group to formulate recommendations. References selected and published in the present document are representative and not all inclusive.An independent Evidence Review Committee was commissioned to perform a formal systematic review of a critical clinical question (Table 1) related to secondary stroke prevention, the results of which were considered by the writing group for incorporation into the present guideline. Concurrently with this process, writing group members evaluated study data relevant to the rest of the guideline. The results of these evidence reviews were evaluated by the writing group for incorporation into the present guideline.Table 1. Evidence Review Committee QuestionQuestion No.QuestionSection No.1In patients with an ischemic stroke or TIA, what are the benefits and risks of DAPT compared to single antiplatelet therapy within 5 y for prevention of recurrent stroke?5.19DAPT indicates dual antiplatelet therapy; and TIA, transient ischemic attack.Each topic area was assigned a primary author and a primary, and sometimes secondary, reviewer. Author assignments were based on the areas of expertise of the members of the writing group members and their lack of any relationships with industry related to the section material. All recommendations were fully reviewed and discussed among the full committee to allow diverse perspectives and considerations for this guideline. Recommendations were then voted on to reach consensus. The systematic review has been published in conjunction with this guideline and includes its respective data supplements.151.2. Organization of the Writing GroupThe writing group consisted of neurologists, neurological surgeons, cardiologists, internists, and a lay/patient representative. The writing group included representatives from the AHA/ASA and the American Academy of Neurology. Appendix 1 lists writing group members’ relevant relationships with industry and other entities. For the purposes of full transparency, the writing group members’ comprehensive disclosure information is available online.1.3. Document Review and ApprovalThis document was reviewed by the AHA’s Stroke Council Scientific Statement Oversight Committee; the AHA’s Science Advisory and Coordinating Committee; the AHA’s Executive Committee; reviewers from the American Academy of Neurology, from the Society of Vascular and Interventional Neurology, and from the American Association of Neurological Surgeons and Congress of Neurological Surgeons; as well as by 55 individual content reviewers. The individual reviewers’ relationships with industry information is available in Appendix 2.This document was approved for publication by the governing bodies of the ASA and the AHA. It was reviewed for evidence-based integrity and endorsed by the American Association of Neurological Surgeons and Congress of Neurological Surgeons, was endorsed by the Society of Vascular and Interventional Neurology, and the American Academy of Neurology affirmed the value of the guideline.1.4. Scope of the GuidelineThe aim of the present guideline is to provide clinicians with evidence-based recommendations for the prevention of future stroke among survivors of ischemic stroke or TIA. It should be noted that this guideline does not cover the following topics, which have been addressed elsewhere:Acute management decisions (covered in the “2019 Update to the 2018 Guidelines for the Early Management of Patients With Acute Ischemic Stroke”16),Intracerebral hemorrhage (ICH; covered in the “Guidelines for the Management of Spontaneous Intracerebral Hemorrhage”17),Primary prevention (covered in the “Guidelines for the Primary Prevention of Stroke”18 and “2019 American College of Cardiology/American Heart Association Guideline on the Primary Prevention of Cardiovascular Disease”19),Special considerations for stroke prevention in women (covered in the “Guidelines for the Prevention of Stroke in Women”20), andCerebral venous sinus thrombosis (covered in “Diagnosis and Management of Cerebral Venous Thrombosis”22).In general, with very few exceptions, the literature supports the concept that patients with TIA and those with ischemic stroke should be treated the same in terms of secondary prevention.This guideline is divided into 4 sections:Diagnostic Evaluation for Secondary Stroke PreventionVascular Risk Factor ManagementManagement by EtiologySystems of Care for Secondary Ischemic Stroke Prevention.The structure and scope of this guideline differ from those of the 2014 Guidelines for the prevention of stroke in patients with stroke and TIA9 in several ways. First, the current guideline reflects numerous innovations and modifications that were incorporated into the AHA clinical practice guideline format. Introduced in 2017, modifications to AHA guidelines included making the text shorter and more user friendly; focusing guidelines on recommendations and patient management flow diagrams and less on extensive text and background information; formatting guidelines so that they can be easily updated with guideline focused updates; and including “chunks” of information after each recommendation.23 Second, the Diagnostic Evaluation and Systems of Care for Secondary Prevention sections are new. The Diagnostic Evaluation for Secondary Stroke Prevention section focuses on the evidence base for laboratory and imaging studies for guiding secondary stroke prevention decisions. Often these tests are completed in the inpatient setting. The Systems of Care for Secondary Prevention section contains 3 subsections: (1) Health Systems–Based Interventions for Secondary Stroke Prevention, (2) Interventions Aimed at Changing Patient Behavior, and (3) Health Equity. The Health Equity subsection is a refocus of the 2014 guideline’s section guiding management of high-risk populations. Third, this guideline does not include a separate section on metabolic syndrome because there are no unique recommendations for metabolic syndrome aside from managing each of the individual components of the syndrome. Fourth, the section on alcohol use was expanded to include the use of other substances. Finally, several additional conditions were included in the Management by Etiology section: congenital heart disease, cardiac tumors, moyamoya disease, migraine, malignancy, vasculitis, other genetic disorders, carotid web, fibromuscular dysplasia, dolichoectasia, and embolic stroke of undetermined source (ESUS).In developing the 2021 secondary stroke prevention guideline, the writing group reviewed prior published AHA/ASA guidelines and scientific statements. Table 2 contains a list of these other guidelines and statements deemed pertinent to this writing effort and is intended for use as a reader resource, thus reducing the need to repeat existing guideline recommendations.Table 2. Associated AHA/ASA Guidelines and StatementsTitleOrganizationPublication yearAHA/ASA guidelines Guidelines for Carotid Endarterectomy24AHA/ASA1998 Guideline on the Management of Patients With Extracranial Carotid and Vertebral Artery Disease25ASA/ACCF/AHA/AANN/AANS/ACR/ASNR/CNS/SAIP/SCAI/SIR/SNIS/SVM/SVS2011 Guideline on Lifestyle Management to Reduce Cardiovascular Risk26AHA/ACC2013 Guideline for the Management of Overweight and Obesity in Adults27AHA/ACC/TOS2013 Guideline for the Management of Patients With Atrial Fibrillation28AHA/ACC/HRS2014 Guidelines for the Management of Spontaneous Intracerebral Hemorrhage17AHA/ASA2014 Guidelines for the Prevention of Stroke in Patients With Stroke and Transient Ischemic Attack9AHA/ASA2014 Guidelines for the Prevention of Stroke in Women20AHA/ASA2014 Guidelines for the Primary Prevention of Stroke18AHA/ASA2014 Guideline for the Prevention, Detection, Evaluation and Management of High Blood Pressure in Adults29ACC/AHA/AAPA/ABC/ACPM/AGS/APhA/ASH/ASPC/NMA/PCNA2017 Guideline for the Management of Adults With Congenital Heart Disease30AHA/ACC2018 Guideline on the Management of Blood Cholesterol31AHA/ACC/AACVPR/AAPA/ABC/ACPM/ADA/AGS/APhA/ASPC/NLA/PCNA2018 Guidelines for the Early Management of Patients With Acute Ischemic Stroke: 2019 Update to the 2018 Guidelines for the Early Management of Acute Ischemic Stroke16AHA/ASA2019 Guideline on the Primary Prevention of Cardiovascular Disease19ACC/AHA2019 Focused Update of the 2014 AHA/ACC/HRS Guideline for the Management of Patients with Atrial Fibrillation32AHA/ACC/HRS2019 Guideline for the Management of Patients With Valvular Heart Disease33ACC/AHA2020AHA/ASA statements Diagnosis and Management of Cerebral Venous Thrombosis22AHA/ASA2011 Cervical Arterial Dissections and Association With Cervical Manipulative Therapy21AHA/ASA2014 Physical Activity and Exercise Recommendations for Stroke Survivors34AHA/ASA2014 Spontaneous Coronary Artery Dissection: Current State of the Science34aAHA/ASA2018AHA/ASA presidential advisory Defining Optimal Brain Health in Adults35AHA/ASA2017AACVPR indicates American Association of Cardiovascular and Pulmonary Rehabilitation; AANN, American Association of Neuroscience Nurses; AANS, American Association of Neurological Surgeons; AAPA, American Academy of Physician Assistants; ABC, Association of Black Cardiologists; ACC, American College of Cardiology; ACCF, American College of Cardiology Foundation; ACPM, American College of Preventive Medicine; ACR, American College of Radiology; ADA, American Diabetes Association; AGS, American Geriatrics Society; AHA, American Heart Association; ASA, American Stroke Association; APhA, American Pharmacists Association; ASH, American Society of Hypertension; ASNR, American Society of Neuroradiology; ASPC, American Society for Preventive Cardiology; CNS, Congress of Neurological Surgeons; HRS, Heart Rhythm Society; NLA, National Lipid Association; NMA, National Medical Association; PCNA, Preventive Cardiovascular Nurses Association; SAIP, Society of Atherosclerosis Imaging and Prevention; SCAI, Society for Cardiovascular Angiography and Interventions; SIR, Society of Interventional Radiology; SNIS, Society of NeuroInterventional Surgery; SVM, Society for Vascular Medicine; SVS, Society for Vascular Surgery; and TOS, The Obesity Society.1.5. Class of Recommendation and Level of EvidenceRecommendations are designated both a Class of Recommendation (COR) and a Level of Evidence (LOE). The COR indicates the strength of recommendation, encompassing the estimated magnitude and certainty of benefit in proportion to risk. The LOE rates the quality of scientific evidence supporting the intervention on the basis of the type, quantity, and consistency of data from clinical trials and other sources (Table 3).Table 3. Applying Class of Recommendation and Level of Evidence to Clinical Strategies, Interventions, Treatments, or Diagnostic Testing in Patient Care (Updated May 2019)*Table 3. Applying Class of Recommendation and Level of Evidence to Clinical Strategies, Interventions, Treatments, or Diagnostic Testing in Patient Care (Updated May 2019)*Numerous studies have evaluated strategies for stroke prevention in individuals without a history of stroke/TIA (ie, primary prevention studies) or included individuals with a history of stroke/TIA mixed into the pools of patients studied in smaller numbers. After carefully reviewing the literature and discussing with AHA methodologists, the writing group decided that many of these prevention strategies were important to include in any guideline on the prevention of recurrent stroke. There is often no reason to think that the mechanism of stroke prevention and benefits would be different in primary versus secondary prevention, although not studied within a purely secondary stroke prevention trial. Therefore, this writing group occasionally includes recommendations with evidence based in the primary prevention of atherosclerotic cardiovascular disease (ASCVD), atherosclerosis, or combined end points of cardiac disease and stroke in this guideline.To acknowledge that some studies were not performed in a purely ischemic stroke population, the LOE was downgraded. In this way, the writing group agreed that this would provide the best and most complete recommendations to the clinician about important strategies for secondary stroke prevention. Principles guiding inclusion and extrapolation of the results of these studies were as follows:The quality of the trial/trials was acceptable.(Ideally, stroke or TIA occurrence or recurrence was a prespecified end point, with clear protocols for assessing stroke end points.)From a physiological perspective, the primary prevention strategy used in the study will likely be effective for secondary prevention.Patients with ischemic stroke were included in the population studied when possible.1.6. AbbreviationsAbbreviationMeaning/PhraseACCAmerican College of CardiologyACSacute coronary syndromeACTIVE WAtrial Fibrillation Clopidogrel Trial With Irbesartan for Prevention of Vascular EventsAFatrial fibrillationAHAAmerican Heart AssociationAHIapnea-hypopnea indexARCHAortic Arch Related Cerebral Hazard TrialARISTOTLEApixaban for Reduction in Stroke and Other Thromboembolic Events in Atrial FibrillationASAAmerican Stroke AssociationASAPAddressing Sleep Apnea Post Stroke/TIAASTRO-APSApixaban for Secondary Prevention of Thromboembolism Among Patients With Antiphospholipid SyndromeASCVDatherosclerotic cardiovascular diseaseBMIbody mass indexBPblood pressureBUST-StrokeBreaking Up Sitting Time After StrokeCADISSCervical Artery Dissection in Stroke StudyCARDIACoronary Artery Risk Development in Young AdultsCAPContinued Access RegistryCAPRIEClopidogrel Versus Aspirin in Patients at Risk of Ischaemic EventsCAScarotid artery stentingCATHARSISCilostazol-Aspirin Therapy Against Recurrent Stroke With Intracranial Artery StenosisCEAcarotid endarterectomyCHANCEClopidogrel in High-Risk Patients With Acute Non-Disabling Cerebrovascular EventsCICASChinese Intracranial AtherosclerosisCLAIRClopidogrel Plus Aspirin for Infarction ReductionCLOSEPatent Foramen Ovale Closure or Anticoagulants Versus Antiplatelet Therapy to Prevent Stroke RecurrenceCNScentral nervous systemCOMMANDER HFA Study to Assess the Effectiveness and Safety of Rivaroxaban in Reducing the Risk of Death, Myocardial Infarction or Stroke in Participants With Heart Failure and Coronary Artery Disease Following an Episode of Decompensated Heart FailureCOMPASSCardiovascular Outcomes for People Using Anticoagulation StrategiesCORClass of RecommendationCOSSCarotid Occlusion Surgery StudyCPAPcontinuous positive airway pressureCRESTCarotid Revascularization Endarterectomy versus Stenting TrialCSPSCilostazol for Prevention of Secondary StrokeCTcomputed tomographyCTAcomputed tomographic angiographyCVDcardiovascular diseaseDAPTdual antiplatelet therapyDASHDietary Approaches to Stop HypertensionDCCTDiabetes Control and Complication TrialDESERVEDischarge Educational Strategies for Reduction of Vascular EventsDHAdocosahexaenoic acidDiRECTDiabetes Remission Clinical TrialDOACdirect-acting oral anticoagulantECSTEuropean Carotid Surgery TrialEFejection fractionENGAGE AF-TIMI 48Global Study to Assess the Safety and Effectiveness of Edoxaban (DU-176b) vs Standard Practice of Dosing With Warfarin in Patients With Atrial FibrillationEPAeicosapentaenoic acidEPIC-CVDEuropean Prospective Investigation into Cancer and Nutrition-CVD case-cohort studyESH-CHL-SHOTEuropean Society of Hypertension and Chinese Hypertension League Stroke in Hypertension Optimal Treatment TrialESPRITEuropean/Australasian Stroke Prevention in Reversible Ischaemia TrialESPS2Second European Stroke Prevention StudyESUSembolic stroke of undetermined sourceExStrokePhysical Exercise After Acute Ischaemic StrokeFASTESTEfficacy and Safety of a TIA/Stroke Electronic Support ToolFMDfibromuscular dysplasiaFOURIERFurther Cardiovascular Outcomes Research With PCSK9 Inhibition in Subjects With Elevated RiskGELIAGerman Experience With Low Intensity AnticoagulationGLP-1glucagon-like protein 1HbA1chemoglobin A1cHRhazard ratioICAinternal carotid arteryICARUSSIntegrated Care for the Reduction of Secondary StrokeICASintracranial atherosclerotic stenosisICHintracerebral hemorrhageIEinfective endocarditisIMPROVE-ITImproved Reduction of Outcomes: Vytorin Efficacy International TrialINRinternational normalized ratioINSPiRE-TMSIntensified Secondary Prevention Intending a Reduction of Recurrent Events in TIA and Minor Stroke PatientsIPEicosapent ethylIRISInsulin Resistance Intervention After StrokeJAMJapan Adult MoyamoyaJELISJapan EPA Lipid Intervention StudyLDLlow-density lipoproteinLDL-Clow-density lipoprotein cholesterolLOELevel of EvidenceLVleft ventricularLVADleft ventricular assist devicesMACEmajor adverse cardiovascular eventMDmean differenceMImyocardial infarctionMISTMotivational Interviewing in StrokeMRAmagnetic resonance angiographyMRImagnetic resonance imagingNAILED StrokeNurse Based Age Independent Intervention to Limit Evolution of Disease After StrokeNASCETNorth American Symptomatic Carotid Endarterectomy TrialNAVIGATE ESUSRivaroxaban Versus Aspirin in Secondary Prevention of Stroke and Prevention of Systemic Embolism in Patients With Recent Embolic Stroke of Undetermined SourceNIHSSNational Institutes of Health Stroke ScaleODYSSEY OUTCOMESEvaluation of Cardiovascular Outcomes After an Acute Coronary Syndrome During Treatment With AlirocumabOMEMIOmega-3 Fatty Acids in Elderly Patients With Acute Myocardial InfarctionORodds ratioOSAobstructive sleep apneaOXVASCOxford Vascular StudyPARpopulation-attributable riskPAST-BPPrevention After Stroke–Blood PressurePCSK9proprotein convertase subtilisin/kexin type 9PFOpatent foramen ovalePODCASTPrevention of Decline in Cognition after Stroke TrialPOINTPlatelet-Oriented Inhibition in New TIA and Minor Ischemic StrokePRAISEPrevent Recurrence of All Inner-City Strokes Through EducationPREDIMEDPrevención con Dieta MediterráneaPREVAILProspective Randomised Evaluation of the Watchman LAA Closure Device in Patients With Atrial Fibrill

Jonathan L. Halperin, MD, FACC, FAHA, Chair Glenn N. Levine, MD, FACC, FAHA, Chair-Elect Sana M. Al-Khatib, MD, MHS, FACC, FAHA Kim K. Birtcher, PharmD, MS, AACC Biykem Bozkurt, MD, PhD, FACC, FAHA Ralph G. Brindis, MD, MPH, MACC, FAHA Joaquin E. Cigarroa, MD, FACC Lesley H. Curtis, PhD,

HomeCirculationVol. 117, No. 22007 Focused Update of the ACC/AHA 2004 Guidelines for the Management of Patients With ST-Elevation Myocardial Infarction Free AccessReview ArticlePDF/EPUBAboutView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toFree AccessReview ArticlePDF/EPUB2007 Focused Update of the ACC/AHA 2004 Guidelines for the Management of Patients With ST-Elevation Myocardial InfarctionA Report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines: Developed in Collaboration With the Canadian Cardiovascular Society Endorsed by the American Academy of Family Physicians: 2007 Writing Group to Review New Evidence and Update the ACC/AHA 2004 Guidelines for the Management of Patients With ST-Elevation Myocardial Infarction, Writing on Behalf of the 2004 Writing Committee Elliott M. Antman, MD, FACC, FAHA, Co-Chair, Mary Hand, MSPH, RN, FAHA, Co-Chair, Paul W. Armstrong, MD, FACC, FAHA, Eric R. Bates, MD, FACC, FAHA, Lee A. Green, MD, MPH, Lakshmi K. Halasyamani, MD, Judith S. Hochman, MD, FACC, FAHA, Harlan M. Krumholz, MD, FACC, FAHA, Gervasio A. Lamas, MD, FACC, Charles J. Mullany, MB, MS, FACC, David L. Pearle, MD, FACC, FAHA, Michael A. Sloan, MD, FACC, Sidney C. SmithJr, MD, FACC, FAHA, 2004 Writing Committee Members Elliott M. Antman, MD, FACC, FAHA, Chair, Daniel T. Anbe, MD, FACC, FAHA, Paul W. Armstrong, MD, FACC, FAHA, Eric R. Bates, MD, FACC, FAHA, Lee A. Green, MD, MPH, Mary Hand, MSPH, RN, FAHA, Judith S. Hochman, MD, FACC, FAHA, Harlan M. Krumholz, MD, FACC, FAHA, Frederick G. Kushner, MD, FACC, FAHA, Gervasio A. Lamas, MD, FACC, Charles J. Mullany, MB, MS, FACC, Joseph P. Ornato, MD, FACC, FAHA, David L. Pearle, MD, FACC, FAHA, Michael A. Sloan, MD, FACC, Sidney C. SmithJr, MD, FACC, FAHA, Sidney C. SmithJr, Task Force Members:, MD, FACC, FAHA, Chair, Alice K. Jacobs, MD, FACC, FAHA, Vice-Chair, Cynthia D. Adams, MSN, PhD, FAHA, Jeffrey L. Anderson, MD, FACC, FAHA, Christopher E. Buller, MD, FACC, Mark A. Creager, MD, FACC, FAHA, Steven M. Ettinger, MD, FACC, Jonathan L. Halperin, MD, FACC, FAHA, Sharon A. Hunt, MD, FACC, FAHA, Harlan M. Krumholz, MD, FACC, FAHA, Frederick G. Kushner, MD, FACC, FAHA, Bruce W. Lytle, MD, FACC, FAHA, Rick Nishimura, MD, FACC, FAHA, Richard L. Page, MD, FACC, FAHA, Barbara Riegel, DNSc, RN, FAHA, Lynn G. Tarkington, RN and Clyde W. Yancy, MD, FACC Elliott M. AntmanElliott M. Antman Search for more papers by this author , Mary HandMary Hand Search for more papers by this author , Paul W. ArmstrongPaul W. Armstrong Search for more papers by this author , Eric R. BatesEric R. Bates Search for more papers by this author , Lee A. GreenLee A. Green Search for more papers by this author , Lakshmi K. HalasyamaniLakshmi K. Halasyamani Search for more papers by this author , Judith S. HochmanJudith S. Hochman Search for more papers by this author , Harlan M. KrumholzHarlan M. Krumholz Search for more papers by this author , Gervasio A. LamasGervasio A. Lamas Search for more papers by this author , Charles J. MullanyCharles J. Mullany Search for more papers by this author , David L. PearleDavid L. Pearle Search for more papers by this author , Michael A. SloanMichael A. Sloan Search for more papers by this author , Sidney C. SmithJrSidney C. SmithJr Search for more papers by this author , 2004 Writing Committee Members Search for more papers by this author , Elliott M. AntmanElliott M. Antman Search for more papers by this author , Daniel T. AnbeDaniel T. Anbe Search for more papers by this author , Paul W. ArmstrongPaul W. Armstrong Search for more papers by this author , Eric R. BatesEric R. Bates Search for more papers by this author , Lee A. GreenLee A. Green Search for more papers by this author , Mary HandMary Hand Search for more papers by this author , Judith S. HochmanJudith S. Hochman Search for more papers by this author , Harlan M. KrumholzHarlan M. Krumholz Search for more papers by this author , Frederick G. KushnerFrederick G. Kushner Search for more papers by this author , Gervasio A. LamasGervasio A. Lamas Search for more papers by this author , Charles J. MullanyCharles J. Mullany Search for more papers by this author , Joseph P. OrnatoJoseph P. Ornato Search for more papers by this author , David L. PearleDavid L. Pearle Search for more papers by this author , Michael A. SloanMichael A. Sloan Search for more papers by this author , Sidney C. SmithJrSidney C. SmithJr Search for more papers by this author , Sidney C. SmithJrSidney C. SmithJr Search for more papers by this author , Alice K. JacobsAlice K. Jacobs Search for more papers by this author , Cynthia D. AdamsCynthia D. Adams Search for more papers by this author , Jeffrey L. AndersonJeffrey L. Anderson Search for more papers by this author , Christopher E. BullerChristopher E. Buller Search for more papers by this author , Mark A. CreagerMark A. Creager Search for more papers by this author , Steven M. EttingerSteven M. Ettinger Search for more papers by this author , Jonathan L. HalperinJonathan L. Halperin Search for more papers by this author , Sharon A. HuntSharon A. Hunt Search for more papers by this author , Harlan M. KrumholzHarlan M. Krumholz Search for more papers by this author , Frederick G. KushnerFrederick G. Kushner Search for more papers by this author , Bruce W. LytleBruce W. Lytle Search for more papers by this author , Rick NishimuraRick Nishimura Search for more papers by this author , Richard L. PageRichard L. Page Search for more papers by this author , Barbara RiegelBarbara Riegel Search for more papers by this author , Lynn G. TarkingtonLynn G. Tarkington Search for more papers by this author and Clyde W. YancyClyde W. Yancy Search for more papers by this author Originally published10 Dec 2007https://doi.org/10.1161/CIRCULATIONAHA.107.188209Circulation. 2008;117:296–329is corrected byCorrectionOther version(s) of this articleYou are viewing the most recent version of this article. Previous versions: December 10, 2007: Previous Version 1 Preamble…2971. Introduction…299 1.1. Evidence Review…299 1.2. Organization of Committee and Relationships With Industry…299 1.3. Review and Approval…3002. Analgesia…3003. Beta Blockers…300 3.1. COMMIT/CCS-2 (Metoprolol)…300 3.2. Conclusion…3014. Reperfusion…302 4.1. Logistics of Care…3025. Facilitated PCI…3046. Immediate or Emergency Invasive Strategy and Rescue PCI…3057. PCI After Fibrinolysis or for Patients Not Undergoing Primary Reperfusion…307 7.1. The Late Open Artery Hypothesis: Clinical Outcomes…307 7.2. The Late Open Artery Hypothesis: Angiographic Outcomes…308 7.3. Conclusion…3088. Ancillary Therapy…308 8.1. Conclusion…3129. Thienopyridines…313 9.1. Conclusion…31410. Anticoagulants…31511. Invasive Evaluation…31512. Secondary Prevention…31513. Antiplatelet Therapy…320References…321Appendix 1…324Appendix 2…326PreambleA primary challenge in the development of clinical practice guidelines is keeping pace with the stream of new data upon which recommendations are based. In an effort to respond more quickly to new evidence, the American College of Cardiology/American Heart Association (ACC/AHA) Task Force on Practice Guidelines has created a new “focused update” process to revise the existing guideline recommendations that are affected by evolving data or opinion. Before the initiation of this focused approach, periodic updates and revisions of existing guidelines required up to 3 years to complete. Now, however, new evidence will be reviewed in an ongoing fashion to more efficiently respond to important science and treatment trends that could have a major impact on patient outcomes and quality of care. Evidence will be reviewed at least twice a year, and updates will be initiated on an as needed basis as quickly as possible, while maintaining the rigorous methodology that the ACC and AHA have developed during their more than 20 years of partnership.These updated guideline recommendations reflect a consensus of expert opinion following a thorough review that consisted primarily of late-breaking clinical trials identified through a broad-based vetting process as important to the relevant patient population and of other new data deemed to have an impact on patient care (see Section 1.1 for details on this focused update). It is important to note that this focused update is not intended to represent an update based on a full literature review from the date of the previous guideline publication. Specific criteria/considerations for inclusion of new data include: •Publication in a peer-reviewed journal•Large, randomized, placebo-controlled trial(s)•Nonrandomized data deemed important on the basis of results that impact current safety and efficacy assumptions•Strengths/weakness of research methodology and findings•Likelihood of additional studies influencing current findings•Impact on current performance measure(s) and/or likelihood of the need to develop new performance measure(s)•Requests and requirements for review and update from the practice community, key stakeholders, and other sources free of relationships with industry or other potential bias•Number of previous trials showing consistent results•Need for consistency with other guidelines or guideline revisionsIn analyzing the data and developing updated recommendations and supporting text, the focused update writing group used evidence-based methodologies developed by the ACC/AHA Task Force on Practice Guidelines, which are described elsewhere.1,2The schema for class of recommendation and level of evidence is summarized in Table 1, which also illustrates how the grading system provides estimates of the size of the treatment effect and the certainty of the treatment effect. Note that a recommendation with Level of Evidence B or C does not imply that the recommendation is weak. Many important clinical questions addressed in guidelines do not lend themselves to clinical trials. Although randomized trials may not be available, there may be a very clear clinical consensus that a particular test or therapy is useful and effective. Both the class of recommendation and level of evidence listed in the focused updates are based on consideration of the evidence reviewed in previous iterations of the guidelines as well as the focused update. Of note, the implications of older studies that have informed recommendations but have not been repeated in contemporary settings are carefully considered. Download figureDownload PowerPointTable 1. Applying Classification of Recommendations and Level of Evidence†*Data available from clinical trials or registries about the usefulness/efficacy in different subpopulations, such as gender, age, history of diabetes, history of prior myocardial infarction, history of heart failure, and prior aspirin use. A recommendation with Level of Evidence B or C does not imply that the recommendation is weak. Many important clinical questions addressed in the guidelines do not lend themselves to clinical trials. Even though randomized trials are not available, there may be a very clear clinical consensus that a particular test or therapy is useful or effective.†In 2003, the ACC/AHA Task Force on Practice Guidelines developed a list of suggested phrases to use when writing recommendations. All guideline recommendations have been written in full sentences that express a complete thought, such that a recommendation, even if separated and presented apart from the rest of the document (including headings above sets of recommendations), would still convey the full intent of the recommendation. It is hoped that this will increase readers’ comprehension of the guidelines and will allow queries at the individual recommendation level.The ACC/AHA practice guidelines address patient populations (and health care providers) residing in North America. As such, drugs that are not currently available in North America are discussed in the text without a specific class of recommendation. For studies performed in large numbers of subjects outside of North America, each writing committee reviews the potential impact of different practice patterns and patient populations on the treatment effect and on the relevance to the ACC/AHA target population to determine whether the findings should inform a specific recommendation.The ACC/AHA practice guidelines are intended to assist health care providers in clinical decision making by describing a range of generally acceptable approaches for the diagnosis, management, and prevention of specific diseases or conditions. The guidelines attempt to define practices that meet the needs of most patients in most circumstances. The ultimate judgment regarding care of a particular patient must be made by the health care provider and patient in light of all the circumstances presented by that patient. Thus, there are circumstances in which deviations from these guidelines may be appropriate. Clinical decision making should consider the quality and availability of expertise in the area where care is provided. These guidelines may be used as the basis for regulatory or payer decisions, but the ultimate goal is quality of care and serving the patient’s best interests.Prescribed courses of treatment in accordance with these recommendations are only effective if they are followed by the patient. Because lack of patient adherence may adversely affect treatment outcomes, health care providers should make every effort to engage the patient in active participation with prescribed treatment.The ACC/AHA Task Force on Practice Guidelines makes every effort to avoid any actual, potential, or perceived conflict of interest arising from industry relationships or personal interests of a writing committee member. All writing committee members and peer reviewers were required to provide disclosure statements of all such relationships pertaining to the trials and other evidence under consideration (see Appendixes 1 and 2). Final recommendations were balloted to all writing committee members. Writing committee members with significant (greater than $10 000) relevant relationships with industry (RWI) were required to recuse themselves from voting on that recommendation. Writing committee members who did not participate are not listed as authors of this focused update.With the exception of the recommendations presented here, the full guidelines remain current. Only the recommendations from the affected section(s) of the full guidelines are included in this focused update. For easy reference, all recommendations from any section of guidelines impacted by a change are presented with a notation as to whether they remain current, are new, or have been modified. When evidence impacts recommendations in more than 1 set of guidelines, those guidelines are updated concurrently.The recommendations in this focused update will be considered current until they are superseded by another focused update or the full-text guidelines are revised. This focused update is published in the January 15, 2008, issue of the Journal of the American College of Cardiology and the January 15, 2008, issue of Circulation as an update to the full-text guidelines and is also posted on the ACC (www.acc.org) and AHA (www.americanheart.org) Web sites. Copies of the focused update are available from both organizations.Sidney C. Smith, Jr., MD, FACC, FAHAChair, ACC/AHA Task Force on Practice GuidelinesAlice K. Jacobs, MD, FACC, FAHAVice-Chair, ACC/AHA Task Force on Practice Guidelines1. Introduction1.1. Evidence ReviewLate-breaking clinical trials presented at the 2005 and 2006 annual scientific meetings of the ACC, AHA, and European Society of Cardiology, as well as selected other data, were reviewed by the standing guideline writing committee along with the parent Task Force and other experts to identify those trials and other key data that might impact guidelines recommendations. On the basis of the criteria/considerations noted above, recent trial data and other clinical information were considered important enough to prompt a focused update of the 2004 ACC/AHA Guidelines for the Management of Patients With ST-Elevation Myocardial Infarction [see Chen ZM et al.3; Chen ZM et al.4; ASSENT-4 PCI5; Antman EM et al.6; Yusuf S et al.7; Bhatt DL et al.8; Sabatine MS et al.9; Bennett JS et al.10; Smith SC Jr et al.11; OAT12,13 and TOSCA14].When considering the new data for this focused update, the writing group faced the task of weighing evidence from studies enrolling large numbers of subjects outside North America. Although noting that practice patterns and the rigor applied to data collection, as well as the genetic makeup of subjects, might influence the observed magnitude of a treatment effect, the writing group believed the data were relevant to formulation of recommendations for management of ST-elevation myocardial infarction (STEMI) in North America. The reasons for this decision include that 1) a broad array of management strategies was represented, including substantial proportions of subjects who received some form of reperfusion therapy, 2) concomitant treatments with proven efficacy (e.g., aspirin, beta blockers, inhibitors of the renin-angiotensin-aldosterone system, and statins) were used in the majority of patients, and 3) it was considered an impractical expectation that the tens of thousands of patients with STEMI needed to meet the estimated sample size for contemporary clinical trials be enrolled exclusively at North American sites.To provide clinicians with a comprehensive set of data, whenever possible the exact event rates in various treatment arms of clinical trials are presented to permit calculation of the absolute risk difference (ARD) and number needed to treat (NNT) or harm (NNH); the relative treatment effects are described either as odds ratio (OR), relative risk (RR), or hazard ratio (HR), depending on the format in the original publication.Consult the full-text version or executive summary of the 2004 ACC/AHA Guidelines for the Management of Patients With ST-Elevation Myocardial Infarction15 for policy on clinical areas not covered by the focused update. Individual recommendations updated in this focused update will be incorporated into future revisions and/or updates of the full-text guidelines.1.2. Organization of Committee and Relationships With IndustryFor this focused update, all members of the 2004 STEMI writing committee were invited to participate; those who agreed (referred to as the 2007 focused update writing group) were required to disclose all RWI relevant to the data under consideration.2 Focused update writing group members who had no significant relevant RWI wrote the first draft of the focused update; the draft was then reviewed and revised by the full writing group. Each recommendation required a confidential vote by the writing group members before external review of the document. Any writing committee member with a significant (greater than $10 000) relationship with industry relevant to the recommendation was recused from voting on that recommendation.1.3. Review and ApprovalThis document was reviewed by 3 outside reviewers nominated by the ACC and 3 outside reviewers nominated by the AHA, as well as 1 reviewer each from the American Academy of Family Physicians and the Canadian Cardiovascular Society (CCS) and 58 individual content reviewers. All reviewer RWI information was collected and distributed to the writing committee and is published in this document (see Appendix 2 for details).This document was approved for publication by the governing bodies of the American College of Cardiology Foundation and the American Heart Association and endorsed by the American Academy of Family Physicians and the Canadian Cardiovascular Society.2. AnalgesiaAnalysis of retrospective data16 has raised a question about the potentially adverse effects of morphine in patients with unstable angina (UA)/non–ST-elevation myocardial infarction (NSTEMI). As a result, the recommendation for morphine pain relief has been reduced to a Class IIa recommendation for that patient population. Use of morphine remains a Class I recommendation for patients with STEMI, however, because STEMI patients should either have received reperfusion or are not candidates for reperfusion, and continuing pain requires relief in either case (Table 2). Table 2. Updates to Section 6.3.1.3: Analgesia2004 STEMI Guideline Recommendation2007 STEMI Focused Update RecommendationCommentsCOX-2 indicates cyclooxygenase-2; IV, intravenous/intravenously; NSAIDs, nonsteroidal anti-inflammatory drugs; and STEMI, ST-elevation myocardial infarction.Class IMorphine sulfate (2 to 4 mg IV with increments of 2 to 8 mg IV repeated at 5- to 15-minute intervals) is the analgesic of choice for management of pain associated with STEMI. (Level of Evidence: C)1. Morphine sulfate (2 to 4 mg IV with increments of 2 to 8 mg IV repeated at 5- to 15-minute intervals) is the analgesic of choice for management of pain associated with STEMI. (Level of Evidence: C)2004 recommendation remains current in 2007 Update2. Patients routinely taking NSAIDs (except for aspirin), both nonselective as well as COX-2 selective agents, before STEMI should have those agents discontinued at the time of presentation with STEMI because of the increased risk of mortality, reinfarction, hypertension, heart failure, and myocardial rupture associated with their use. (Level of Evidence: C)New recommendationClass III1. NSAIDs (except for aspirin), both nonselective as well as COX-2 selective agents, should not be administered during hospitalization for STEMI because of the increased risk of mortality, reinfarction, hypertension, heart failure, and myocardial rupture associated with their use. (Level of Evidence: C)New recommendationBecause of the known increased risk of cardiovascular events among patients taking cyclooxygenase-2 (COX-2) inhibitors and other nonsteroidal anti-inflammatory drugs (NSAIDs),17–19 these drugs should be discontinued immediately at the time of STEMI (see 2004 STEMI Guidelines, Section 7.12.5, for additional discussion).3,15,20,21 A substudy analysis from the ExTRACT TIMI-25 (Enoxaparin and Thrombolysis Reperfusion for Acute Myocardial Infarction Treatment–Thrombolysis in Myocardial Infarction) trial22 demonstrated an increased risk of death, reinfarction, heart failure, or shock among patients who were taking NSAIDs within 7 days of enrollment. Longer-term management considerations and a discussion of the gradient of risk with the various NSAIDS are found in Section 7.12.5 of the 2004 STEMI Guidelines.153. Beta BlockersThe 2004 STEMI Guidelines recommendations (Table 3) were based on studies that showed a reduced incidence of subsequent reinfarction and recurrent ischemia in patients receiving both fibrinolytic therapy and intravenous (IV) beta blockers. However, uncertainty about the use of IV beta blockers in the setting of fibrinolytic therapy has increased following 2 later randomized trials of IV beta blockade,23,24 a post-hoc analysis of the use of atenolol in the GUSTO-I (Global Utilization of Streptokinase and TPA for Occluded Coronary Arteries) trial,25 and a review of early beta-blocker therapy in myocardial infarction (MI)26 that did not find significant reductions in mortality.15Table 3. Updates to Section 6.3.1.5: Beta Blockers2004 STEMI Guideline Recommendation2007 STEMI Focused Update RecommendationComments*Risk factors for cardiogenic shock (the greater the number of risk factors present, the higher the risk of developing cardiogenic shock) are age greater than 70 years, systolic blood pressure less than 120 mm Hg, sinus tachycardia greater than 110 bpm or heart rate less than 60 bpm, and increased time since onset of symptoms of STEMI.IV indicates intravenous; LOE, level of evidence; LV, left ventricular; PCI, percutaneous coronary intervention; and STEMI, ST-elevation myocardial infarction.Class IOral beta-blocker therapy should be administered promptly to those patients without a contraindication, irrespective of concomitant fibrinolytic therapy or performance of primary PCI. (Level of Evidence: A)1. Oral beta-blocker therapy should be initiated in the first 24 hours for patients who do not have any of the following: 1) signs of heart failure, 2) evidence of a low output state, 3) increased risk* for cardiogenic shock, or 4) other relative contraindications to beta blockade (PR interval greater than 0.24 seconds, second- or third-degree heart block, active asthma, or reactive airway disease). (Level of Evidence: B)Modified recommendation (changed LOE and text)Patients with early contraindications within the first 24 hours of STEMI should be reevaluated for candidacy for beta-blocker therapy as secondary prevention. (Level of Evidence: C)2. Patients with early contraindications within the first 24 hours of STEMI should be reevaluated for candidacy for beta-blocker therapy as secondary prevention. (Level of Evidence: C)2004 recommendation remains current in 2007 UpdatePatients with moderate or severe LV failure should receive beta-blocker therapy as secondary prevention with a gradual titration scheme. (Level of Evidence: B)3. Patients with moderate or severe LV failure should receive beta-blocker therapy as secondary prevention with a gradual titration scheme. (Level of Evidence: B)2004 recommendation remains current in 2007 UpdateClass IIaIt is reasonable to administer IV beta blockers promptly to STEMI patients without contraindications, especially if a tachyarrhythmia or hypertension is present. (Level of Evidence: B)1. It is reasonable to administer an IV beta blocker at the time of presentation to STEMI patients who are hypertensive and who do not have any of the following: 1) signs of heart failure, 2) evidence of a low output state, 3) increased risk* for cardiogenic shock, or 4) other relative contraindications to beta blockade (PR interval greater than 0.24 seconds, second- or third-degree heart block, active asthma, or reactive airway disease). (Level of Evidence: B)Modified recommendation (changed text)Class III1. IV beta blockers should not be administered to STEMI patients who have any of the following: 1) signs of heart failure, 2) evidence of a low output state, 3) increased risk* for cardiogenic shock, or 4) other relative contraindications to beta blockade (PR interval greater than 0.24 seconds, second- or third-degree heart block, active asthma, or reactive airway disease). (Level of Evidence: A)New recommendation3.1. COMMIT/CCS-2 (Metoprolol)The COMMIT/CCS-2 (Clopidogrel and Metoprolol in Myocardial Infarction Trial/Second Chinese Cardiac Study) (4) randomized 45 852 patients within 24 hours of onset of suspected MI to receive metoprolol (up to 3 doses of 5 mg IV each in the first 15 minutes, followed by 200 mg orally daily) or matching placebo. Fifteen minutes after the IV doses, a 50-mg tablet of metoprolol or placebo was administered orally and repeated every 6 hours during Days 0 to 1 of hospitalization. From Day 2 onward, 200 mg of controlled-release metoprolol or placebo was administered orally daily (this is the Food and Drug Administration [FDA]-approved regimen for metoprolol in MI) until discharge from the hospital or up to a maximum of 4 weeks in hospital (in survivors, the mean was 15 days). The 2 prespecified co-primary outcomes were the composite of death, reinfarction, or cardiac arrest and death from any cause during the scheduled treatment period.Neither of the co-primary study end points was significantly reduced by allocation to metoprolol. For every 1000 patients treated, allocation to metoprolol was associated with 5 fewer episodes of reinfarction, 5 fewer episodes of ventricular defibrillation, but 11 more episodes of cardiogenic shock. The excess of cardiogenic shock was seen chiefly from Days 0 to 1 after hospitalization, whereas the reductions in reinfarction and ventricular fibrillation appeared from Day 2 onward.Allocation to metoprolol produced an average relative increase in cardiogenic shock of 30%, with higher rates for those greater than 70 years of age, or with systolic blood pressure less than 120 mm Hg, or with presenting heart rate greater than 110 bpm, or with Killip class greater than 1. On average across the whole study population, the absolute reduction in arrhythmia-related deaths and the absolute increase in cardiogenic shock–related deaths were of similar magnitude. No apparent difference was noted between the 2 treatment groups in the other attributed causes of death, either individually or in aggregate. Metoprolol allocation was associated with significantly more persistent hypotension and more cases of bradycardia.Though patients at high or low risk could be identified, the authors noted that they were not able to identify any subgroups in which the benefits clearly outweighed the risks.3.2. ConclusionThis focused update expands on the concepts introduced in the 2004 STEMI Guidelines, underscoring the potential risk of administering IV beta blockers to patients with severe heart failure or cardiogenic shock. There are several circumstances in which it can be useful (Class IIa) to administer an IV beta blocker acutely to a STEMI patient (Table 3), and these situations are discussed below. It is reasonable to administer IV beta-blocker therapy on Days 0 to 1 of hospitalization for STEMI when hypertension is present and the patient is not at an increased risk of cardiogenic shock on the basis of the risk factors defined above. Patients

The Adult Treatment Panel III (ATP III) of the National Cholesterol Education Program issued an evidence-based set of guidelines on cholesterol management in 2001. Since the publication of ATP III, 5 major clinical trials of statin therapy with clinical end points have been published. These trials addressed issues that were not examined in previous clinical trials of cholesterol-lowering therapy. The present document reviews the results of these recent trials and assesses their implications for cholesterol management. Therapeutic lifestyle changes (TLC) remain an essential modality in clinical management. The trials confirm the benefit of cholesterol-lowering therapy in high-risk patients and support the ATP III treatment goal of low-density lipoprotein cholesterol (LDL-C) <100 mg/dL. They support the inclusion of patients with diabetes in the high-risk category and confirm the benefits of LDL-lowering therapy in these patients. They further confirm that older persons benefit from therapeutic lowering of LDL-C. The major recommendations for modifications to footnote the ATP III treatment algorithm are the following. In high-risk persons, the recommended LDL-C goal is <100 mg/dL, but when risk is very high, an LDL-C goal of <70 mg/dL is a therapeutic option, ie, a reasonable clinical strategy, on the basis of available clinical trial evidence. This therapeutic option extends also to patients at very high risk who have a baseline LDL-C <100 mg/dL. Moreover, when a high-risk patient has high triglycerides or low high-density lipoprotein cholesterol (HDL-C), consideration can be given to combining a fibrate or nicotinic acid with an LDL-lowering drug. For moderately high-risk persons (2+ risk factors and 10-year risk 10% to 20%), the recommended LDL-C goal is <130 mg/dL, but an LDL-C goal <100 mg/dL is a therapeutic option on the basis of recent trial evidence. The latter option extends also to moderately high-risk persons with a baseline LDL-C of 100 to 129 mg/dL. When LDL-lowering drug therapy is employed in high-risk or moderately high-risk persons, it is advised that intensity of therapy be sufficient to achieve at least a 30% to 40% reduction in LDL-C levels. Moreover, any person at high risk or moderately high risk who has lifestyle-related risk factors (eg, obesity, physical inactivity, elevated triglycerides, low HDL-C, or metabolic syndrome) is a candidate for TLC to modify these risk factors regardless of LDL-C level. Finally, for people in lower-risk categories, recent clinical trials do not modify the goals and cutpoints of therapy.

Alice K. Jacobs, MD, FACC, FAHA, Chair, 2009–2011 Sidney C. Smith, Jr, MD, FACC, FAHA, Immediate Past Chair, 2006–2008 [⁎⁎⁎][1] Jeffrey L. Anderson, MD, FACC, FAHA, Chair-Elect Nancy Albert, PhD, CCNS, CCRN Christopher E. Buller, MD, FACC[⁎⁎⁎][1] Mark A. Creager, MD, FACC,

HomeCirculationVol. 100, No. 13Assessment of Cardiovascular Risk by Use of Multiple-Risk-Factor Assessment Equations

HomeCirculationVol. 104, No. 24ACC/AHA Guidelines for the Evaluation and Management of Chronic Heart Failure in the Adult: Executive Summary A Report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Committee to Revise the 1995 Guidelines for the Evaluation and Management of Heart Failure) Free AccessOtherPDF/EPUBAboutView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toFree AccessOtherPDF/EPUBACC/AHA Guidelines for the Evaluation and Management of Chronic Heart Failure in the Adult: Executive Summary A Report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Committee to Revise the 1995 Guidelines for the Evaluation and Management of Heart Failure) Committee Members Sharon A. Hunt, MD, FACC, David W. Baker, MD, MPH, FACP, Marshall H. Chin, MD, MPH, Michael P. Cinquegrani, MD, FACC, Arthur M. Feldmanmd, PhD, FACC, Gary S. Francis, MD, FACC, Theodore G. Ganiats, MD, Sidney Goldstein, MD, FACC, Gabriel Gregoratos, MD, FACC, Mariell L. Jessup, MD, FACC, R. Joseph Noble, MD, FACC, Milton Packer, MD, FACC, Marc A. Silver, MD, FACC, FACP, FCCP, FCGC, Lynne Warner Stevenson, MD, FACC, Raymond J. Gibbons, Task Force Members:, MD, FACC, Elliott M. Antman, MD, FACC, Joseph S. Alpert, MD, FACC, David P. Faxon, MD, FACC, Valentin Fuster, MD, PhD, FACC, Gabriel Gregoratos, MD, FACC, Alice K. Jacobs, MD, FACC, Loren F. Hiratzka, MD, FACC, Richard O. Russell, MD, FACC and Sidney C. SmithJr, MD, FACC Committee Members Search for more papers by this author , Sharon A. HuntSharon A. Hunt Search for more papers by this author , David W. BakerDavid W. Baker Search for more papers by this author , Marshall H. ChinMarshall H. Chin Search for more papers by this author , Michael P. CinquegraniMichael P. Cinquegrani Search for more papers by this author , Arthur M. FeldmanmdArthur M. Feldmanmd Search for more papers by this author , Gary S. FrancisGary S. Francis Search for more papers by this author , Theodore G. GaniatsTheodore G. Ganiats Search for more papers by this author , Sidney GoldsteinSidney Goldstein Search for more papers by this author , Gabriel GregoratosGabriel Gregoratos Search for more papers by this author , Mariell L. JessupMariell L. Jessup Search for more papers by this author , R. Joseph NobleR. Joseph Noble Search for more papers by this author , Milton PackerMilton Packer Search for more papers by this author , Marc A. SilverMarc A. Silver Search for more papers by this author , Lynne Warner StevensonLynne Warner Stevenson Search for more papers by this author , Raymond J. GibbonsRaymond J. Gibbons Search for more papers by this author , Elliott M. AntmanElliott M. Antman Search for more papers by this author , Joseph S. AlpertJoseph S. Alpert Search for more papers by this author , David P. FaxonDavid P. Faxon Search for more papers by this author , Valentin FusterValentin Fuster Search for more papers by this author , Gabriel GregoratosGabriel Gregoratos Search for more papers by this author , Alice K. JacobsAlice K. Jacobs Search for more papers by this author , Loren F. HiratzkaLoren F. Hiratzka Search for more papers by this author , Richard O. RussellRichard O. Russell Search for more papers by this author and Sidney C. SmithJrSidney C. SmithJr Search for more papers by this author Originally published11 Dec 2001https://doi.org/10.1161/hc4901.102568Circulation. 2001;104:2996–3007Heart failure (HF) is a major public health problem in the United States. Nearly 5 million patients in this country have HF, and nearly 500,000 patients are diagnosed with HF for the first time each year. The disorder is the underlying reason for 12 to 15 million office visits and 6.5 million hospital days each year (1). During the last 10 years, the annual number of hospitalizations has increased from approximately 550,000 to nearly 900,000 for HF as a primary diagnosis and from 1.7 to 2.6 million for HF as a primary or secondary diagnosis (2). Nearly 300,000 patients die of HF as a primary or contributory cause each year, and the number of deaths has increased steadily despite advances in treatment.HFs primarily a disease of the elderly (3). Approximately 6% to 10% of people older than 65 years have HF (4), and approximately 80% of patients hospitalized with HF are more than 65 years old (2). HF is the most common Medicare diagnosis-related group, and more Medicare dollars are spent for the diagnosis and treatment of HF than for any other diagnosis (5). The total inpatient and outpatient costs for HF in 1991 were approximately $38.1 billion, which was approximately 5.4% of the healthcare budget that year (1). In the United States, approximately $500 million annually is spent on drugs for the treatment of HF.The American College of Cardiology (ACC) and the American Heart Association (AHA) first published guidelines for the evaluation and management of HF in 1995 (6). Since that time, a great deal of progress has been made in the development of both pharmacological and nonpharmacological approaches to treatment for this common, costly, disabling, and generally fatal disorder. For this reason, the 2 organizations believed that the time was right to reassess and update these guidelines, fully recognizing that the optimal therapy of HF remains a work in progress and that future guidelines will supersede these.The writing committee was composed of 7 members who represented the ACC and AHA, as well as invited participants from the American College of Chest Physicians, the Heart Failure Society of America, the International Society for Heart and Lung Transplantation, the American Academy of Family Physicians, and the American College of Physicians–American Society of Internal Medicine. Both the academic and private practice sectors were represented. This document was reviewed by 3 official reviewers nominated by the ACC, 3 official reviewers nominated by the AHA, 1 reviewer nominated by the Heart Failure Society of America, 1 reviewer nominated by the International Society for Heart and Lung Transplantation, 1 reviewer nominated by the American Academy of Family Physicians, 1 reviewer nominated by the National Heart Foundation of Australia, the ACC Hypertensive Disease Committee and 16 content reviewers.In formulating the present document, the writing committee decided to take a new approach to the classification of HF that emphasized both the evolution and progression of the disease. In doing so, we identified 4 stages of HF. Stage A identifies the patient who is at high risk for developing HF but has no structural disorder of the heart; Stage B refers to a patient with a structural disorder of the heart but who has never developed symptoms of HF; Stage C denotes the patient with past or current symptoms of HF associated with underlying structural heart disease; and Stage D designates the patient with end-stage disease who requires specialized treatment strategies such as mechanical circulatory support, continuous inotropic infusions, cardiac transplantation, or hospice care (see Table 1 and Fig. 1). Only the latter 2 stages, of course, qualify for the traditional clinical diagnosis of HF for diagnostic or coding purposes. This classification recognizes that there are established risk factors and structural prerequisites for the development of HF and that therapeutic interventions performed even before the appearance of left ventricular dysfunction or symptoms can reduce the morbidity and mortality of HF. This classification system is intended to complement but not to replace the New York Heart Association (NYHA) functional classification, which primarily gauges the severity of symptoms in patients who are in stage C or D. It has been recognized for many years, however, that the NYHA functional classification reflects a subjective assessment by a physician and changes frequently over short periods of time and that the treatments used do not differ significantly across the classes. Therefore, the committee believed that a staging system was needed that would reliably and objectively identify patients in the course of their disease and would be linked to treatments that were uniquely appropriate at each stage of their illness. According to this new approach, patients would be expected to advance from one stage to the next unless progression of the disease was slowed or stopped by treatment. This new classification scheme adds a useful dimension to our thinking about HF similar to that achieved by staging systems for other disorders (e.g., those used in the classification of cancer). Stages of HFStageDescriptionExamplesHF indicates heart failure.APatients at high risk of developing HF because of the presence of conditions that are strongly associated with the development of HF. Such patients have no identified structural or functional abnormalities of the pericardium, myocardium, or cardiac valves and have never shown signs or symptoms of HF.Systemic hypertension; coronary artery disease; diabetes mellitus; history of cardiotoxic drug therapy or alcohol abuse; personal history of rheumatic fever; family history of cardiomyopathy.BPatients who have developed structural heart disease that is strongly associated with the development of HF but who have never shown signs or symptoms of HF.Left ventricular hypertrophy or fibrosis; left ventricular dilatation or hypocontractility; asymptomatic valvular heart disease; previous myocardial infarction.CPatients who have current or prior symptoms of HF associated with underlying structural heart disease.Dyspnea or fatigue due to left ventricular systolic dysfunction; asymptomatic patients who are undergoing treatment for prior symptoms of HF.DPatients with advanced structural heart disease and marked symptoms of HF at rest despite maximal medical therapy and who require specialized interventions.Patients who are frequently hospitalized for HF or cannot be safely discharged from the hospital; patients in the hospital awaiting heart transplantation; patients at home receiving continuous intravenous support for symptom relief or being supported with a mechanical circulatory assist device; patients in a hospice setting for the management of HF.Download figureDownload PowerPointFigure 1. Stages in the evolution of HF and recommended therapy by stage. FHx CM indicates family history of cardiomyopathy; MI, myocardial infarction; LV, left ventricular; and IV,intravenous.All recommendations provided in this document follow the format of previous ACC/AHA guidelines:Class I: Conditions for which there is evidence for and/or general agreement that the procedure or treatment is useful and effective.Class II: Conditions for which there is conflicting evidence and/or a divergence of opinion about the usefulness/efficacy of a procedure or treatment.Class IIa: The weight of evidence or opinion is in favor of the procedure or treatment.Class IIb: Usefulness/efficacy is less well established by evidence or opinion.Class III: Conditions for which there is evidence and/or general agreement that the procedure or treatment is not useful/effective and in some cases can be harmful.The recommendations listed in this document are evidence based whenever possible. Pertinent medical literature in the English language was identified through a series of computerized literature searches (including Medline and EMBASE) and a manual search of selected articles. References selected and published in this document are representative but not all-inclusive.The levels of evidence on which these recommendations are based were ranked as level A if the data were derived from multiple randomized clinical trials, level B when data were derived from a single randomized trial or nonrandomized studies, and level C when the consensus opinion of experts was the primary source of recommendation. The strength of evidence does not necessarily reflect the strength of a recommendation. A treatment may be considered controversial although it has been evaluated in controlled clinical trials; conversely, a strong recommendation may be based on years of clinical experience and be supported only by historical data or by no data at all.The committee elected to focus this document on the prevention of HF, as well as the evaluation and management of chronic HF in the adult patient with left ventricular systolic and diastolic dysfunction. It specifically did not consider acute HF, which might merit a separate set of guidelines and which is addressed in part in the ACC/AHA guidelines for the management of patients with acute myocardial infarction (7). We have also excluded HF in children, both because the underlying causes of HF in children differ from those in adults and because none of the controlled trials of treatments for HF have included children. We have not considered the management of HF due to primary valvular disease (see ACC/AHA guidelines on management of patients with valvular heart disease) (8) or congenital malformations, and we have not included recommendations for the treatment of specific myocardial disorders (e.g., hemochromatosis, sarcoidosis, or amyloidosis).The ACC/AHA guidelines for the evaluation and management of chronic heart failure in the adult were approved for publication by the governing bodies of the ACC and AHA. These guidelines will be reviewed annually after publication and will be considered current unless the ACC/AHA Task Force on Practice Guidelines revises or withdraws them from circulation.These practice guidelines are intended to assist physicians in clinical decision making by describing a range of generally acceptable approaches for the prevention, diagnosis, and management of HF. The guidelines attempt to define practices that meet the needs of most patients under most circumstances. However, the ultimate judgment regarding the care of a particular patient must be made by the physician in light of all of the circumstances that are relevant to that patient. The various therapeutic strategies described in this document can be viewed as a checklist to be considered for each patient in an attempt to individualize treatment for an evolving disease process. Every patient is unique, not only in terms of his or her cause and course of HF, but also in terms of his or her personal and cultural approach to the disease. Guidelines can only provide an outline for evidence-based decisions or recommendations for individual care; these guidelines are meant to provide that outline.II. Characterization of HF as a Clinical SyndromeHF is a complex clinical syndrome that can result from any structural or functional cardiac disorder that impairs the ability of the ventricle to fill with or eject blood. The cardinal manifestations of HF are dyspnea and fatigue, which may limit exercise tolerance, and fluid retention, which may lead to pulmonary and peripheral edema. Both abnormalities can impair the functional capacity and quality of life of affected individuals, but they may not necessarily dominate the clinical picture at the same time.Coronary artery disease is the underlying cause of HF in approximately two thirds of patients with left ventricular systolic dysfunction (9). The remainder have nonischemic causes of systolic dysfunction and may have an identifiable cause (e.g., hypertension, valvular disease, myocardial toxins, or myocarditis) or may have no discernible cause (e.g., idiopathic dilated cardiomyopathy).The classification system that is most commonly used to quantify the degree of functional limitation imposed by HF is one first developed by the NYHA (10). This system assigns patients to 1 of 4 functional classes depending on the degree of effort needed to elicit symptoms: patients may have symptoms of HF at rest (class IV), on less-than-ordinary exertion (class III), on ordinary exertion (class II), or only at levels that would limit normal individuals (class I). The mechanisms responsible for exercise intolerance in patients with chronic HF have not been clearly defined. Patients with a very low ejection fraction may be asymptomatic, whereas patients with preserved left ventricular systolic function may have severe disability. The apparent discordance between the severity of systolic dysfunction and the degree of functional impairment is not well understood despite intense investigation.Left ventricular dysfunction begins with some injury to the myocardium and is usually a progressive process, even in the absence of a new identifiable insult to the myocardium. The principal manifestation of such progression is a process known as remodeling, which occurs in association with homeostatic attempts to decrease wall stress through increases in wall thickness. This ultimately results in a change in the geometry of the left ventricle such that the chamber dilates, hypertrophies, and becomes more spherical. The process of cardiac remodeling generally precedes the development of symptoms, occasionally by months or even years. The process of remodeling continues after the appearance of symptoms and may contribute importantly to worsening of symptoms despite treatment.The committee struggled with its perception that many clinicians do not appreciate the progressive nature of left ventricular dysfunction and HF or the importance of screening and prophylaxis for them, principles that are quite analogous to well-recognized strategies in the field of oncology. For this reason, it believed that the progression to and evolution of HF could appropriately be characterized by considering 4 stages in the evolution of the disease as described in the Introduction and Table 1. This classification scheme recognizes that HF, like coronary artery disease, has established risk factors; that the evolution of HF has asymptomatic and symptomatic phases; and that treatments prescribed at each stage can reduce the morbidity and mortality of HF.III. Assessment of PatientsA. Initial Evaluation of Patients and Detection of Predisposing Conditions1. Identification of Patients.In general, patients with left ventricular dysfunction present to the physician in 1 of 3 ways: with a syndrome of decreased exercise tolerance; with a syndrome of fluid retention; or with no symptoms and incidentally discovered left ventricular dysfunction.2. Identification of Structural Abnormality.A complete history and physical examination are the first steps in evaluating the structural abnormality or cause responsible for the development of HF. Although the history and physical examination may provide important clues about the nature of the underlying cardiac abnormality, identification of the structural abnormality leading to HF generally requires either noninvasive or invasive imaging of the cardiac structures. The single most useful diagnostic test in the evaluation of patients with HF is the 2-dimensional echocardiogram, coupled with Doppler flow studies. Other tests may be used to provide information regarding the nature and severity of the cardiac abnormality. Radionuclide ventriculography can provide highly accurate measurements of global and regional function and assessment of ventricular enlargement, but it is unable to directly assess valvular abnormalities or cardiac hypertrophy. Both chest radiography and 12-lead electrocardiograms are considered to provide baseline information in most patients, but because they are both insensitive and nonspecific, neither the chest radiograph nor the electrocardiogram alone should form the primary basis for determining the specific cardiac abnormality responsible for the development of HF.Recently, the measurement of circulating levels of brain natriuretic peptide has become available as a means of identifying patients with elevated left ventricular filling pressures who are likely to exhibit signs and symptoms of HF. The assessment of this peptide cannot reliably distinguish patients with systolic from those with diastolic dysfunction. However, it has been widely investigated as a biochemical marker of morbidity and mortality in patients with known HF (11) and as an aid in differentiating dyspnea due to HF from dyspnea due to other causes in an emergency setting (12). The role of brain natriuretic peptide measurement in the identification and management of patients with symptomatic or asymptomatic left ventricular dysfunction remains to be fully clarified.3. Evaluation of the Cause of Ventricular Dysfunction.Identification of the disorder leading to HF may be important, because some causes of left ventricular dysfunction are reversible or treatable. However, it may not be possible to discern the cause of HF in many patients who present with this syndrome, and in others, the underlying condition may not be amenable to treatment. Hence, physicians should focus their efforts on diagnoses that have some potential for improvement with therapy directed at the underlying condition. Evaluation of potential causative factors should include taking a patient and family history, general laboratory testing, evaluation of the possibility of coronary artery disease, and evaluation of the possibility of primary myocardial disease.B. Ongoing Evaluation of HFOnce the nature and cause of the structural abnormalities leading to the development of HF have been defined, physicians should focus on the clinical assessment of patients, both during the initial presentation and during subsequent visits. This ongoing review of the patient’s clinical status is critical to the appropriate selection and monitoring of treatment. It should include assessment of functional capacity, assessment of volume status, laboratory evaluation, and assessment of prognosis.Recommendations for the Evaluation of Patients With HFClass IThorough history and physical examination to identify cardiac and noncardiac disorders that might lead to the development of HF or accelerate the progression of HF. (Level of Evidence: C)Initial and ongoing assessment of patient’s ability to perform routine and desired activities of daily living. (Level of Evidence: C)Initial and ongoing assessment of volume status. (Level of Evidence: C)Initial measurement of complete blood count, urinalysis, serum electrolytes (including calcium and magnesium), blood urea nitrogen, serum creatinine, blood glucose, liver function tests, and thyroid-stimulating hormone. (Level of Evidence: C)Serial monitoring of serum electrolytes and renal function. (Level of Evidence: C)Initial 12-lead electrocardiogram and chest radiograph. (Level of Evidence: C)Initial 2-dimensional echocardiography with Doppler or radionuclide ventriculography to assess left ventricular systolic function. (Level of Evidence: C)Cardiac catheterization with coronary arteriography in patients with angina who are candidates for revascularization. (Level of Evidence: B)Class IIaCardiac catheterization with coronary arteriography in patients with chest pain who have not had evaluation of their coronary anatomy and who have no contraindications to coronary revascularization. (Level of Evidence: C)Cardiac catheterization with coronary arteriography in patients with known or suspected coronary artery disease but without angina who are candidates for revascularization. (Level of Evidence: C)Noninvasive imaging to detect ischemia and viability in patients with known coronary artery disease and no angina who are being considered for revascularization. (Level of Evidence: C)Maximal exercise testing with measurement of respiratory gas exchange and/or blood oxygen saturation to help determine whether HF is the cause of exercise limitation when the contribution of HF is uncertain. (Level of Evidence: C)Maximal exercise testing with measurement of respiratory gas exchange to identify high-risk patients who are candidates for cardiac transplantation or other advanced treatments. (Level of Evidence: B)Echocardiography in asymptomatic first-degree relatives of patients with idiopathic dilated cardiomyopathy. (Level of Evidence: C)Repeat measurement of ejection fraction in patients who have had a change in clinical status or who have experienced or recovered from a clinical event or received treatment that might have had a significant effect on cardiac function. (Level of Evidence: C)Screening for hemochromatosis. (Level of Evidence: C)Measurement of serum antinuclear antibody, rheumatoid factor, urinary vanillylmandelic acid, and metanephrines in selected patients. (Level of Evidence: C)Class IIbNoninvasive imaging to define the likelihood of coronary artery disease in patients with left ventricular dysfunction. (Level of Evidence: C)Maximal exercise testing with measurement of respiratory gas exchange to facilitate prescription of an appropriate exercise program. (Level of Evidence: C)Endomyocardial biopsy in patients in whom an inflammatory or infiltrative disorder of the heart is suspected. (Level of Evidence: C)Assessment of human immunodeficiency virus status. (Level of Evidence: C)Class IIIEndomyocardial biopsy in the routine evaluation of patients with HF. (Level of Evidence: C)Routine Holter monitoring or signal-averaged electrocardiography. (Level of Evidence: C)Repeat coronary arteriography or noninvasive testing for ischemia in patients for whom coronary artery disease has previously been excluded as the cause of left ventricular dysfunction. (Level of Evidence: C)Routine measurement of circulating levels of norepinephrine or endothelin. (Level of Evidence: C)IV. TherapyA. Patients at High Risk of Developing Left Ventricular Dysfunction (Stage A)Many conditions or behaviors that are associated with an increased risk of HF can be identified before patients show any evidence of structural heart disease. Because early modification of these factors can often reduce the risk of HF, working with patients with these risk factors provides the earliest opportunity to reduce the impact of HF on public and individual health.Recommendations for Patients at High Risk of Developing HF (Stage A)Class IControl of systolic and diastolic hypertension in accordance with recommended guidelines. (Level of Evidence: A)Treatment of lipid disorders in accordance with recommended guidelines. (Level of Evidence: B)Avoidance of patient behaviors that may increase the risk of HF (e.g., smoking, alcohol consumption, and illicit drug use). (Level of Evidence: C)Angiotensin converting enzyme (ACE) inhibition in patients with a history of atherosclerotic vascular disease, diabetes mellitus, or hypertension and associated cardiovascular risk factors. (Level of Evidence: B)Control of ventricular rate in patients with supraventricular tachyarrhythmias. (Level of Evidence: B)Treatment of thyroid disorders. (Level of Evidence: C)Periodic evaluation for signs and symptoms of HF. (Level of Evidence: C)Class IIaNoninvasive evaluation of left ventricular function in patients with a strong family history of cardiomyopathy or in those receiving cardiotoxic interventions. (Level of Evidence: C)Class IIIExercise to prevent the development of HF. (Level of Evidence: C)Reduction of dietary salt beyond that which is prudent for healthy individuals in patients without hypertension or fluid retention. (Level of Evidence: C)Routine testing to detect left ventricular dysfunction in patients without signs or symptoms of HF or evidence of structural heart disease. (Level of Evidence: C)Routine use of nutritional supplements to prevent the development of structural heart disease. (Level of Evidence: C)B. Patients With Left Ventricular Dysfunction Who Have Not Developed Symptoms (Stage B)Patients without symptoms but who have had a myocardial infarction and patients without symptoms who have evidence of left ventricular dysfunction are at considerable risk of developing HF. The likelihood of developing clinical HF can be diminished by the use of therapies that reduce the risk of additional injury, the process of remodeling, and the progression of left ventricular dysfunction. However, as with patients with no structural heart disease, there is no evidence that control of dietary sodium, participation in regular exercise, or use of nutritional supplements can prevent the development of HF in patients with a recent or remote myocardial infarction with or without left ventricular systolic dysfunction.Recommendations for Patients With Asymptomatic Left Ventricular Systolic Dysfunction (Stage B)Class IACE inhibition in patients with a recent or remote history of myocardial infarction regardless of ejection fraction. (Level of Evidence: A)ACE inhibition in patients with a reduced ejection fraction, whether or not they have experienced a myocardial infarction. (Level of Evidence: B)Beta-blockade in patients with a recent myocardial infarction regardless of ejection fraction. (Level of Evidence: A)Beta-blockade in patients with a reduced ejection fraction, whether or not they have experienced a myocardial infarction. (Level of Evidence: B)Valve replacement or repair for patients with hemodynamically significant valvular stenosis or regurgitation. (Level of Evidence: B)Regular evaluation for signs and symptoms of HF. (Level of Evidence: C)Measures listed as class I recommendations for patients in stage A. (Levels of Evidence: A, B, and C as appropriate).Class IIbLong-term treatment with systemic vasodilators in patients with severe aortic regurgitation. (Level of Evidence: B)Class IIITreatment with digoxin in patients with left ventricular dysfunction who are in sinus rhythm. (Level of Evidence: C)Reduction of dietary salt beyond that which is prudent for healthy individuals in patients without hypertension or fluid retention. (Level of Evidence: C)Exercise to prevent

HomeCirculationVol. 122, No. 252010 ACCF/AHA Guideline for Assessment of Cardiovascular Risk in Asymptomatic Adults Free AccessResearch ArticlePDF/EPUBAboutView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toFree AccessResearch ArticlePDF/EPUB2010 ACCF/AHA Guideline for Assessment of Cardiovascular Risk in Asymptomatic AdultsA Report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines Writing Committee Members Philip Greenland, MD, FACC, FAHA, Joseph S. Alpert, MD, FACC, FAHA, George A. Beller, MD, MACC, FAHA, Emelia J. Benjamin, MD, ScM, FACC, FAHA, Matthew J. Budoff, MD, FACC, FAHA, Zahi A. Fayad, PhD, FACC, FAHA, Elyse Foster, MD, FACC, FAHA, Mark. A. Hlatky, MD, FACC, FAHA, John McB. Hodgson, MD, FACC, FAHA, FSCAI, Frederick G. Kushner, MD, FACC, FAHA, Michael S. Lauer, MD, FACC, FAHA, Leslee J. Shaw, PhD, FACC, FAHA, Sidney C. SmithJr, MD, FACC, FAHA, Allen J. Taylor, MD, FACC, FAHA, William S. Weintraub, MD, FACC, FAHA and Nanette K. Wenger, MD, MACC, FAHA Writing Committee Members Search for more papers by this author , Philip GreenlandPhilip Greenland Search for more papers by this author , Joseph S. AlpertJoseph S. Alpert Search for more papers by this author , George A. BellerGeorge A. Beller Search for more papers by this author , Emelia J. BenjaminEmelia J. Benjamin Search for more papers by this author , Matthew J. BudoffMatthew J. Budoff Search for more papers by this author , Zahi A. FayadZahi A. Fayad Search for more papers by this author , Elyse FosterElyse Foster Search for more papers by this author , Mark. A. HlatkyMark. A. Hlatky Search for more papers by this author , John McB. HodgsonJohn McB. Hodgson Search for more papers by this author , Frederick G. KushnerFrederick G. Kushner Search for more papers by this author , Michael S. LauerMichael S. Lauer Search for more papers by this author , Leslee J. ShawLeslee J. Shaw Search for more papers by this author , Sidney C. SmithJrSidney C. SmithJr Search for more papers by this author , Allen J. TaylorAllen J. Taylor Search for more papers by this author , William S. WeintraubWilliam S. Weintraub Search for more papers by this author and Nanette K. WengerNanette K. Wenger Search for more papers by this author Originally published15 Nov 2010https://doi.org/10.1161/CIR.0b013e3182051b4cCirculation. 2010;122:e584–e636Other version(s) of this articleYou are viewing the most recent version of this article. Previous versions: January 1, 2010: Previous Version 1 Jacobs Alice K., MD, FACC, FAHAPreambleIt is essential that the medical profession play a central role in critically evaluating the evidence related to drugs, devices, and procedures for the detection, management, or prevention of disease. Properly applied, rigorous, expert analysis of the available data documenting absolute and relative benefits and risks of these therapies and procedures can improve the effectiveness of care, optimize patient outcomes, and favorably affect the cost of care by focusing resources on the most effective strategies. One important use of such data is the production of clinical practice guidelines that, in turn, can provide a foundation for a variety of other applications, such as performance measures, appropriate use criteria, clinical decision support tools, and quality improvement tools.The American College of Cardiology Foundation (ACCF) and the American Heart Association (AHA) have jointly engaged in the production of guidelines in the area of cardiovascular disease since 1980. The ACCF/AHA Task Force on Practice Guidelines (Task Force) is charged with developing, updating, and revising practice guidelines for cardiovascular diseases and procedures, and the Task Force directs and oversees this effort. Writing committees are charged with assessing the evidence as an independent group of authors to develop, update, or revise recommendations for clinical practice.Experts in the subject under consideration have been selected from both organizations to examine subject-specific data and write guidelines in partnership with representatives from other medical practitioner and specialty groups. Writing committees are specifically charged to perform a formal literature review; weigh the strength of evidence for or against particular tests, treatments, or procedures; and include estimates of expected health outcomes where data exist. Patient-specific modifiers, comorbidities, and issues of patient preference that may influence the choice of tests or therapies are considered. When available, information from studies on cost is considered, but data on efficacy and clinical outcomes constitute the primary basis for recommendations in these guidelines.In analyzing the data and developing recommendations and supporting text, the writing committee used evidence-based methodologies developed by the Task Force that are described elsewhere.1 The committee reviewed and ranked evidence supporting current recommendations, with the weight of evidence ranked as Level A if the data were derived from multiple randomized clinical trials or meta-analyses. The committee ranked available evidence as Level B when data were derived from a single randomized trial or nonrandomized studies. Evidence was ranked as Level C when the primary source of the recommendation was consensus opinion, case studies, or standard of care. In the narrative portions of these guidelines, evidence is generally presented in chronological order of development. Studies are identified as observational, retrospective, prospective, or randomized when appropriate. For certain conditions for which inadequate data are available, recommendations are based on expert consensus and clinical experience and ranked as Level C. An example is the use of penicillin for pneumococcal pneumonia, where there are no randomized trials and treatment is based on clinical experience. When recommendations at Level C are supported by historical clinical data, appropriate references (including clinical reviews) are cited if available. For issues where sparse data are available, a survey of current practice among the clinicians on the writing committee was the basis for Level C recommendations and no references are cited. The schema for Classification of Recommendations (COR) and Level of Evidence (LOE) is summarized in Table 1, which also illustrates how the grading system provides an estimate of the size as well as the certainty of the treatment effect. A new addition to the ACCF/AHA methodology is a separation of the Class III recommendations to delineate whether the recommendation is determined to be of “no benefit” or associated with “harm” to the patient. In addition, in view of the increasing number of comparative effectiveness studies, comparator verbs and suggested phrases for writing recommendations for the comparative effectiveness of one treatment/strategy with respect to another for COR I and IIa, LOE A or B only, have been added.Table 1. Applying Classification of Recommendations and Level of EvidenceTable 1. Applying Classification of Recommendations and Level of Evidence* Data available from clinical trials or registries about the usefulness/efficacy in different subpopulations, such as gender, age, history of diabetes, history of prior myocardial infarction, history of heart failure, and prior aspirin use. A recommendation with Level of Evidence B or C does not imply that the recommendation is weak. Many important clinical questions addressed in the guidelines do not lend themselves to clinical trials. Even though randomized trials are not available, there may be a very clear clinical consensus that a particular test or therapy is useful or effective.†For comparative effectiveness recommendations (Class I and IIa; Level of Evidence: A and B only), studies that support the use of comparator verbs should involve direct comparisons of the treatments or strategies being evaluated.The Task Force on Practice Guidelines makes every effort to avoid actual, potential, or perceived conflicts of interest that may arise as a result of industry relationships or personal interests among the writing committee. Specifically, all members of the writing committee, as well as peer reviewers of the document, are asked to disclose ALL relevant relationships and those existing 24 months before initiation of the writing effort. All guideline recommendations require a confidential vote by the writing committee and must be approved by a consensus of the members voting. Members who were recused from voting are noted on the title page of this document and in Appendix 1. Members must recuse themselves from voting on any recommendation to which their relationship with industry and other entities (RWI) applies. Any writing committee member who develops a new RWI during his or her tenure is required to notify guideline staff in writing. These statements are reviewed by the Task Force on Practice Guidelines and all members during each conference call and meeting of the writing committee and are updated as changes occur. For detailed information about guideline policies and procedures, please refer to the ACCF/AHA methodology and policies manual.1 Authors' and peer reviewers' RWI pertinent to this guideline are disclosed in Appendixes 1 and 2, respectively. In addition, to ensure complete transparency, writing committee members' comprehensive disclosure information—including RWI not pertinent to this document—is available online as a supplement to this document. Disclosure information for the ACCF/AHA Task Force on Practice Guidelines is available online at www.cardiosource.org/ACC/About-ACC/Leadership/Guidelines-and-Documents-Task-Forces.aspx. The work of the writing committee was supported exclusively by the ACCF and AHA without commercial support. Writing group members volunteered their time for this effort.The ACCF/AHA practice guidelines address patient populations (and healthcare providers) residing in North America. As such, drugs that are not currently available in North America are discussed in the text without a specific class of recommendation. For studies performed in large numbers of subjects outside of North America, each writing committee reviews the potential impact of different practice patterns and patient populations on the treatment effect and the relevance to the ACCF/AHA target population to determine whether the findings should inform a specific recommendation.The ACCF/AHA practice guidelines are intended to assist healthcare providers in clinical decision making by describing a range of generally acceptable approaches to the diagnosis, management, and prevention of specific diseases or conditions. These practice guidelines represent a consensus of expert opinion after a thorough and systematic review of the available current scientific evidence and are intended to improve patient care. The guidelines attempt to define practices that meet the needs of most patients in most situations. The ultimate judgment regarding care of a particular patient must be made by the healthcare provider and patient in light of all the circumstances presented by that patient. Thus, there are circumstances in which deviations from these guidelines may be appropriate. Clinical decision making should consider the quality and availability of expertise in the area where care is provided. When these guidelines are used as the basis for regulatory or payer decisions, the goal should be improvement in quality of care. The Task Force recognizes that situations arise in which additional data are needed to better inform patient care; these areas will be identified within each respective guideline when appropriate.Prescribed courses of treatment in accordance with these recommendations are effective only if they are followed. Because lack of patient understanding and adherence may adversely affect outcomes, physicians and other healthcare providers should make every effort to engage the patient's active participation in prescribed medical regimens and lifestyles.The guidelines will be reviewed annually by the Task Force and considered current until they are updated, revised, or withdrawn from distribution. The executive summary and recommendations are published in the Journal of the American College of Cardiology, Circulation, and the Journal of Cardiovascular Computed Tomography.1. Introduction1.1. Methodology and Evidence ReviewThe recommendations listed in this document are, whenever possible, evidence based. An extensive evidence review was conducted for the period beginning March 2008 through April 2010. Searches were limited to studies, reviews, and other evidence conducted in human subjects and published in English. Key search words included, but were not limited to, African Americans, Asian Americans, albuminuria, asymptomatic, asymptomatic screening and brachial artery reactivity, atherosclerosis imaging, atrial fibrillation, brachial artery testing for atherosclerosis, calibration, cardiac tomography, compliance, carotid intima-media thickness (IMT), coronary calcium, coronary computed tomography angiography (CCTA), C-reactive protein (CRP), detection of subclinical atherosclerosis, discrimination, endothelial function, family history, flow-mediated dilation, genetics, genetic screening, guidelines, Hispanic Americans, hemoglobin A, glycosylated, meta-analysis, Mexican Americans, myocardial perfusion imaging (MPI), noninvasive testing, noninvasive testing and type 2 diabetes, outcomes, patient compliance, peripheral arterial tonometry (PAT), peripheral tonometry and atherosclerosis, lipoprotein-associated phospholipase A2, primary prevention of coronary artery disease (CAD), proteinuria, cardiovascular risk, risk scoring, receiver operating characteristics (ROC) curve, screening for brachial artery reactivity, stress echocardiography, subclinical atherosclerosis, subclinical and Framingham, subclinical and Multi-Ethnic Study of Atherosclerosis (MESA), and type 2 diabetes. Additionally, the writing committee reviewed documents related to the subject matter previously published by the ACCF and AHA, American Diabetes Association (ADA), European Society of Cardiology, and the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure (JNC) 7. References selected and published in this document are representative and not all-inclusive.To provide clinicians with a comprehensive set of data, whenever deemed appropriate or when published in the article, data from the clinical trial will be used to calculate the absolute risk difference and number needed to treat or harm; data related to the relative treatment effects will also be provided, such as odds ratio (OR), relative risk (RR), hazard ratio (HR), or incidence rate ratio (IRR), along with confidence interval (CI) when available.The focus of this guideline is the initial assessment of the apparently healthy adult for risk of developing cardiovascular events associated with atherosclerotic vascular disease. The goal of this early assessment of cardiovascular risk in an asymptomatic individual is to provide the foundation for targeted preventive efforts based on that individual's predicted risk. It is based on the long-standing concept of targeting the intensity of drug treatment interventions to the severity of the patient's risk.2 This clinical approach serves as a complement to the population approach to prevention of cardiovascular disease (CVD), in which population-wide strategies are used regardless of an individual's risk.This guideline pertains to initial assessment of cardiovascular risk in the asymptomatic adult. Although there is no clear age cut point for defining the onset of risk for CVD, elevated risk factor levels and subclinical abnormalities can be detected in adolescents as well as young adults. To maximize the benefits of prevention-oriented interventions, especially those involving lifestyle changes, the writing committee advises that these guidelines be applied in asymptomatic persons beginning at age 20. The writing committee recognizes that the decision about a starting point is an arbitrary one.This document specifically excludes from consideration patients with a diagnosis of CVD or a coronary event, for example, angina or anginal equivalent, myocardial infarction (MI), or revascularization with percutaneous coronary intervention or coronary artery bypass graft surgery. It also excludes testing for patients with known peripheral artery disease (PAD) and cerebral vascular disease. This guideline is not intended to replace other sources of information on cardiovascular risk assessment in specific disease groups or higher-risk groups such as those with known hypertension or diabetes who are receiving treatment.1.2. Organization of the Writing CommitteeThe committee was composed of physicians and others expert in the field of cardiology. The committee included representatives from the American Society of Echocardiography (ASE), American Society of Nuclear Cardiology (ASNC), Society of Atherosclerosis Imaging and Prevention (SAIP), Society for Cardiovascular Angiography and Interventions (SCAI), Society of Cardiovascular Computed Tomography (SCCT), and Society for Cardiovascular Magnetic Resonance (SCMR).1.3. Document Review and ApprovalThis document was reviewed by 2 outside reviewers nominated by the ACCF and 2 outside reviewers nominated by the AHA, as well as 2 reviewers each from ASE, ASNC, SAIP, SCAI, SCCT, and SCMR, and 23 individual content reviewers (including members from the Appropriate Use Criteria Task Force, ACCF Cardiac Catheterization Committee, ACCF Imaging Council, and ACCF Prevention of Cardiovascular Disease Committee). All reviewer RWI information was collected and distributed to the writing committee and is published in this document (Appendix 2).This document was approved for publication by the governing bodies of the ACCF and AHA and endorsed by ASE, ASNC, SAIP, SCCT, and SCMR.1.4. Magnitude of the Problem of Cardiovascular Risk in Asymptomatic AdultsAtherosclerotic CVD is the leading cause of death for both men and women in the United States.3 Risk factors for the development of atherosclerotic disease are widespread in the U.S. population. In 2003, approximately 37% of American adults reported having ≥2 risk factors for CVD. Ninety percent of patients with coronary heart disease (CHD) have at least 1 atherosclerotic risk factor.4 Approximately half of all coronary deaths are not preceded by cardiac symptoms or diagnoses.5 One aim of this guideline is to provide an evidence-based approach to risk assessment in an effort to lower this high burden of coronary deaths in asymptomatic adults.CVD was mentioned on the death certificates of 56% of decedents in 2005. It was listed as the underlying cause of death in 35.3% (864,480) of all deaths (2,448,017) in 2005 or 1 of every 2.8 deaths in the U.S.6 In every year since 1900 (except 1918), CVD accounted for more deaths than any other major cause of death in the United States.6 It is estimated that if all forms of major CVD were eliminated, life expectancy would rise by almost 7 years.6 Analyses suggest that the decrease in U.S. deaths due to CHD from 1980 to 2000 was partly attributable (approximately 47%) to evidence-based medical therapies, and about 44% of the reduction has been attributed to changes in risk factors in the population.7 The estimated direct and indirect cost of CVD for 2009 is $475.3 billion.6CHD has a long asymptomatic latent period, which provides an opportunity for early preventive interventions. Atherosclerosis begins in childhood and progresses into adulthood due to multiple coronary risk factors such as unfavorable levels of blood lipids, blood pressure, body weight and body fat, smoking, diabetes, and genetic predisposition.8–10 The lifetime risk of CHD and its various manifestations has been calculated for the Framingham Heart Study population at different ages. In nearly 8000 persons initially free of clinical evidence of CHD, the lifetime risk of developing clinically manifest CHD (angina pectoris, MI, coronary insufficiency, or death from CHD) at age 40 was 48.6% for men and 31.7% for women.11 At age 70, the lifetime risk of developing CHD was 34.9% for men and 24.2% for women. The lifetime risk for all CVD combined is nearly 2 of every 3 Americans.12 Thus, the problem is immense, but the preventive opportunity is also great.1.5. Assessing the Prognostic Value of Risk Factors and Risk MarkersMany risk factors have been proposed as predictors of CHD.13,14 New risk factors or markers are frequently identified and evaluated as potential additions to standard risk assessment strategies. The AHA has published a scientific statement on appropriate methods for evaluating the predictive value of new risk factors or risk markers.15 The scientific statement endorsed previously published guidelines for proper reporting of observational studies in epidemiology16 but also went beyond those guidelines to specifically address criteria for evaluation of established and new risk markers. The current writing committee endorses this scientific statement and incorporated these principles into the assessments for this guideline. The general concepts and requirements for new risk marker validation and evaluation are briefly reviewed to provide a basis for the assessments in this document.For any new risk marker to be considered useful for risk prediction, it must, at the very least, have an independent statistical association with risk after accounting for established readily available and inexpensive risk markers. This independent statistical association should be based on studies that include large numbers of outcome events. Traditionally, reports of novel risk markers have only gone this far, reporting adjusted HRs with CIs and P values.17 Although this level of basic statistical association is often regarded by researchers as meaningful in prediction of a particular outcome of interest, the AHA scientific statement called for considerably more rigorous assessments that include analysis of the calibration, discrimination, and reclassification of the predictive model. Many of the tests reviewed in this guideline fail to provide these more comprehensive measures of test evaluation, and for this reason, many tests that are statistically associated with clinical outcomes cannot be judged to be useful beyond a standard risk assessment profile. In the absence of this evidence of “additive predictive information,” the writing committee generally concluded that a new risk marker was not ready for routine use in risk assessment.Calibration and discrimination are 2 separate concepts that do not necessarily track with each other. Calibration refers to the ability to correctly predict the proportion of subjects within any given group who will experience disease events. Among patients predicted to be at higher risk, there will be a higher number of events, whereas among patients identified as being at lower risk, there will be fewer events. For example, if a diagnostic test or a multivariable model splits patients into 3 groups with predicted risks of 5%, 10%, and 15% within each group, calibration would be considered good if in a separate group of cohorts with similar predicted risks, the actual rates of events were close to 5%, 10%, and 15%. Calibration is best presented by displaying observed versus expected event rates across quantiles of predicted risk for models that do and do not include the new risk marker.Discrimination is a different concept that refers to the probability of a diagnostic test or a risk prediction instrument to distinguish between patients who are at higher compared with lower risk. For example, a clinician sees 2 random patients, 1 of whom is ultimately destined to experience a clinical event. A diagnostic test or risk model discriminates well if it usually correctly predicts which of the 2 subjects is at higher risk for an event. Mathematically this is described by calculating a C index or C statistic, parameters that are analogous to the area under the ROC curve. These statistics define the probability that a randomly selected person from the “affected group” will have a higher test score than a randomly selected person from the “nonaffected group.” A test with no discrimination would have a C statistic of 0.50 and a perfect test would have a C statistic of 1.0. Throughout this document, C statistic information is cited where available.As an example of a risk marker that improves discrimination, MESA investigators found that the addition of coronary artery calcium (CAC) scores to standard risk factors improved the area under the ROC curve from 0.77 to 0.82 (P<0.001).18 In contrast, a score based on 9 genes that code for cholesterol levels added no predictive value over established risk factors and family history.19 Similarly, a study comparing the predictive capacity of conventional and newer biomarkers for prediction of cardiovascular events derived a C statistic of 0.760 for coronary events for the conventional risk factor model. Adding a number of newer biomarkers changed the C statistic by only 0.009 (P=0.08).20 Small changes such as these in the C statistic suggest limited or rather modest improvement in risk discrimination with additional risk markers.Some investigators have called for evaluating the number of subjects reclassified into other risk categories based on models that include the new risk marker.21 For example, in a model of cardiovascular risk in a large cohort of healthy women, the addition of CRP resulted in reclassification of a large proportion of subjects who were thought to be at intermediate risk based on standard risk markers alone.22 One problem with this approach is that not all reclassification is necessarily clinically useful. If a patient is deemed to be at intermediate risk and is then reclassified as being at high or low risk, the clinician might find that information helpful. It may not be known, however, whether or not these reclassifications are correct for individual subjects. Pencina and colleagues introduced 2 new approaches, namely “net reclassification improvement” and “integrated with classification improvement,” which provide quantitative estimates of correct reclassifications.23 Correct reclassifications are associated with higher predicted risks for cases and lower predicted risks for noncases.1.6. Usefulness in Motivating Patients or Guiding TherapyIn 1996 the American College of Cardiology Bethesda Conference reviewed the concept of risk stratification, an approach that is now standard for identifying the appropriate degree of therapeutic or preventive interventions.2 Patients deemed to be at low risk for clinical events are unlikely to gain substantial benefits from pharmaceutical interventions and therefore might best be managed with lifestyle modifications. Conversely, patients deemed to be at high risk for events are more likely to benefit from pharmacologic interventions and therefore are appropriate candidates for intensive risk factor modification efforts. Among patients at intermediate risk, further testing may be indicated to refine risks and assess the need for treatment. Although this model is attractive and has been shown to be appropriate in certain situations, there is no definitive evidence that it directly leads to improved patient outcomes. Further research is clearly needed, and it is appropriate to point out that the risk stratification paradigm has not been subjected to rigorous evaluation by randomized trials. Indeed, the impact of various risk assessment modalities on patient outcomes is rarely studied and not well documented in the few studies that have been conducted.241.7. Economic Evaluation of Novel Risk MarkersThe progressively rising costs of medical care have increased interest in documenting the economic effects of new tests and therapies. The most basic goal is to estimate the economic consequences of a decision to order a new test. The ultimate goal is to determine whether performing the test provides sufficient value to justify its use.A complete economic evaluation of the test has to account for all the subsequent costs induced by ordering the test, not just the cost of the test itself. The results of the test should change subsequent clinical management, which might include ordering follow-up tests, starting or stopping drug therapy, or using a device or procedure. The costs of these subsequent clinical management choices must be included in an “intention-to-test” analysis of the economic consequences of the initial decision to use the test. Ideally, the analysis should be extended to account for clinical events that are either averted or caused as a result of the strategy based on performing the test.An example of the economic consequences of testing will illustrate the importance of these principles. Suppose a patient with diabetes who has no cardiac symptoms undergoes a computed tomography (CT) coronary angiogram, which reveals obstructive CAD but also leads to contrast-induced nephropathy. Further suppose this patient has a follow-up invasive coronary angiogram, undergoes insertion of a coronary stent, and is treated for renal insufficiency. The costs of all these “downstream events” should be included in any economic assessment of the use of CCTA because they all resulted from the initial decision to perform the test. Note that the total costs of a “test strategy” may greatly exceed the cost of the initial test itself.The cost of any medical intervention has to be placed in the context of the clinic

The Clinical Efficacy Assessment Subcommittee of the American College of Physicians–American Society of Internal Medicine acknowledges the scientific validity of this product as a background paper and as a review that captures the levels of evidence in the management of patients with chronic stable angina as of November 17, 2002. The American College of Cardiology (ACC)/American Heart Association (AHA) Task Force on Practice Guidelines regularly reviews existing guidelines to determine when an update or a full revision is needed. This process gives priority to areas in which major changes in text, and particularly recommendations, are merited on the basis of new understanding or evidence. Minor changes in verbiage and references are discouraged. The ACC/AHA/American College of Physicians–American Society of Internal Medicine (ACP-ASIM) Guidelines for the Management of Patients With Chronic Stable Angina, which were published in June 1999, have now been updated. The full-text guideline incorporating the updated material is available on the Internet (www.acc.org or www.americanheart.org) in both a track-changes version showing the changes in the 1999 guideline in strike-out (deleted text) and highlighting …

The American College of Cardiology (ACC)/American Heart Association (AHA) Task Force on Practice Guidelines regularly reviews existing guidelines to determine when an update or full revision is needed. This process gives priority to areas where major changes in text, and particularly recommendations, are mentioned on the basis of new understanding or evidence. Minor changes in verbiage and references are discouraged. The ACC/AHA guidelines for exercise testing that were published in 1997 have now been updated. The full-text guidelines incorporating the updated material are available on the Internet (www.acc.org or www.americanheart.org) in both a version that shows the changes in the 1997 guidelines in strike-over (deleted text) and highlighting (new text) and a “clean” version that fully incorporates the changes. This article describes the 10 major areas of change reflected in the update in a format that we hope can be read and understood as a stand-alone document. The table of contents from the full-length guideline (see next page) indicates the location of these changes. Interested readers are referred to the full-length Internet version to completely understand the context of these changes. All new references appear in boldface type; all original references appear in normal type.⇓ View this table: Table of Contents The ACC/AHA classifications, I, II, and III are used to summarize indications as follows: Class I: Conditions for which there is evidence and/or general agreement that a given procedure or treatment is useful and effective. Class II: Conditions for which there is conflicting evidence and/or a divergence of opinion about the usefulness/efficacy of a procedure or treatment. IIa: Weight of evidence/opinion is in favor of usefulness/efficacy. IIb: Usefulness/efficacy is less well established by evidence/opinion. Class III: Conditions for which there is evidence and/or general agreement that the procedure/treatment is not useful/effective and in some cases may be harmful. In the original …

HomeCirculationVol. 134, No. 102016 ACC/AHA Guideline Focused Update on Duration of Dual Antiplatelet Therapy in Patients With Coronary Artery Disease: A Report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines: An Update of the 2011 ACCF/AHA/SCAI Guideline for Percutaneous Coronary Intervention, 2011 ACCF/AHA Guideline for Coronary Artery Bypass Graft Surgery, 2012 ACC/AHA/ACP/AATS/PCNA/SCAI/STS Guideline for the Diagnosis and Management of Patients With Stable Ischemic Heart Disease, 2013 ACCF/AHA Guideline for the Management of ST-Elevation Myocardial Infarction, 2014 AHA/ACC Guideline for the Management of Patients With Non–ST-Elevation Acute Coronary Syndromes, and 2014 ACC/AHA Guideline on Perioperative Cardiovascular Evaluation and Management of Patients Undergoing Noncardiac Surgery Free AccessResearch ArticlePDF/EPUBAboutView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissionsDownload Articles + Supplements ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toSupplemental MaterialFree AccessResearch ArticlePDF/EPUB2016 ACC/AHA Guideline Focused Update on Duration of Dual Antiplatelet Therapy in Patients With Coronary Artery Disease: A Report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines: An Update of the 2011 ACCF/AHA/SCAI Guideline for Percutaneous Coronary Intervention, 2011 ACCF/AHA Guideline for Coronary Artery Bypass Graft Surgery, 2012 ACC/AHA/ACP/AATS/PCNA/SCAI/STS Guideline for the Diagnosis and Management of Patients With Stable Ischemic Heart Disease, 2013 ACCF/AHA Guideline for the Management of ST-Elevation Myocardial Infarction, 2014 AHA/ACC Guideline for the Management of Patients With Non–ST-Elevation Acute Coronary Syndromes, and 2014 ACC/AHA Guideline on Perioperative Cardiovascular Evaluation and Management of Patients Undergoing Noncardiac Surgery Glenn N. Levine, MD, FACC, FAHA, Chair, Eric R. Bates, MD, FACC, FAHA, FSCAI, John A. Bittl, MD, FACC, Ralph G. Brindis, MD, MPH, MACC, FAHA, Stephan D. Fihn, MD, MPH, Lee A. Fleisher, MD, FACC, FAHA, Christopher B. Granger, MD, FACC, FAHA, Richard A. Lange, MD, MBA, FACC, Michael J. Mack, MD, FACC, Laura Mauri, MD, MSc, FACC, FAHA, FSCAI, Roxana Mehran, MD, FACC, FAHA, FSCAI, Debabrata Mukherjee, MD, FACC, FAHA, FSCAI, L. Kristin Newby, MD, MHS, FACC, FAHA, Patrick T. O’Gara, MD, FACC, FAHA, Marc S. Sabatine, MD, MPH, FACC, FAHA, Peter K. Smith, MD, FACC and Sidney C. SmithJr, MD, FACC, FAHA Glenn N. LevineGlenn N. Levine *, †, ‡, §, ‖, ¶, # Search for more papers by this author , Eric R. BatesEric R. Bates *, †, ‡, §, ‖, ¶, # Search for more papers by this author , John A. BittlJohn A. Bittl *, †, ‡, §, ‖, ¶, # Search for more papers by this author , Ralph G. BrindisRalph G. Brindis *, †, ‡, §, ‖, ¶, # Search for more papers by this author , Stephan D. FihnStephan D. Fihn *, †, ‡, §, ‖, ¶, # Search for more papers by this author , Lee A. FleisherLee A. Fleisher *, †, ‡, §, ‖, ¶, # Search for more papers by this author , Christopher B. GrangerChristopher B. Granger *, †, ‡, §, ‖, ¶, # Search for more papers by this author , Richard A. LangeRichard A. Lange *, †, ‡, §, ‖, ¶, # Search for more papers by this author , Michael J. MackMichael J. Mack *, †, ‡, §, ‖, ¶, # Search for more papers by this author , Laura MauriLaura Mauri *, †, ‡, §, ‖, ¶, # Search for more papers by this author , Roxana MehranRoxana Mehran *, †, ‡, §, ‖, ¶, # Search for more papers by this author , Debabrata MukherjeeDebabrata Mukherjee *, †, ‡, §, ‖, ¶, # Search for more papers by this author , L. Kristin NewbyL. Kristin Newby *, †, ‡, §, ‖, ¶, # Search for more papers by this author , Patrick T. O’GaraPatrick T. O’Gara *, †, ‡, §, ‖, ¶, # Search for more papers by this author , Marc S. SabatineMarc S. Sabatine *, †, ‡, §, ‖, ¶, # Search for more papers by this author , Peter K. SmithPeter K. Smith *, †, ‡, §, ‖, ¶, # Search for more papers by this author and Sidney C. SmithJrSidney C. SmithJr *, †, ‡, §, ‖, ¶, # Search for more papers by this author Originally published29 Mar 2016https://doi.org/10.1161/CIR.0000000000000404Circulation. 2016;134:e123–e155is corrected byCorrection to: 2016 ACC/AHA Guideline Focused Update on Duration of Dual Antiplatelet Therapy in Patients With Coronary Artery Disease: A Report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines: An Update of the 2011 ACCF/AHA/SCAI Guideline for Percutaneous Coronary Intervention, 2011 ACCF/AHA Guideline for Coronary Artery Bypass Graft Surgery, 2012 ACC/AHA/ACP/AATS/PCNA/SCAI/STS Guideline for the Diagnosis and Management of Patients With Stable Ischemic Heart Disease, 2013 ACCF/AHA Guideline for the Management of ST-Elevation Myocardial Infarction, 2014 AHA/ACC Guideline for the Management of Patients With Non–ST-Elevation Acute Coronary Syndromes, and 2014 ACC/AHA Guidelineon Perioperative Cardiovascular Evaluation and Management of Patients Undergoing Noncardiac SurgeryOther version(s) of this articleYou are viewing the most recent version of this article. Previous versions: January 1, 2016: Previous Version 1 Table of ContentsPreamble e124Introduction e1251.1. Methodology and Evidence Review e1261.1. Organization of the Writing Group e1271.3. Review and Approval e127Critical Questions and Systematic Review Findings e1272.1. Critical Questions on Duration of DAPT e1272.2. Studies of Shorter-Duration DAPT After Stent Implantation e1272.3. Studies of Longer-Duration DAPT After Stent Implantation e1282.4. Other Studies Relevant to DAPT >1 Year After MI e1282.5. Prolonged/Extended DAPT and Mortality Rate e128Overriding Concepts and Recommendations for DAPT and Duration of Therapy e1293.1. General Overriding Concepts e1293.2. Factors Associated With Increased Ischemic and Bleeding Risk e1293.3. Specific P2Y12 Inhibitors: Recommendations e1313.4. Platelet Function Testing, Genetic Testing, and Switching of P2Y12 Inhibitors e1313.5. Proton Pump Inhibitors and DAPT e1323.6. Aspirin Dosing in Patients Treated With DAPT: Recommendation e1323.7. Triple Therapy (Aspirin, P2Y12 Inhibitor, and Oral Anticoagulant) e132Percutaneous Coronary Intervention e1334.1. Duration of DAPT in Patients With SIHD Treated With PCI: Recommendations e1334.2. Duration of DAPT in Patients With ACS Treated With PCI: Recommendations e1334.3. Duration of DAPT in Patients With SIHD and ACS Treated with PCI e134Recommendations for Duration of DAPT in Patients Undergoing CABG e134Recommendations for Duration of DAPT in Patients With SIHD e135Acute Coronary Syndrome (NSTE-ACS and STEMI) e1377.1. Duration of DAPT in Patients With ACS Treated With Medical Therapy Alone (Without Revascularization or Fibrinolytic Therapy): Recommendations e1377.2. Duration of DAPT in Patients With STEMI Treated With Fibrinolytic Therapy: Recommendations e1387.3. Duration of DAPT in Patients With ACS Treated With PCI: Recommendations e1387.4. Duration of DAPT in Patients With ACS Treated With CABG: Recommendation e1387.5. Duration of DAPT in Patients With ACS e138Perioperative Management–Timing of Elective Noncardiac Surgery in Patients Treated With PCI and DAPT: Recommendations e140References e143Appendix 1. Author Relationships With Industry and Other Entities (Relevant) e149Appendix 2. Reviewer Relationships With Industry and Other Entities (Relevant) e151PreambleIncorporation of new study results, medications, or devices that merit modification of existing clinical practice guideline recommendations, or the addition of new recommendations, is critical to ensuring that guidelines reflect current knowledge, available treatment options, and optimum medical care. To keep pace with evolving evidence, the American College of Cardiology (ACC)/American Heart Association (AHA) Task Force on Clinical Practice Guidelines (“Task Force”) has issued this focused update to revise existing guideline recommendations on the basis of recently published study data. This update has been subject to rigorous, multilevel review and approval, similar to the full guidelines. For specific focused update criteria and additional methodological details, please see the ACC/AHA guideline methodology manual.1ModernizationProcesses have evolved over time in response to published reports from the Institute of Medicine2,3 and ACC/AHA mandates,4–7 leading to adoption of a “knowledge byte” format. This process entails delineation of a recommendation addressing a specific clinical question, followed by concise text (ideally <250 words per recommendation) and hyperlinked to supportive evidence. This approach better accommodates time constraints on busy clinicians, facilitates easier access to recommendations via electronic search engines and other evolving technology, and supports the evolution of guidelines as “living documents” that can be dynamically updated as needed.Class of Recommendation and Level of EvidenceThe Class of Recommendation (COR) and Level of Evidence (LOE) are derived independently of each other according to established criteria. The COR indicates the strength of recommendation, encompassing the estimated magnitude and certainty of benefit of a clinical action in proportion to risk. The LOE rates the quality of scientific evidence supporting the intervention on the basis of the type, quantity, and consistency of data from clinical trials and other sources (Table 1). Recommendations in this focused update reflect the new 2015 COR/LOE system, in which LOE B and C are subcategorized for the purpose of increased granularity.1,7,8Table 1. Applying Class of Recommendation and Level of Evidence to Clinical Strategies, Interventions, Treatments, or Diagnostic Testing in Patient Care* (Updated August 2015)Table 1. Applying Class of Recommendation and Level of Evidence to Clinical Strategies, Interventions, Treatments, or Diagnostic Testing in Patient Care* (Updated August 2015)Relationships With Industry and Other EntitiesThe ACC and AHA exclusively sponsor the work of guideline writing committees (GWCs) without commercial support, and members volunteer time for this activity. Selected organizations and professional societies with related interests and expertise are invited to participate as partners or collaborators. The Task Force makes every effort to avoid actual, potential, or perceived conflicts of interest that might arise through relationships with industry or other entities (RWI). All GWC members and reviewers are required to fully disclose current industry relationships or personal interests, beginning 12 months before initiation of the writing effort. Management of RWI involves selecting a balanced GWC and requires that both the chair and a majority of GWC members have no relevant RWI (see Appendix 1 for the definition of relevance). GWC members are restricted with regard to writing or voting on sections to which RWI apply. Members of the GWC who recused themselves from voting are indicated and specific section recusals are noted in Appendixes 1 and 2. In addition, for transparency, GWC members’ comprehensive disclosure information is available as an Online Supplement (http://circ.ahajournals.org/lookup/suppl/doi:10.1161/CIR.0000000000000404/-/DC1). Comprehensive disclosure information for the Task Force is also available at http://www.acc.org/guidelines/about-guidelines-and-clinical-documents/guidelines-and-documents-task-forces. The Task Force strives to avoid bias by selecting experts from a broad array of backgrounds representing different geographic regions, genders, ethnicities, intellectual perspectives, and scopes of clinical activities.Intended UseGuidelines provide recommendations applicable to patients with or at risk of developing cardiovascular disease. The focus is on medical practice in the United States, but guidelines developed in collaboration with other organizations may have a broader target. Although guidelines may be used to inform regulatory or payer decisions, the intent is to improve quality of care and align with patients’ interests. The guidelines are reviewed annually by the Task Force and are official policy of the ACC and AHA. Each guideline is considered current unless and until it is updated, revised, or superseded by a published addendum.Related IssuesFor additional information pertaining to the methodology for grading evidence, assessment of benefit and harm, shared decision making between the patient and clinician, structure of evidence tables and summaries, standardized terminology for articulating recommendations, organizational involvement, peer review, and policies regarding periodic assessment and updating of guideline documents, we encourage readers to consult the ACC/AHA guideline methodology manual.1Jonathan L. Halperin, MD, FACC, FAHAChair, ACC/AHA Task Force on Clinical Practice Guidelines1. IntroductionThe scope of this focused update is limited to addressing recommendations on duration of dual antiplatelet therapy (DAPT) (aspirin plus a P2Y12 inhibitor) in patients with coronary artery disease (CAD). Recommendations considered are those in 6 guidelines: “2011 ACCF/AHA/SCAI Guideline for Percutaneous Coronary Intervention”,9 “2011 ACCF/AHA Guideline for Coronary Artery Bypass Graft Surgery”,10 “2012 ACCF/AHA/ACP/AATS/PCNA/SCAI/STS Guideline for the Diagnosis and Management of Patients With Stable Ischemic Heart Disease”,11,12 “2013 ACC/AHA Guideline for the Management of ST-Elevation Myocardial Infarction”,13 “2014 ACC/AHA Guideline for Non–ST-Elevation Acute Coronary Syndromes”,14 and “2014 ACC/AHA Guideline on Perioperative Cardiovascular Evaluation and Management of Patients Undergoing Noncardiac Surgery”.15The impetus for this focused update review is 11 studies16–27 of patients treated with coronary stent implantation (predominantly with drug-eluting stents [DES]) assessing shorter-duration or longer-duration DAPT, as well as a large, randomized controlled trial (RCT) of patients 1 to 3 years after myocardial infarction (MI) assessing the efficacy of DAPT compared with aspirin monotherapy.28 These studies were published after the formulation of recommendations for duration of DAPT in prior guidelines. The specific mandate of the present writing group is to evaluate, update, harmonize, and, when possible, simplify recommendations on duration of DAPT.Although there are several potential combinations of antiplatelet therapy, the term and acronym DAPT has been used to specifically refer to combination antiplatelet therapy with aspirin and a P2Y12 receptor inhibitor (clopidogrel, prasugrel, or ticagrelor) and will be used similarly in this focused update. Recommendations in this focused update on duration of DAPT, aspirin dosing in patients treated with DAPT, and timing of elective noncardiac surgery in patients treated with percutaneous coronary intervention (PCI) and DAPT supersede prior corresponding recommendations in the 6 relevant guidelines. These recommendations for duration of DAPT apply to newer-generation stents and, in general, only to those not treated with oral anticoagulant therapy. For the purposes of this focused update, patients with a history of acute coronary syndrome (ACS) >1 year prior who have since remained free of recurrent ACS are considered to have transitioned to stable ischemic heart disease (SIHD) and are addressed in the section on SIHD. Issues and recommendations with regard to P2Y12 inhibitor “pretreatment,” “preloading,” and loading are beyond the scope of this document but are addressed in other guidelines.9,14,29This focused update is designed to function both as a standalone document and to serve as an update to the relevant sections on duration of DAPT in the 6 clinical practice guidelines, replacing relevant text, figures, and recommendations. Thus, by necessity, there is some redundancy in different sections of this document. When possible, the “knowledge byte” format was used for recommendations. In some cases, the complexity of this document required a modification of the knowledge byte format, with several interrelated recommendations grouped together, followed by concise associated text (<250 words of text per recommendation).1.1. Methodology and Evidence ReviewClinical trials published since the 2011 PCI guideline9 and the 2011 coronary artery bypass graft (CABG) guideline,10 published in a peer-reviewed format through December 2015, were reviewed by the Task Force to identify trials and other key data that might affect guideline recommendations. The information considered important enough to prompt updated recommendations is included in evidence tables in the Data Supplement.In accord with recommendations by the Institute of Medicine2,3 and the ACC/AHA Task Force Methodology Summit,1,6 3 critical (PICOTS-formatted; population, intervention, comparison, outcome, timing, setting) questions were developed to address the critical questions related to duration of DAPT. These 3 critical questions were the basis of a formal systematic review and evaluation of the relevant study data by an Evidence Review Committee (ERC).30 Concurrent with this process, writing group members evaluated study data relevant to the numerous current recommendations in the 6 guidelines, including topics not covered in the 3 critical questions (eg, DAPT after CABG). The findings of the ERC and the writing group members were formally presented and discussed, and then modifications to existing recommendations were considered. Recommendations that are based on a body of evidence that includes a systematic review conducted by the ERC are denoted by the superscript SR (eg, LOE B-R SR). See the ERC systematic review report, “Duration of Dual Antiplatelet Therapy: A Systematic Review for the 2016 ACC/AHA Guideline Focused Update on Duration of Dual Antiplatelet Therapy in Patients With Coronary Artery Disease,” for the complete evidence review report.301.2. Organization of the Writing GroupRecommendations on duration of DAPT are currently included in 6 clinical practice guidelines, which are interrelated and overlapping because they address the management of patients with CAD. Therefore, the writing group consisted of the chairs/vice chairs and/or members of all 6 guidelines, representing the fields of cardiovascular medicine, interventional cardiology, cardiac surgery, internal medicine, and cardiovascular anesthesia, as well as expertise in trial design and statistical analysis.1.3. Review and ApprovalThis focused update was reviewed by the writing committee members from the 6 guidelines; by 5 official reviewers from the ACC and AHA; 2 reviewers each from the American Association for Thoracic Surgery, American College of Emergency Physicians, American Society of Anesthesiologists, Preventive Cardiovascular Nurses Association, Society for Cardiovascular Angiography and Interventions, Society of Cardiovascular Anesthesiologists, and the Society of Thoracic Surgeons; and by 23 additional content reviewers. Reviewers’ RWI information is published in this document (Appendix 2).This document was approved for publication by the governing bodies of the ACC and the AHA and was endorsed by the American Association for Thoracic Surgery, American Society of Anesthesiologists, Preventive Cardiovascular Nurses Association, Society for Cardiovascular Angiography and Interventions, Society of Cardiovascular Anesthesiologists, Society of Thoracic Surgeons, and Society for Vascular Surgery.2. Critical Questions and Systematic Review Findings2.1. Critical Questions on Duration of DAPTThe 3 critical (PICOTS-formatted) questions on DAPT duration are listed in Table 2. Most contemporary studies of DAPT have compared either shorter (3 to 6 months)17–21 or longer (18 to 48 months)16,22–26 duration of therapy with 12 months of DAPT, which is the recommended or minimal duration of therapy for most patients in ACC/AHA9,13,14 and European Society of Cardiology31–33 guidelines published between 2011 and 2014. Recommendations based on the findings from the critical question–focused systemic reviews are provided in Sections 4 to 8 of the present document.Table 2. Critical (PICOTS-Formatted) Questions on DAPT DurationQ1: In patients treated with newer (non-first) generation DES for (1) SIHD or (2) ACS, compared with 12 months of DAPT, is 3–6 months of DAPT as effective in preventing stent thrombosis, preventing MACE and/or reducing bleeding complications?Q2: In patients treated with newer (non-first) generation DES, compared with 12 months of DAPT, does >12 (18–48) months of DAPT result in differences in mortality rate, decreased MACE, decreased stent thrombosis, and/or increased bleeding?Q3: In post-MI (NSTEMI or STEMI) patients who are clinically stable and >12 months past their event, does continued DAPT, compared with aspirin monotherapy, result in differences in mortality rate, decreased nonfatal MI, decreased MACE, and/or increased bleeding?ACS indicates acute coronary syndrome; DAPT, dual antiplatelet therapy; DES, drug-eluting stents; MACE, major adverse cardiac events; MI, myocardial infarction; NSTEMI, non–ST-elevation myocardial infarction; PICOTS, population, intervention, comparison, outcome, timing, and setting; SIHD, stable ischemic heart disease; and STEMI, ST-elevation myocardial infarction.2.2. Studies of Shorter-Duration DAPT After Stent ImplantationFive RCTs of patients treated with elective DES implantation have compared shorter-duration (3 to 6 months) DAPT with 12 months of DAPT17–21 (Data Supplement 1). The trials primarily enrolled low-risk (non-ACS) patients, with only a small proportion having had a recent MI. The main endpoints of these noninferiority trials were composite ischemic events (or net composite events) and stent thrombosis. These studies, as well as several meta-analyses34–37 and an analysis by the ERC,30 did not find any increased risk of stent thrombosis with shorter-duration DAPT. A shorter duration of DAPT results in fewer bleeding complications.30,34–36 Shorter-duration DAPT may be most reasonable in patients currently being treated with “newer-generation” (eg, everolimus- or zotarolimus-eluting) DES, which are associated with lower stent thrombosis and MI rates than those of “first-generation” (eg, sirolimus- and paclitaxel-eluting) DES, which are rarely, if ever, used in current clinical practice.16,36,382.3. Studies of Longer-Duration DAPT After Stent ImplantationSix RCTs, consisting predominantly of patients treated with elective DES implantation, compared prolonged DAPT (total therapy duration: 18 to 48 months) with 6 to 12 months of DAPT to determine whether extended therapy reduces late and very late stent thrombosis and prevents ischemic events associated with disease progression and plaque rupture at other nonstented sites16,22–27 (Data Supplement 2). In the Dual Antiplatelet Therapy study—the largest of these trials—patients who had undergone DES implantation, had been treated with DAPT for 12 months, and were without ischemic or bleeding events during this period were randomized to an additional 18 months of DAPT or to aspirin monotherapy.16 Extended DAPT resulted in a 0.7% absolute reduction in very late stent thrombosis, a 2.0% absolute reduction in MI, a 1.6% absolute reduction in major adverse cardiac events (MACE), and a 0.9% absolute increase in moderate or severe bleeding. In the subgroup of patients treated with everolimus-eluting stents—currently the most commonly used stent—extended DAPT resulted in a 0.4% absolute reduction in stent thrombosis, a 1.1% absolute reduction in MI, and a 1.2% absolute increase in moderate/severe bleeding.39Taken as a whole, studies of longer-duration (“prolonged” or “extended”) DAPT16,22–27 for an additional 18 to 36 months after DES found an absolute decrease in late stent thrombosis and ischemic complications of ≈1% to 2% and an absolute increase in bleeding complications of ≈1% (Data Supplements 2 and 3). A weighted risk-benefit analysis by the ERC of studies of patients treated with DES found 6 fewer MIs and 3 fewer stent thromboses but 5 additional major bleeds per 1000 patients treated with prolonged DAPT per year.302.4. Other Studies Relevant to DAPT >1 Year After MIThe CHARISMA (Clopidogrel for High Atherothrombotic Risk and Ischemic Stabilization, Management, and Avoidance) trial randomized patients with established atherosclerosis or at high risk of clinical atherosclerotic disease to either DAPT (with clopidogrel) or aspirin monotherapy; with DAPT, no significant reduction was found in ischemic effects at a median follow-up of 28 months, but there was a 0.4% absolute increase in severe bleeding.40 A post hoc analysis of patients enrolled in the study with prior MI found a 1.7% absolute decrease in the composite endpoint of cardiovascular death, MI, or stroke events with DAPT, with no benefit in those with CAD without prior MI.40,41Patients in the PEGASUS-TIMI 54 (Prevention of Cardiovascular Events in Patients with Prior Heart Attack Using Ticagrelor Compared to Placebo on a Background of Aspirin—Thrombolysis In Myocardial Infarction 54) trial were randomized 1 to 3 years after MI with additional high-risk features to either DAPT (with ticagrelor 60 mg or 90 mg twice daily) or continued aspirin monotherapy.28 After a mean of 33 months of therapy, DAPT, when compared with aspirin monotherapy, resulted in a 1.2% to 1.3% absolute reduction in the primary composite endpoint of cardiovascular death, MI, or stroke and a 1.2% to 1.5% absolute increase in major bleeding, with no excess in fatal bleeding or intracranial hemorrhage. In subgroup analysis, the greatest reduction in ischemic events with prolonged DAPT was in patients in whom P2Y12 inhibitor therapy either had not been discontinued or had been discontinued for ≤30 days (absolute reduction in MACE: 1.9% to 2.5%). No benefit was seen in patients in whom P2Y12 inhibitor therapy had been discontinued >1 year before enrollment in the study.42In the Dual Antiplatelet Therapy study, the benefit/risk ratio for prolonged DAPT was more favorable for those presenting with MI than those with SIHD.43 In an analysis of patients with a history of prior MI enrolled in 6 RCTs of extended/prolonged DAPT, extended DAPT significantly decreased the absolute risk of MACE by 1.1% and significantly increased the absolute risk of major bleeding by 0.8%.44Taken as a whole, trials of prolonged or extended DAPT suggest that the benefit/risk ratio of prolonged DAPT may be more favorable for those with prior MI, with an absolute decrease in ischemic events of ≈1% to 3% at the cost of an absolute increase in bleeding events of ≈1% over the course of several years of prolonged or extended therapy (median durations of therapy: 18 to 33 months) (Data Supplements 3 and 4). This appears biologically plausible because patients with prior MI (usually mediated by plaque rupture) may be at greater risk for future plaque rupture than those without prior MI.37,40,412.5. Prolonged/Extended DAPT and Mortality RateAn unexpected finding in the Dual Antiplatelet Therapy study16 was a borderline-significant increase in overall mortality rate (0.5% absolute increase) with 30 months of DAPT versus 12 months of DAPT in DES-treated patients, which was due to significantly increased deaths from noncardiovascular causes (most commonly cancer), with no increase in cardiovascular deaths, and no significant increase in fatal bleeding.45 Five subsequent meta-analyses35–37,46,47 restricted to RCTs of studies enrolling patients treated with predominantly newer generation DES, published prior to the presentation of the OPTIDUAL (Optimal Dual Antiplatelet Therapy) trial, found numerically36,47 or statistically35,37,46 significant increased risk of all-cause (though not cardiovascular) death associated with prolonged duration of DAPT (Data Supplements 3 and 4).In contrast, a meta-analysis that combined studies of DAPT duration after stent implantation with studies of DAPT duration for other indications48 and an analysis of 6 trials restricted to post-MI patients treated with DAPT44 found no increase in cardiovascular or noncardiovascular mortality rate associated with prolonged DAPT (Data Supplement 3). A US Food and Drug Administration drug safety communication, based on an evaluation of long-term clinical trials of patients with cardiovascular disease or stroke treated with clopidogrel, concluded that long-term clopidogrel treatment did not increase the risk of all-cause death or cancer-related death.49 The primary analysis by the ERC of 11 RCTs (including OPTIDUAL) compared use of DAPT for 18 to 48 months with use of DAPT for 6 to 12 months in patients who had received predominantly newer-generation DES and found no statistically significant difference in all-cause mortality rate.30A majority of writing group members believe the data as a whole do not seem to suggest prolonged DAPT results in increased mortality.3. Overriding Concepts and Recommendations for DAPT and Duration of Therapy3.1. General Overriding ConceptsOverriding concepts and relevant recommendations for DAPT and duration of therapy are summarized in Table 3. Intensification of antiplatelet therapy, with the addition of a P2Y12 inhibitor to aspirin monotherapy, necessitates a fundamental tradeoff between decreasing ischemic risk and increasing bleeding risk.40,41,50–52 Similarly, longer compared with shorter duration of DAPT generally results in decreased ischemic risk at the expense of increased bleeding risk.16,24,28,30,46 Use of more potent P2Y12 inhibitors (ticagrelor or prasugrel) in place of clopidogrel also results in decreased ischemic risk and increased bleeding risk.53–55Table 3. Overriding Concepts and Updated Recommendations for DAPT and DurationIntensifi

There is increasing interest in utilizing novel markers of cardiovascular disease risk, and consequently, there is a need to assess the value of their use. This scientific statement reviews current concepts of risk evaluation and proposes standards for the critical appraisal of risk assessment methods. An adequate evaluation of a novel risk marker requires a sound research design, a representative at-risk population, and an adequate number of outcome events. Studies of a novel marker should report the degree to which it adds to the prognostic information provided by standard risk markers. No single statistical measure provides all the information needed to assess a novel marker, so measures of both discrimination and accuracy should be reported. The clinical value of a marker should be assessed by its effect on patient management and outcomes. In general, a novel risk marker should be evaluated in several phases, including initial proof of concept, prospective validation in independent populations, documentation of incremental information when added to standard risk markers, assessment of effects on patient management and outcomes, and ultimately, cost-effectiveness.

HomeCirculationVol. 113, No. 1ACC/AHA/SCAI 2005 Guideline Update for Percutaneous Coronary Intervention—Summary Article Free AccessReview ArticlePDF/EPUBAboutView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toFree AccessReview ArticlePDF/EPUBACC/AHA/SCAI 2005 Guideline Update for Percutaneous Coronary Intervention—Summary ArticleA Report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (ACC/AHA/SCAI Writing Committee to Update the 2001 Guidelines for Percutaneous Coronary Intervention) WRITING COMMITTEE MEMBERS Sidney C. SmithJr, MD, FACC, FAHA, Chair, Ted E. Feldman, MD, FACC, FSCAI, John W. HirshfeldJr, MD, FACC, FSCAI, Alice K. Jacobs, MD, FACC, FAHA, FSCAI, Morton J. Kern, MD, FACC, FAHA, FSCAI, Spencer B. KingIII, MD, MACC, FSCAI, Douglass A. Morrison, MD, PhD, FACC, FSCAI, William W. O'Neill, MD, FACC, FSCAI, Hartzell V. Schaff, MD, FACC, FAHA, Patrick L. Whitlow, MD, FACC, FAHA, David O. Williams, MD, FACC, FAHA, FSCAI, Elliott M. Antman, TASK FORCE MEMBERS:, MD, FACC, FAHA, Chair, Sidney C. SmithJr, MD, FACC, FAHA, Vice-Chair, Cynthia D. Adams, MSN, APRN-BC, FAHA, Jeffrey L. Anderson, MD, FACC, FAHA, David P. Faxon, MD, FACC, FAHA, Valentin Fuster, MD, PhD, FACC, FAHA, FESC, Jonathan L. Halperin, MD, FACC, FAHA, Loren F. Hiratzka, MD, FACC, FAHA, Sharon Ann Hunt, MD, FACC, FAHA, Alice K. Jacobs, MD, FACC, FAHA, Rick Nishimura, MD, FACC, FAHA, Joseph P. Ornato, MD, FACC, FAHA, Richard L. Page, MD, FACC, FAHA and Barbara Riegel, DNSc, RN, FAHA WRITING COMMITTEE MEMBERS , Sidney C. SmithJrSidney C. SmithJr , Ted E. FeldmanTed E. Feldman , John W. HirshfeldJrJohn W. HirshfeldJr , Alice K. JacobsAlice K. Jacobs , Morton J. KernMorton J. Kern , Spencer B. KingIIISpencer B. KingIII , Douglass A. MorrisonDouglass A. Morrison , William W. O'NeillWilliam W. O'Neill , Hartzell V. SchaffHartzell V. Schaff , Patrick L. WhitlowPatrick L. Whitlow , David O. WilliamsDavid O. Williams , Elliott M. AntmanElliott M. Antman , Sidney C. SmithJrSidney C. SmithJr , Cynthia D. AdamsCynthia D. Adams , Jeffrey L. AndersonJeffrey L. Anderson , David P. FaxonDavid P. Faxon , Valentin FusterValentin Fuster , Jonathan L. HalperinJonathan L. Halperin , Loren F. HiratzkaLoren F. Hiratzka , Sharon Ann HuntSharon Ann Hunt , Alice K. JacobsAlice K. Jacobs , Rick NishimuraRick Nishimura , Joseph P. OrnatoJoseph P. Ornato , Richard L. PageRichard L. Page and Barbara RiegelBarbara Riegel Originally published3 Jan 2006https://doi.org/10.1161/CIRCULATIONAHA.105.170815Circulation. 2006;113:156–175The American College of Cardiology/American Heart Association/Society for Cardiovascular Angiography and Interventions (ACC/AHA/SCAI) 2005 Guideline Update for Percutaneous Coronary Intervention (PCI) contains changes in the recommendations, along with supporting text. For the purpose of comparison, this summary contains a list of the updated recommendations (middle column) alongside a list of the 2001 recommendations (left column), with each set accompanied by a comment (right column) that provides the rationale for the changes, additions, or deletions (see Table 1). References that support either the 2001 recommendations that have changed or the new or revised recommendations are cited in parentheses at the end of each recommendation or comment. A list of abbreviations is included in the Appendix. The reader is referred to the full-text guideline posted on the World Wide Web sites of the ACC, the AHA, and the SCAI for a more detailed explanation of the changes discussed here. Please note that we have changed the table of contents headings in the 2001 ACC/AHA Guidelines for Percutaneous Coronary Intervention from roman numerals to unique identifying numbers. 2001 Recommendation2005 New or Revised RecommendationComments3. Outcomes3.2 Acute Outcome: Procedural ComplicationsClass IClass INoneAll patients who have signs or symptoms suggestive of MI during or after PCI and those with complicated procedures should have CK-MB and troponin I or T measured after the procedure. (Level of Evidence: B)This recommendation appeared in the text of the 2001 revision for CK-MB only. Troponin I or T measurement has been added, and it is now listed as a class I, level of evidence B recommendation (1–10).Class IIaClass IIaNoneRoutine measurement of cardiac biomarkers (CK-MB and/or troponin I or T) in all patients undergoing PCI is reasonable 8 to 12 hours after the procedure. (Level of Evidence: C)Routine measurement of CK-MB or troponin I or T is added as a new class IIa, level of evidence C recommendation. The committee did not think that evidence regarding the clinical utility of routine measurement of biomarkers in all patients was strong enough to warrant a class I recommendation.4. Institutional and Operator Competency4.1 Quality AssuranceClass IClass INone1. An institution that performs PCI should establish an ongoing mechanism for valid peer review of its quality and outcomes. Review should be conducted both at the level of the entire program and at the level of the individual practitioner. Quality-assessment reviews should take risk adjustment, statistical power, and national benchmark statistics into consideration. Quality-assessment reviews should include both tabulation of adverse event rates for comparison with benchmark values and case review of complicated procedures and some uncomplicated procedures. (Level of Evidence: C)Quality assurance is an important responsibility for all institutions in which PCI is performed. Institutions must monitor the PCI program with respect to process, appropriateness, and outcomes and correct any circumstances in which quality falls below accepted norms. The quality assessment should be conducted at the level of both the entire program and the individual practitioner.2. An institution that performs PCI should participate in a recognized PCI data registry for the purpose of benchmarking its outcomes against current national norms. (Level of Evidence: C)Participation in a recognized PCI registry for benchmarking outcomes against current national norms is an important part of the quality-improvement process. The ACC–National Cardiovascular Data Registry® or other databases may serve as a valuable resource in this regard.4.2 Operator and Institutional VolumeClass IClass IPCI done by operators with acceptable volume (greater than or equal to 75) at high-volume centers (greater than 400). (Level of Evidence: B)1. Elective PCI should be performed by operators with acceptable annual volume (at least 75 procedures) at high-volume centers (more than 400 procedures) with on-site cardiac surgery. (Level of Evidence: B)Wording has been added to clarify this statement and emphasize that it relates to elective PCI performed at centers with on-site cardiac surgery.2. Elective PCI should be performed by operators and institutions whose historical and current risk-adjusted outcomes statistics are comparable to those reported in contemporary national data registries. (Level of Evidence: C)This recommendation was added to emphasize that historical and current risk-adjusted outcomes for operators and institutions are an essential part of the quality-improvement process.3. Primary PCI for STEMI should be performed by experienced operators who perform more than 75 elective PCI procedures per year and, ideally, at least 11 PCI procedures for STEMI per year. Ideally, these procedures should be performed in institutions that perform more than 400 elective PCIs per year and more than 36 primary PCI procedures for STEMI per year. (Level of Evidence: B)This recommendation is expanded based on data from the New York State registry indicating that physicians performing more than 10 primary PCI procedures per year have lower mortality rates (11–13).Class IIaClass IIa1. PCI done by operators with acceptable volume (75 or more) at low-volume centers (200–400). (Level of Evidence: C)1. It is reasonable that operators with acceptable volume (at least 75 PCI procedures per year) perform PCI at low-volume centers (200 to 400 PCI procedures per year) with on-site cardiac surgery. (Level of Evidence: B)Wording has been changed to comply with current recommended phrasing for class IIa recommendation. The fact that this recommendation applies to centers with on-site cardiac surgery is emphasized. Level of evidence has been changed to B based on accumulated published evidence (14).2001 Recommendation2005 New or Revised RecommendationComments2. PCI done by low-volume operators (fewer than 75) at high-volume centers (more than 400). Note: Ideally operators with an annual procedure volume less than 75 should only work at institutions with an activity level of more than 600 procedures/year.* (Level of Evidence: C)2. It is reasonable that low-volume operators (fewer than 75 PCI procedures per year) perform PCI at high-volume centers (more than 400 PCI procedures per year) with on-site cardiac surgery. Ideally, operators with an annual procedure volume less than 75 should only work at institutions with an activity level of more than 600 procedures per year. Operators who perform fewer than 75 procedures per year should develop a defined mentoring relationship with a highly experienced operator who has an annual procedural volume of at least 150 procedures per year. (Level of Evidence: B)Wording has been changed to comply with current recommended phasing. Level of evidence has been changed to B based on accumulated published evidence (15).*Operators who perform fewer than 75 procedures per year should develop a defined mentoring relationship with a highly experienced operator who has an annual procedural volume of at least 150 procedures per year.Class IIbClass IIbNoneThe benefit of primary PCI for STEMI patients eligible for fibrinolysis when performed by an operator who performs fewer than 75 procedures per year (or fewer than 11 PCIs for STEMI per year) is not well established. (Level of Evidence: C)This recommendation has been added to address the issue of low-volume operators performing primary PCI. It reflects the relative lack of evidence supporting a benefit of primary PCI for low-volume operators.Class IIIClass IIIPCI done by low-volume operators (fewer than 75) at low-volume centers (200–400). Note: An institution with a volume of fewer than 200 procedures/year, unless in a region that is underserved because of geography, should carefully consider whether it should continue to offer service.* (Level of Evidence: C)It is not recommended that elective PCI be performed by low-volume operators (fewer than 75 procedures per year) at low-volume centers (200 to 400) with or without on-site cardiac surgery. An institution with a volume of fewer than 200 procedures per year, unless in a region that is underserved because of geography, should carefully consider whether it should continue to offer this service. (Level of Evidence: B)Wording has been changed to reflect current preferred phrasing. Level of evidence changed to B on the basis of published data indicating poorer outcomes at low-volume centers (15).* Operators who perform fewer than 75 procedures per year should develop a defined mentoring relationship with a highly experienced operator who has an annual procedural volume of at least 150 procedures per year.4.3. Role of On-Site Cardiac Surgical Back-upClass IClass I1. Patients undergoing elective PCI in facilities with on-site cardiac surgery. (Level of Evidence: B)1. Elective PCI should be performed by operators with acceptable annual volume (at least 75 procedures per year) at high-volume centers (more than 400 procedures annually) that provide immediately available on-site emergency cardiac surgical services. (Level of Evidence: B)Phrasing has been changed to reflect current terminology and volume criteria; otherwise, no significant changes.2. Patients undergoing primary PCI in facilities with on-site cardiac surgery. (Level of Evidence: B)2. Primary PCI for patients with STEMI should be performed in facilities with on-site cardiac surgery. (Level of Evidence: B)Phrasing has been changed to reflect current terminology and to be consistent with the ACC/AHA Guidelines for the Management of Patients With ST-Elevation Myocardial Infarction.Class IIIClass IIIPatients undergoing elective PCI in facilities without on-site cardiac surgery. (Level of Evidence: C)Elective PCI should not be performed at institutions that do not provide on-site cardiac surgery. * (Level of Evidence: C)Phrasing has been changed to reflect current terminology. As with many dynamic areas in interventional cardiology, these recommendations may be subject to revision as clinical data and experience increase.*Several centers have reported satisfactory results based on careful case selection with well-defined arrangements for immediate transfer to a surgical program (18–28). A small, but real fraction of patients undergoing elective PCI will experience a life-threatening complication that could be managed with the immediate on-site availability of cardiac surgical support but cannot be managed effectively by urgent transfer. Wennberg et al. found higher mortality in the Medicare database for patients undergoing elective PCI in institutions without onsite cardiac surgery (29). These recommendations may be subject to revision as clinical data and experience increase.2001 Recommendation2005 New or Revised RecommendationCommentsSection 4.4 Primary PCI for STEMI Without On-Site Cardiac SurgeryClass IIbClass IIbPatients undergoing primary PCI in facilities without on-site cardiac surgery, but with a proven plan for rapid access (within 1 h) to a cardiac surgery operating room in a nearby facility with appropriate hemodynamic support capability for transfer. The procedure should be limited to patients with ST-segment elevation MI or new LBBB on ECG, and done in a timely fashion (balloon inflation within 90 plus or minus 30 min of admission) by persons skilled in the procedure (at least 75 PCIs/year) and only at facilities performing a minimum of 36 primary PCI procedures per year. (Level of Evidence: B)Primary PCI for patients with STEMI might be considered in hospitals without on-site cardiac surgery, provided that appropriate planning for program development has been accomplished, including appropriately experienced physician operators (more than 75 total PCIs and, ideally, at least 11 primary PCIs per year for STEMI), an experienced catheterization team on a 24 hours per day, 7 days per week call schedule, and a well-equipped catheterization laboratory with digital imaging equipment, a full array of interventional equipment, and intra-aortic balloon pump capability, and provided that there is a proven plan for rapid transport to a cardiac surgery operating room in a nearby hospital with appropriate hemodynamic support capability for transfer. The procedure should be limited to patients with STEMI or MI with new or presumably new LBBB on ECG and should be performed in a timely fashion (goal of balloon inflation within 90 minutes of presentation) by persons skilled in the procedure (at least 75 PCIs per year) and at hospitals that perform a minimum of 36 primary PCI procedures per year. (Level of Evidence: B)Phrasing has been changed to reflect current terminology. Recommendations have been added that 1) physicians perform at least 11 primary PCIs per year for STEMI, 2) a 24 hours per day, 7 days per week call schedule be maintained, and 3) the catheterization laboratory be well equipped with digital imaging equipment, a full array of interventional equipment, and intra-aortic balloon pump capability. The intent is to ensure optimal experience availability and capability to perform primary PCI in patients with STEMI (16,17).Class IIIClass IIIPatients undergoing primary PCI in facilities without on-site cardiac surgery and without a proven plan for rapid access (within 1 h) to a cardiac surgery operating room in a nearby facility with appropriate hemodynamic support capability for transfer or when performed by lower-skilled operators (fewer than 75 PCIs per year) in a facility performing fewer than 36 primary PCI procedures per year. (Level of Evidence: C)Primary PCI should not be performed in hospitals without on-site cardiac surgery and without a proven plan for rapid transport to a cardiac surgery operating room in a nearby hospital or without appropriate hemodynamic support capability for transfer. (Level of Evidence: C)Phrasing has been changed to reflect current terminology and to place emphasis on need for inter-institutional planning and support.4.5 Elective PCI Without On-Site SurgeryClass IIIClass IIIPatients undergoing elective PCI in facilities without on-site cardiac surgery. (Level of Evidence: C)Elective PCI should not be performed at institutions that do not provide on-site cardiac surgery. (Level of Evidence: C) *Several centers have reported satisfactory results based on careful case selection with well-defined arrangements for immediate transfer to a surgical program (18–28). A small, but real fraction of patients undergoing elective PCI will experience a life-threatening complication that could be managed with the immediate on-site availability of cardiac surgical support but cannot be managed effectively by urgent transfer. Wennberg et al. found higher mortality in the Medicare database for patients undergoing elective PCI in institutions without onsite cardiac surgery (29). These recommendations may be subject to revision as clinical data and experience increase.Repeated from previous section for consistency. Phrasing has been changed to reflect current terminology.5.1. Patients With Asymptomatic Ischemia or Canadian Cardiovascular Society (CCS) Class I or II AnginaClass IClass IIaPatients who do not have treated diabetes with asymptomatic ischemia or mild angina with 1 or more significant lesions in 1 or 2 coronary arteries suitable for PCI with a high likelihood of success and a low risk of morbidity and mortality. The vessels to be dilated must subtend a large area of viable myocardium. (Level of Evidence: B)1. PCI is reasonable in patients with asymptomatic ischemia or CCS class I or II angina and with 1 or more significant lesions in 1 or 2 coronary arteries suitable for PCI with a high likelihood of success and a low risk of morbidity and mortality. The vessels to be dilated must subtend a moderate to large area of viable myocardium or be associated with a moderate to severe degree of ischemia on noninvasive testing. (Level of Evidence: B)Phrasing has been changed to reflect current terminology. This recommendation and all of those that follow in Section 5 have been reworded to be consistent with the CCS classification system of angina. This recommendation has been changed to class IIa to reflect the published data and Writing Committee consensus that not all patients in this clinical category must have PCI performed (30,31).Class IIa1. The same clinical and anatomic requirements for Class I, except the myocardial area at risk is of moderate size or the patient has treated diabetes. (Level of Evidence: B)This recommendation has been merged with other class IIa recommendations of this section, and the phrasing has been changed to reflect current terminology.2001 Recommendation2005 New or Revised RecommendationComments2. PCI is reasonable for patients with asymptomatic ischemia or CCS class I or II angina, and recurrent stenosis after PCI with a large area of viable myocardium or high-risk criteria on noninvasive testing. (Level of Evidence: C)This is a new recommendation dealing with the management of recurrent stenosis after PCI among patients with asymptomatic ischemia or class I or II angina.3. Use of PCI is reasonable in patients with asymptomatic ischemia or CCS class I or II angina with significant left main CAD (greater than 50% diameter stenosis) who are candidates for revascularization but are not eligible for CABG. (Level of Evidence: B)This recommendation for PCI among patients who are eligible for CABG who have significant left main disease has been added to reflect the favorable results noted by several trials with PCI (32–35).Class IIbPatients with asymptomatic ischemia or mild angina with greater than or equal to 3 coronary arteries suitable for PCI with a high likelihood of success and a low risk of morbidity and mortality. The vessels to be dilated must subtend at least a moderate area of viable myocardium. In the physician's judgment, there should be evidence of myocardial ischemia by ECG exercise testing, stress nuclear imaging, stress echocardiography or ambulatory ECG monitoring or intracoronary physiologic measurements. (Level of Evidence: B)This recommendation has been eliminated and replaced by the following 2 recommendations. For each, the phrasing has been constructed to reflect current terminology.Class IIb1. The effectiveness of PCI for patients with asymptomatic ischemia or CCS class I or II angina who have 2- or 3-vessel disease with significant proximal LAD CAD who are otherwise eligible for CABG with 1 arterial conduit and who have treated diabetes or abnormal LV function is not well established. (Level of Evidence: B)Phrasing has been changed to reflect current terminology. Among patients who are eligible, CABG with 1 arterial conduit is generally preferred for treatment of multivessel disease with significant proximal LAD obstruction in patients with treated diabetes and/or abnormal LV function (36).2. PCI might be considered for patients with asymptomatic ischemia or CCS class I or II angina with nonproximal LAD CAD that subtends a moderate area of viable myocardium and demonstrates ischemia on noninvasive testing. (Level of Evidence: C)Phrasing has been changed to reflect current terminology. PCI might be considered in this clinical setting.Class IIIClass IIIPatients with asymptomatic ischemia or mild angina who do not meet the criteria as listed under Class I or Class II and who have:PCI is not recommended in patients with asymptomatic ischemia or CCS class I or II angina who do not meet the criteria as listed under the class II recommendations or who have 1 or more of the following:Phrasing has been changed to reflect current terminology. Recommendation has been reworded to be consistent with CCS classification system for angina. Level of evidence has been added for each subgroup. a. Only a small area of viable myocardium at risk a. Only a small area of viable myocardium at risk (Level of Evidence: C) b. No objective evidence of ischemia b. No objective evidence of ischemia (Level of Evidence: C) c. Lesions that have a low likelihood of successful dilatation c. Lesions that have a low likelihood of successful dilatation (Level of Evidence: C) d. Mild symptoms that are unlikely to be due to myocardial ischemia d. Mild symptoms that are unlikely to be due to myocardial ischemia (Level of Evidence: C) e. Factors associated with increased risk of morbidity or mortality e. Factors associated with increased risk of morbidity or mortality (Level of Evidence: C) f. Left main disease f. Left main disease and eligibility for CABG (Level of Evidence: C) g. Insignificant disease less than 50% (Level of Evidence: C) g. Insignificant disease (less than 50% coronary stenosis) (Level of Evidence: C)5.2 Patients With CCS Class III AnginaClass IClass IIaPatients with 1 or more significant lesions in 1 or more coronary arteries suitable for PCI with a high likelihood of success and low risk of morbidity or mortality. The vessel(s) to be dilated must subtend a moderate or large area of viable myocardium and have high risk. (Level of Evidence: B)1. It is reasonable that PCI be performed in patients with CCS class III angina and single-vessel or multivessel CAD who are undergoing medical therapy and who have 1 or more significant lesions in 1 or more coronary arteries suitable for PCI with a high likelihood of success and low risk of morbidity or mortality. (Level of Evidence: B)Phrasing has been changed to reflect current terminology. Recommendation has been reworded to be consistent with CCS classification system for angina. The recommendation class has been changed to IIa to reflect published data and Writing Committee consensus. Criteria regarding viable and high-risk myocardium have been deleted from this recommendation (30, 31).2001 Recommendation2005 New or Revised RecommendationCommentsClass IIaPatients with focal saphenous vein graft lesions or multiple stenoses who are poor candidates for reoperative surgery. (Level of Evidence: C)2. It is reasonable that PCI be performed in patients with CCS class III angina with single-vessel or multivessel CAD who are undergoing medical therapy with focal saphenous vein graft lesions or multiple stenoses who are poor candidates for reoperative surgery. (Level of Evidence: C)Phrasing has been changed to reflect current terminology.3. Use of PCI is reasonable in patients with CCS class III angina with significant left main CAD (greater than 50% diameter stenosis) who are candidates for revascularization but are not eligible for CABG. (Level of Evidence: B)This recommendation for PCI among patients with significant left main disease who are not eligible for CABG has been added to reflect the favorable results noted by several trials with PCI (32–35).Class IIbClass IIbPatient has 1 or more lesions to be dilated with reduced likelihood of success or the vessel(s) subtend a less than moderate area of viable myocardium. Patients with 2- or 3-vessel disease, with significant proximal LAD CAD and treated diabetes or abnormal LV function. (Level of Evidence: B)1. PCI may be considered in patients with CCS class III angina with single-vessel or multivessel CAD who are undergoing medical therapy and who have 1 or more lesions to be dilated with a reduced likelihood of success. (Level of Evidence: B)Phrasing has been changed to reflect current terminology. The 2001 recommendation has been split into 2 separate recommendations.2. PCI may be considered in patients with CCS class III angina and no evidence of ischemia on noninvasive testing or who are undergoing medical therapy and have 2- or 3-vessel CAD with significant proximal LAD CAD and treated diabetes or abnormal LV function. (Level of Evidence: B)Phrasing has been changed to reflect current terminology. The use of noninvasive testing to evaluate for evidence of ischemia has been added.Class IIIClass IIIPatient has no evidence of myocardial injury or ischemia on objective testing and has not had a trial of medical therapy, or hasPCI is not recommended for patients with CCS class III angina with single-vessel or multivessel CAD, no evidence of myocardial injury or ischemia on objective testing, and no trial of medical therapy, or who have 1 of the following:Phrasing has been changed to reflect current terminology. Class III recommendations #2 and #3 from the 2001 guidelines have been merged into this recommendation. a. Only a small area of myocardium at risk a. Only a small area of myocardium at risk (Level of Evidence: C) b. All lesions or the culprit lesion to be dilated with morphology with a low likelihood of success b. All lesions or the culprit lesion to be dilated with morphology that conveys a low likelihood of success (Level of Evidence: C) c. A high risk of procedure-related morbidity or mortality. (Level of Evidence: C) c. A high risk of procedure-related morbidity or mortality (Level of Evidence: C) d. Insignificant disease (less than 50% coronary stenosis) (Level of Evidence: C) e. Significant left main CAD and candidacy for CABG (Level of Evidence: C)2. Patients with insignificant coronary stenosis (e.g., less than 50% diameter). (Level of Evidence: C)See above.3. Patients with significant left main CAD who are candidates for CABG. (Level of Evidence: B)See above.5.3 Unstable Angina/Non–ST-Elevation Myocardial Infarction (UA/NSTEMI)(Note: Some of these recommendations have been repeated from above because the sections for the 2005 guideline were revised slightly.)Class IAn early invasive PCI strategy is indicated for patients with UA/NSTEMI who have no serious comorbidity and who have coronary lesions amenable to PCI. Patients must have any of the following high-risk features:Added to maintain consistency with the ACC/AHA 2002 Guideline Update for the Management of Patients With Unstable Angina and Non–ST-Segment Myocardial Infarction (37). a. Recurrent ischemia despite intensive anti-ischemic therapy (Level of Evidence: A) b. Elevated troponin level (Level of Evidence: A) c. New ST-segment depression (Level of Evidence: A) d. CHF symptoms or new or worsening MR (Level of Evidence: A) e. Depressed LV systolic function (Level of Evidence: A) f. Hemodynamic instability (Level of Evidence: A) g. Sustained ventricular tachycardia (Level of Evidence: A) h. PCI within 6 months (Level of Evidence: A) i. Prior CABG (Level of Evidence: A)2001 Recommendation2005 New or Revised RecommendationCommentsClass IIaClass IIa1. Patients with focal saphenous vein graft lesions or multiple stenoses who are poor candidates for reoperative surgery. (Level of Evidence: C)1. It is reasonable that PCI be performed in patients with UA/NSTEMI and single-vessel or multivessel CAD who are undergoing medical therapy with focal saphenous vein graft lesions or multiple stenoses who are poor candidates for reoperative surgery. (Level of Evidence: C)Phrasing has been changed to reflect current terminology.2. In the absence of high-risk features associated with UA/NSTEMI, it is reasonable to perform PCI in patients with amenable lesions and no contraindication for PCI wit

References 1331 The American College of Cardiology (ACC)/American Heart Association (AHA) Task Force on Practice Guidelines regularly reviews existing guidelines to determine when an update or full revision is needed. Guidelines for the Clinical Use of Cardiac Radionuclide Imaging were originally

Preamble…1757 I. Introduction…1758 II. General Considerations Regarding Coronary Angiography…1759 A. Definitions…1759 B. Purpose…1759 C. Morbidity and Mortality…1760 D. Relative Contraindications…1760 E. Utilization…1761 F. Costs…1763 G. Cost-Effectiveness…1764

Atrial fibrillation (AF), the most common sustained cardiac rhythm disturbance, is increasing in prevalence as the population ages. Although it is often associated with heart disease, AF occurs in many patients with no detectable disease. Hemodynamic impairment and thromboembolic events result in significant morbidity, mortality, and cost. Accordingly, the American College of Cardiology (ACC), the American Heart Association (AHA), and the European Society of Cardiology (ESC) created a committee of experts to establish guidelines for management of this arrhythmia. The committee was composed of 8 members representing the ACC and AHA, 4 representing the ESC, 1 from the North American Society of Pacing and Electrophysiology (NASPE), and a representative of the Johns Hopkins University Evidence-Based Practice Center representing the Agency for Healthcare Research and Quality’s report on Atrial Fibrillation in the Elderly. This document was reviewed by 3 official reviewers nominated by the ACC, 3 nominated by the AHA, and 3 nominated by the ESC, as well as by the ACC Clinical Electrophysiology Committee, the AHA ECG and Arrhythmia Committee, NASPE, and 25 reviewers nominated by the writing committee. The document was approved for publication by the governing bodies of the ACC, AHA, and ESC and officially endorsed by NASPE. These guidelines will be reviewed annually by the task force and will be considered current unless the task force revises or withdraws them from distribution. The committee conducted a comprehensive review of the literature from 1980 to June 2000 relevant to AF using the following databases: PubMed/Medline, EMBASE, the Cochrane Library (including the Cochrane Database of Systematic Reviews and the Cochrane Controlled Trials Registry), and Best Evidence. Searches were limited to English language sources and to human subjects. ### A. Atrial Fibrillation AF is a supraventricular tachyarrhythmia characterized by uncoordinated atrial activation with consequent deterioration of atrial mechanical function. On the electrocardiogram (ECG), AF …

### Preamble ### Preamble It is important that the medical profession play a significant role in critically evaluating the use of diagnostic procedures and therapies in the management or prevention of disease states. Rigorous and expert analysis of the available data documenting relative benefits

These guidelines represent an update of those published in 1996 and are intended for physicians who are involved in the preoperative, operative, and postoperative care of patients undergoing noncardiac surgery. They provide a framework for considering cardiac risk of noncardiac surgery in a variety of patient and surgical situations. The overriding theme of these guidelines is that preoperative intervention is rarely necessary simply to lower the risk of surgery unless such intervention is indicated irrespective of the preoperative context. The purpose of preoperative evaluation is not simply to give medical clearance but rather to perform an evaluation of the patient’s current medical status; make recommendations concerning the evaluation, management, and risk of cardiac problems over the entire perioperative period; and provide a clinical risk profile that the patient, primary physician, anesthesiologist, and surgeon can use in making treatment decisions that may influence short- and long-term cardiac outcomes. The goal of the consultation is to identify the most appropriate testing and treatment strategies to optimize care of the patient, provide assessment of both short- and long-term cardiac risk, and avoid unnecessary testing in this era of cost containment. ### A. Development of Guidelines These guidelines are based on an update of a Medline, EMBASE, Cochrane library, and Best Evidence search of the English literature from 1995 through 2000, a review of selected journals, and the expert opinions of 12 committee members representing various disciplines of cardiovascular care, including general cardiology, interventional cardiology, noninvasive testing, vascular medicine, vascular surgery, anesthesiology, and arrhythmia management. As a result of these searches, more than 400 relevant new articles were identified. In addition, draft guidelines were submitted for critical review and amendment to the executive officers representing the American College of Cardiology (ACC) and the American Heart Association (AHA). A large proportion of the data used to develop these guidelines are …

HomeCirculationVol. 120, No. 222009 Focused Updates: ACC/AHA Guidelines for the Management of Patients With ST-Elevation Myocardial Infarction (Updating the 2004 Guideline and 2007 Focused Update) and ACC/AHA/SCAI Guidelines on Percutaneous Coronary Intervention (Updating the 2005 Guideline and 2007 Focused Update) Free AccessReview ArticlePDF/EPUBAboutView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissionsDownload Articles + Supplements ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toSupplemental MaterialFree AccessReview ArticlePDF/EPUB2009 Focused Updates: ACC/AHA Guidelines for the Management of Patients With ST-Elevation Myocardial Infarction (Updating the 2004 Guideline and 2007 Focused Update) and ACC/AHA/SCAI Guidelines on Percutaneous Coronary Intervention (Updating the 2005 Guideline and 2007 Focused Update)A Report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines Frederick G. Kushner, MD, FACC, FAHA, FSCAI, Co-Chair, Mary Hand, MSPH, RN, FAHA, Co-Chair, Sidney C. SmithJr, MD, FACC, FAHA, Chair, Spencer B. KingIII, MD, MACC, FSCAI, Co-Chair, Jeffrey L. Anderson, MD, FACC, FAHA, Elliott M. Antman, MD, FACC, FAHA, Steven R. Bailey, MD, FACC, FSCAI, Eric R. Bates, MD, FACC, FAHA, James C. Blankenship, MD, FACC, FSCAI, Donald E. CaseyJr, MD, MPH, MBA, Lee A. Green, MD, MPH, Judith S. Hochman, MD, FACC, FAHA, Alice K. Jacobs, MD, FACC, FAHA, FSCAI, Harlan M. Krumholz, MD, SM, FACC, FAHA, Douglass A. Morrison, MD, PhD, FACC, FSCAI, Joseph P. Ornato, MD, FACC, FAHA, David L. Pearle, MD, FACC, FAHA, Eric D. Peterson, MD, MPH, FACC, FAHA, Michael A. Sloan, MD, MS, FACC, FAHA, Patrick L. Whitlow, MD, FACC, FAHA and David O. Williams, MD, FACC, FAHA, FSCAI Frederick G. KushnerFrederick G. Kushner Search for more papers by this author , Mary HandMary Hand Search for more papers by this author , Sidney C. SmithJrSidney C. SmithJr Search for more papers by this author , Spencer B. KingIIISpencer B. KingIII Search for more papers by this author , Jeffrey L. AndersonJeffrey L. Anderson Search for more papers by this author , Elliott M. AntmanElliott M. Antman Search for more papers by this author , Steven R. BaileySteven R. Bailey Search for more papers by this author , Eric R. BatesEric R. Bates Search for more papers by this author , James C. BlankenshipJames C. Blankenship Search for more papers by this author , Donald E. CaseyJrDonald E. CaseyJr Search for more papers by this author , Lee A. GreenLee A. Green Search for more papers by this author , Judith S. HochmanJudith S. Hochman Search for more papers by this author , Alice K. JacobsAlice K. Jacobs Search for more papers by this author , Harlan M. KrumholzHarlan M. Krumholz Search for more papers by this author , Douglass A. MorrisonDouglass A. Morrison Search for more papers by this author , Joseph P. OrnatoJoseph P. Ornato Search for more papers by this author , David L. PearleDavid L. Pearle Search for more papers by this author , Eric D. PetersonEric D. Peterson Search for more papers by this author , Michael A. SloanMichael A. Sloan Search for more papers by this author , Patrick L. WhitlowPatrick L. Whitlow Search for more papers by this author and David O. WilliamsDavid O. Williams Search for more papers by this author Originally published18 Nov 2009https://doi.org/10.1161/CIRCULATIONAHA.109.192663Circulation. 2009;120:2271–2306is corrected byCorrectionOther version(s) of this articleYou are viewing the most recent version of this article. Previous versions: November 18, 2009: Previous Version 1 2009 STEMI and PCI Focused Updates…2273Preamble…2273 1. Introduction…2274 1.1. Methodology and Evidence Review…2274 1.2. Organization of Committee and Relationships With Industry and Other Entities…2275 1.3. Document Review and Approval…2275STEMI and PCI Focused Update Section…2276 2. Recommendations for the Use of Glycoprotein IIb/IIIa Receptor Antagonists…2276 2.1. Glycoprotein IIb/IIIa Receptor Antagonists…2276 3. Recommendations for the Use of Thienopyridines…2277 3.1. Thienopyridines…2277 3.1.1. Additional Thienopyridine Information…2280 3.1.2. Choice of Thienopyridine for PCI in STEMI…2281 3.2. Proton Pump Inhibitors and Dual-Antiplatelet Therapy for ACS…2281 4. Recommendations for the Use of Parenteral Anticoagulants…2282 4.1. Parenteral Anticoagulants…2282 5. Recommendations for Triage and Transfer for PCI…2283 5.1. Triage and Transfer for PCI…2283 5.1.1. STEMI Patients Who Are Candidates for Reperfusion…2283 6. Recommendations for Intensive Glucose Control in STEMI…2286 6.1. Intensive Glucose Control…2286 7. Recommendation for Thrombus Aspiration During PCI for STEMI…2287 7.1. Thrombus Aspiration…2287 8. Recommendations for the Use of Stents in STEMI…2288 8.1. Stent Selection for STEMI…2288PCI Focused Update Section…2289 9. Recommendation for Angiography in Patients With Chronic Kidney Disease…2289 9.1. Angiography in Patients With Chronic Kidney Disease…2289 10. Recommendations for Use of Fractional Flow Reserve…2289 10.1. Fractional Flow Reserve…2289 11. Recommendations for PCI for Unprotected Left Main Coronary Artery Disease…2290 11.1. Unprotected Left Main Coronary Artery Disease…2290 12. Recommendations for the Timing of Angiography and Antiplatelet Therapy in UA/NSTEMI…2292 12.1. Timing of Angiography…2292 12.2. Timing of GP IIb/IIIa Receptor Antagonist Therapy in UA/NSTEMI Patients Undergoing Angiography…2292Appendix 1. Author Relationships With Industry and Other Entities—ST-Elevation Myocardial Infarction…2294Appendix 2. Author Relationships With Industry and Other Entities—Percutaneous Coronary Intervention…2295Appendix 3. Reviewer Relationships With Industry and Other Entities—2009 STEMI and PCI Focused Updates…2296Appendix 4. Dosing Table for Antiplatelet and Anticoagulant Therapy Discussed in This Focused Update to Support PCI in STEMI…2299Appendix 5. Triage and Transfer for PCI…2301Appendix 6. Outcomes of PCI Versus CABG for Unprotected Left Main Coronary Artery Disease…2301References…23022009 STEMI and PCI Focused UpdatesPreambleA primary challenge in the development of clinical practice guidelines is keeping pace with the stream of new data on which recommendations are based. In an effort to respond promptly to new evidence, the American College of Cardiology Foundation/American Heart Association (ACCF/AHA) Task Force on Practice Guidelines has created a “focused update” process to revise the existing guideline recommendations that are affected by evolving data or opinion. Before the initiation of this focused approach, periodic updates and revisions of existing guidelines required up to 3 years to complete. Now, however, new evidence will be reviewed in an ongoing fashion to more efficiently respond to important science and treatment trends that could have a major impact on patient outcomes and quality of care. Evidence will be reviewed at least twice a year, and updates will be initiated on an as-needed basis as quickly as possible, while maintaining the rigorous methodology that the ACCF and AHA have developed during their 25 years of partnership.These updated guideline recommendations reflect a consensus of expert opinion after a thorough review primarily of late-breaking clinical trials identified through a broad-based vetting process as being important to the relevant patient population, as well as a review of other new data deemed to have an impact on patient care (see Section 1.1, Methodology and Evidence Review, for details). This focused update is not intended to represent an update based on a full literature review from the date of the previous guideline publication. Specific criteria/considerations for inclusion of new data include the following: publication in a peer-reviewed journal;large randomized, placebo-controlled trial(s);nonrandomized data deemed important on the basis of results that affect current safety and efficacy assumptions;strength/weakness of research methodology and findings;likelihood of additional studies influencing current findings;impact on current performance measure(s) and/or likelihood of need to develop new performance measure(s);requests and requirements for review and update from the practice community, key stakeholders, and other sources free of relationships with industry or other potential bias;number of previous trials showing consistent results; andneed for consistency with a new guideline or guideline revision.In analyzing the data and developing updated recommendations and supporting text, the focused update writing group used evidence-based methodologies developed by the ACCF/AHA Task Force on Practice Guidelines, which are described elsewhere.1The schema for classification of recommendations and level of evidence is summarized in Table 1, which also illustrates how the grading system provides an estimate of the size of the treatment effect and an estimate of the certainty of the treatment effect. Note that a recommendation with level of evidence B or C does not imply that the recommendation is weak. Many important clinical questions addressed in guidelines do not lend themselves to clinical trials. Although randomized trials may not be available, there may be a very clear clinical consensus that a particular test or therapy is useful and effective. Both the classification of recommendations and level of evidence listed in the focused updates are based on consideration of the evidence reviewed in previous iterations of the guideline and the focused update. Of note, the implications of older studies that have informed recommendations but have not been repeated in contemporary settings are considered carefully. Download figureDownload PowerPointTable 1. Applying Classification of Recommendations and Level of Evidence*Data available from clinical trials or registries about the usefulness/efficacy in different subpopulations, such as gender, age, history of diabetes, history of prior myocardial infarction, history of heart failure, and prior aspirin use. A recommendation with Level of Evidence B or C does not imply that the recommendation is weak. Many important clinical questions addressed in the guidelines do not lend themselves to clinical trials. Even though randomized trials are not available, there may be a very clear clinical consensus that a particular test or therapy is useful or effective.†In 2003, the ACCF/AHA Task Force on Practice Guidelines developed a list of suggested phrases to use when writing recommendations. All guideline recommendations have been written in full sentences that express a complete thought, such that a recommendation, even if separated and presented apart from the rest of the document (including headings above sets of recommendations), would still convey the full intent of the recommendation. It is hoped that this will increase readers’ comprehension of the guidelines and will allow queries at the individual recommendation level.The ACCF/AHA practice guidelines address patient populations (and healthcare providers) residing in North America. As such, drugs that are not currently available in North America are discussed in the text without a specific class of recommendation. For studies performed in large numbers of subjects outside of North America, each writing group reviews the potential impact of different practice patterns and patient populations on the treatment effect and on the relevance to the ACCF/AHA target population to determine whether the findings should inform a specific recommendation.The ACCF/AHA practice guidelines are intended to assist healthcare providers in clinical decision making by describing a range of generally acceptable approaches for the diagnosis, management, and prevention of specific diseases or conditions. The guidelines attempt to define practices that meet the needs of most patients in most circumstances. The ultimate judgment regarding care of a particular patient must be made by the healthcare provider and patient in light of all the circumstances presented by that patient. Thus, there are circumstances in which deviations from these guidelines may be appropriate. Clinical decision making should consider the quality and availability of expertise in the area where care is provided. These guidelines may be used as the basis for regulatory or payer decisions, but the ultimate goals are quality of care and serving the patient’s best interests.Prescribed courses of treatment in accordance with these recommendations are effective only if they are followed by the patient. Because a lack of patient adherence may adversely affect treatment outcomes, healthcare providers should engage the patient in active participation with the prescribed treatment.The ACCF/AHA Task Force on Practice Guidelines makes every effort to avoid actual, potential, or perceived conflicts of interest that may arise as a result of industry relationships or personal interests among the writing committee. Specifically, all members of the writing committee, as well as reviewers of the document, are asked to disclose all such relevant relationships pertaining to the trials and other evidence under consideration (see Appendixes 1, 2, and 3). All guideline recommendations require a confidential vote by the writing group and must be approved by a consensus of the members voting. Members who recused themselves from voting are noted on the title page of this document. Members must recuse themselves from voting on any recommendations to which their relationships with industry and other entities apply. Writing group members who did not participate are not listed as authors of this focused update. The work of the writing group was supported exclusively by the ACCF and AHA without commercial support. Writing group members volunteered their time for this effort.With the exception of the recommendations presented here, the full-text guidelines remain current.2,3 Only the recommendations from the affected section(s) of the full-text guidelines are included in this focused update. Recommendations from any section of a guideline affected by a change are presented with notation as to whether they are new or have been modified; however, recommendations that remain unchanged in each section are not included in this focused update. When evidence affects recommendations in more than 1 set of guidelines, those guidelines are updated concurrently whenever possible.The recommendations in this focused update will be considered current until they are superseded by another focused update or the full-text guidelines are revised. This focused update is published in the December 1, 2009, issues of the Journal of the American College of Cardiology and Circulation as an update to the full-text guideline, and it is also posted on the American College of Cardiology (ACC; www.acc.org), AHA (my.americanheart.org), and Society for Cardiovascular Angiography and Interventions (SCAI; scai.org) World Wide Web sites.Alice K. Jacobs, MD, FACC, FAHAChair, ACCF/AHA Task Force on Practice Guidelines1. Introduction1.1. Methodology and Evidence ReviewLate-breaking clinical trials presented at the 2007 and 2008 annual scientific meetings of the ACC, AHA, Transcatheter Cardiovascular Therapeutics, the European Society of Cardiology, and the 2009 annual scientific sessions of the ACC were reviewed by the standing guideline writing committee along with the parent Task Force and other experts to identify those trials and other key data that may impact guideline recommendations. On the basis of the criteria/considerations noted above, recent trial data and other clinical information were considered important enough to prompt a focused update of the ACC/AHA 2004 Guidelines for the Management of Patients With ST-Elevation Myocardial Infarction and the ACC/AHA 2005 Guidelines for Percutaneous Coronary Intervention, inclusive of their respective 2007 focused updates.2–5The ST-elevation myocardial infarction (STEMI) and percutaneous coronary intervention (PCI) writing groups together considered the following studies: Two meta-analyses, “A Comparison of Abciximab and Small Molecule Glycoprotein IIb/IIIa Inhibitors in Patients Undergoing Primary Percutaneous Coronary Intervention,”6 and “Benefits From Small Molecule Administration as Compared With Abciximab Among Patients With ST-Segment Elevation Myocardial Infarction Treated With Primary Angioplasty,”7 FINESSE (Facilitated PCI in Patients With ST-Elevation Myocardial Infarction),8 the HORIZONS-AMI (Harmonizing Outcomes With Revascularization and Stents in Acute Myocardial Infarction),9 BRAVE-3 (Bavarian Reperfusion Alternatives Evaluation-3),10 MULTISTRATEGY (Multicentre Evaluation of Single High-Dose Bolus Tirofiban Versus Abciximab With Sirolimus-Eluting Stent or Bare Metal Stent in Acute Myocardial Infarction Study),11 ON-TIME 2 (Ongoing Tirofiban in Myocardial Infarction Evaluation),12 TRITON-TIMI 38 (Trial to Assess Improvement in Therapeutic Outcomes by Optimizing Platelet Inhibition With Prasugrel–Thrombolysis in Myocardial Infarction),13 TRANSFER-AMI (Trial of Routine ANgioplasty and Stenting after Fibrinolysis to Enhance Reperfusion in Acute Myocardial Infarction),14 CARESS-in-AMI (Combined Abciximab Reteplase Stent Study in Acute Myocardial Infarction),15 NICE-SUGAR (Normoglycemia in Intensive Care Evaluation—Survival Using Glucose Algorithm Regulation),16 TAPAS (Thrombus Aspiration during Percutaneous coronary intervention in Acute myocardial infarction Study),17 and EXPIRA (Thrombectomy With Export Catheter in Infarct-Related Artery During Primary Percutaneous Coronary Intervention).18 Additionally, the PCI writing group considered the CARE (Cardiac Angiography in Renally Impaired Patients),19 FAME (Fractional Flow Reserve versus Angiography for Multivessel Evaluation) study,20 SYNTAX (Synergy Between Percutaneous Intervention With Taxus and Cardiac Surgery),21 Early ACS (Early versus Delayed, Provisional Eptifibatide in Acute Coronary Syndromes),22 and TIMACS (Timing of Intervention in Patients With Acute Coronary Syndromes) studies.23 When considering the new data for this focused update, the writing group faced the task of weighing evidence from studies that had enrolled large numbers of subjects outside North America. Although noting that practice patterns and the rigor applied to data collection, as well as the genetic makeup of subjects, may influence the observed magnitude of a treatment’s effect, the writing group believed the data were relevant to the formulation of recommendations for management of STEMI and PCI in North America. The writing group also notes that the AHA/ACCF and the Heart Rhythm Society have published updated recommendations for the standardization and interpretation of the electrocardiogram with a separate section on acute ischemia/infarction.24To provide clinicians with a comprehensive set of data, whenever possible, the exact event rates in various treatment arms of clinical trials are presented to permit calculation of the absolute risk difference and number needed to treat (NNT) or harm; the relative treatment effects are described either as odds ratio, relative risk (RR), or hazard ratio (HR) depending on the format used in the original publication. Along with all other statistical point estimates, the confidence interval (CI) for those statistics are added when available.Consult the full-text or executive summary versions of the ACC/AHA 2004 Guidelines for the Management of Patients With ST-Elevation Myocardial Infarction or the ACC/AHA/SCAI 2005 Guidelines for Percutaneous Coronary Intervention, as well as their respective 2007 focused updates, for policy on clinical areas not covered by the present focused update.2–5 Unchanged recommendations from previous iterations of the guidelines are not listed in this document and remain current policy. Individual recommendations updated in this focused update will be incorporated into future revisions of the full-text guidelines.1.2. Organization of Committee and Relationships With Industry and Other EntitiesFor this focused update, all members of the 2004 STEMI guideline, 2007 STEMI focused update, 2005 PCI guideline, and 2007 PCI focused update writing committees were invited to participate; those who agreed (referred to as the 2009 Focused Update Writing Group) were required to disclose all relationships with industry and other entities relevant to the data under consideration. The policies used for relationships with industry were those in effect at the initial meeting of this committee, which included disclosure of relationships 12 months prior to initiation and a chair with no relevant relationships except in a situation where more than one chair is named. In this circumstance, one chair will have no relevant relationships and the other may have relationships. Each recommendation required a confidential vote by the writing group members before and after external review of the document. Any writing group member with a relationship with industry relevant to the recommendation was recused from voting on that recommendation. The PCI writing group included 2 representatives from SCAI.1.3. Document Review and ApprovalThis document was reviewed by 3 official reviewers nominated by the ACCF and 4 official reviewers nominated by the AHA, 1 official reviewer nominated by the SCAI, 6 reviewers from the ACCF Interventional Council, 2 reviewers from the ACCF Imaging Council, and 22 content reviewers. All reviewer information on relationships with industry and other entities was collected and distributed to the writing committee and is published in Appendix 3. This document was approved for publication by the governing bodies of the ACCF, the AHA, and the SCAI (specifically, the PCI portion of the guideline).STEMI and PCI Focused Update Section2. Recommendations for the Use of Glycoprotein IIb/IIIa Receptor Antagonists(See Table 2 and Appendix 4.) Table 2. Recommendations for the Use of Glycoprotein IIb/IIIa Receptor Antagonists2004/2005/2007 Recommendations: 2004 STEMI Guideline Section 6.3.1.6.8.2.3; Also 2005 PCI Guideline Section 6.2.22009 Joint STEMI/PCI Focused Update RecommendationsCommentsClass IIa1. It is reasonable to start treatment with abciximab as early as possible before primary PCI (with or without stenting) in patients with STEMI. (Level of Evidence: B)1. It is reasonable to start treatment with glycoprotein IIb/IIIa receptor antagonists (abciximab9,11 [Level of Evidence: A], tirofiban11,12 [Level of Evidence: B] or eptifibatide6,7,9 [Level of Evidence: B]) at the time of primary PCI (with or without stenting) in selected patients with STEMI.Modified recommendation (class of recommendation changed from IIb to IIa for tirofiban and eptifibatide).Class IIb1. Treatment with tirofiban or eptifibatide may be considered before primary PCI (with or without stenting) in patients with STEMI. (Level of Evidence: C)1. The usefulness of glycoprotein IIb/IIIa receptor antagonists (as part of a preparatory pharmacological strategy for patients with STEMI before their arrival in the cardiac catheterization laboratory for angiography and PCI) is uncertain.8,10 (Level of Evidence: B)Modified recommendation (text modified; level of evidence changed from C to B).2.1. Glycoprotein IIb/IIIa Receptor AntagonistsIn considering the use of intravenous glycoprotein (GP) IIb/IIIa receptor antagonists for STEMI, the writing group noted that much of the evidence favoring the use of these agents was established in the era before dual oral antiplatelet therapy and largely by placebo-controlled comparisons. Contemporary management of STEMI patients involves a complex array of antithrombotics, including dual oral antiplatelet therapy (aspirin [acetylsalicylic acid; ASA] plus a thienopyridine) and an anticoagulant. There is a paucity of trials adequately powered for assessment of clinical end points that have reevaluated the current relative role of intravenous GP IIb/IIIa receptor antagonists with respect to other pharmacological therapy in STEMI patients. Accordingly, a reevaluation of the value of GP IIb/IIIa antagonists in STEMI is appropriate, but the ability to draw definitive conclusions is limited.At least 3 trials evaluated GP IIb/IIIa antagonists as adjuncts to oral antiplatelet therapy in the setting of primary PCI. The findings of these trials question whether GP IIb/IIIa antagonists provide significant additional benefit to STEMI patients who have received dual-antiplatelet therapy before catheterization. In the BRAVE-3 study, 800 patients presenting within 24 hours of a STEMI were pretreated with 600 mg of clopidogrel and then randomly assigned in a double-blind manner to receive either abciximab or placebo in the intensive care unit before being sent for PCI.10 The primary end point was infarct size measured by single photon emission computed tomography before hospital discharge. At 30 days, the composite of death, recurrent myocardial infarction (MI), stroke, or urgent revascularization of the infarct-related artery was not significantly different in the 2 groups (abciximab 5%, placebo 3.8%; 95% CI 0.7 to 2.6; P=0.4). There was no significant difference in infarct size or major bleeding.ON-TIME 2 was a randomized, placebo-controlled, multicenter European trial that included 491 patients receiving high-dose tirofiban and 493 receiving placebo within a median of 76 minutes from onset of symptoms.12 Patients receiving high-dose tirofiban (25 mcg/kg bolus followed by 0.15 mcg/kg per min for 18 hours) at first medical contact before transport for primary PCI were also treated with unfractionated heparin (UFH; 5000 U), clopidogrel (600 mg), and ASA. Patients in the high-dose tirofiban group had improved ST-segment resolution (primary end point) before and 1 hour after PCI (P=0.003) compared with those receiving placebo (NNT=100). However, there was no significant difference in Thrombolysis In Myocardial Infarction (TIMI) grade 3 flow or blush grade and no significant difference in major bleeding or minor bleeding. There was no significant difference in death, recurrent MI, or urgent target-vessel revascularization (TVR) between the tirofiban and placebo groups at 30 days.25In the HORIZONS-AMI trial,9 patients undergoing primary PCI for STEMI were randomized to treatment with UFH plus a GP IIb/IIIa receptor antagonist (abciximab or double-bolus eptifibatide) or to bivalirudin alone with provisional IIb/IIIa. Aspirin and a thienopyridine were administered before catheterization. (See the full discussion of the trial under Section 4, Recommendations for the Use of Parenteral Anticoagulants.) Seven hundred fifty-seven of the 1661 patients who received UFH received a double bolus of eptifibatide and infusion, whereas 53 of 1661 in the bivalirudin arm received eptifibatide. At 30 days, rates of major bleeding and total adverse events were higher among patients treated with GP IIb/IIIa antagonists and heparin than among those given bivalirudin alone.Two meta-analyses of randomized trials were published that compared small-molecule GP IIb/IIIa antagonists with abciximab in STEMI patients undergoing primary PCI.6,7 In each case, there was no statistically significant difference in 30-day mortality, reinfarction, or major TIMI bleeding, and there was no significant difference in death or reinfarction at 8 months between groups. There was also no statistically significant difference in postprocedural TIMI flow grade 3 or ST-segment resolution. On the basis of these studies, the present writing group judged that the totality of evidence indicates that the various GP IIb/IIIa antagonists demonstrate similar effectiveness in the setting of primary PCI.MULTISTRATEGY was an open-label, multicenter, randomized European trial with a 2-by-2 factorial design that randomized 745 STEMI patients undergoing primary PCI to high-dose bolus tirofiban versus abciximab infusion and sirolimus-eluting stent versus bare-metal stent (BMS).11 The prespecified primary end points were the achievement of 50% resolution of ST-segment elevation at 90 minutes after PCI, powered for noninferiority, and the rate of major adverse cardiac events (MACE) at 8 months, powered for superiority. All patients received ASA at the usual doses, clopidogrel 300 mg orally then 75 mg per day, and UFH. There was a similar rate of at least 50% ST-segment resolution at 90 minutes after primary PCI with abciximab and tirofiban (RR 1.020; 97.5% CI 0.958 to 1.086; P=0.001 for noninferiority). Rates of MACE, including all-cause death, clinical reinfarction, or TVR, and hemorrhagic (major and minor bleeding) complications were similar. The incidence of severe or moderate thrombocytopenia was more common with abciximab than with tirofiban (4.0% versus 0.8%, P=0.004).In an analysis of the predictors of stent thrombosis after primary PCI in acute MI presented at the 2009 ACC Scientific Sessions, titled “Predictors of Stent Thrombosis After Primary Angioplasty in Acute Myocardial Infarction: The HORIZONS-AMI Trial,”69 there was no significant difference in the 1-year rate of stent thrombosis with the heparin plus GP IIb/IIIa receptor antagonists compared with eptifibatide and abciximab (3.6% versus 2.8%, P=0.93), which suggests that eptifibatide has the same impact as abciximab on stent thrombosis incidence.One investigation, FINESSE, addressed the issue of timing of GP IIb/IIIa antagonist administration. This double-blind, randomized, placebo-controlled study of 2453 patients with STEMI explored the use of pre-PCI treatment with a half-dose fibrinolytic agent plus abciximab, pr

A link between oral health and cardiovascular disease has been proposed for more than a century. Recently, concern about possible links between periodontal disease (PD) and atherosclerotic vascular disease (ASVD) has intensified and is driving an active field of investigation into possible association and causality. The 2 disorders share several common risk factors, including cigarette smoking, age, and diabetes mellitus. Patients and providers are increasingly presented with claims that PD treatment strategies offer ASVD protection; these claims are often endorsed by professional and industrial stakeholders. The focus of this review is to assess whether available data support an independent association between ASVD and PD and whether PD treatment might modify ASVD risks or outcomes. It also presents mechanistic details of both PD and ASVD relevant to this topic. The correlation of PD with ASVD outcomes and surrogate markers is discussed, as well as the correlation of response to PD therapy with ASVD event rates. Methodological issues that complicate studies of this association are outlined, with an emphasis on the terms and metrics that would be applicable in future studies. Observational studies to date support an association between PD and ASVD independent of known confounders. They do not, however, support a causative relationship. Although periodontal interventions result in a reduction in systemic inflammation and endothelial dysfunction in short-term studies, there is no evidence that they prevent ASVD or modify its outcomes.

Preamble......971 I. Introduction ......972 A. Organization of Committee and Evidence Review......972 B. Purpose of These Guidelines......973 C. Overview of the Acute Coronary Syndrome......973 1. Definition of Terms......973 2. Pathogenesis of UA/NSTEMI ......974 3. Presentations of

HomeCirculationVol. 98, No. 18Guidelines for the Management of Patients With Valvular Heart Disease

The previous guideline for the use of echocardiography was published in March 1997. Since that time, there have been significant advances in the technology of echocardiography and growth in its clinical use and in the scientific evidence leading to recommendations for its proper use. Each section has been reviewed and updated in evidence tables, and where appropriate, changes have been made in recommendations. A new section on the use of intraoperative transesophageal echocardiography (TEE) is being added to update the guidelines published by the American Society of Anesthesiologists and the Society of Cardiovascular Anesthesiologists. There are extensive revisions, especially of the sections on ischemic heart disease; congestive heart failure, cardiomyopathy, and assessment of left ventricular (LV) function; and screening and echocardiography in the critically ill. There are new tables of evidence and extensive revisions in the ischemic heart disease evidence tables. Because of space limitations, only those sections and evidence tables with new recommendations will be printed in this summary article. Where there are minimal changes in a recommendation grouping, such as a change from Class IIa to Class I, only that change will be printed, not the entire set of recommendations. Advances for which the clinical applications are still being investigated, such as the use of myocardial contrast agents and three-dimensional echocardiography, will not be discussed. The original recommendations of the 1997 guideline are based on a Medline search of the English literature from 1990 to May 1995. The original search yielded more than 3000 references, which the committee reviewed. For this guideline update, literature searching was conducted in Medline, EMBASE, Best Evidence, and the Cochrane Library for English-language meta-analyses and systematic reviews from 1995 through September 2001. Further searching was conducted for new clinical trials on the following topics: echocardiography in adult congenital heart disease, echocardiography for evaluation …

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HomeCirculationVol. 106, No. 16ACC/AHA/NASPE 2002 Guideline Update for Implantation of Cardiac Pacemakers and Antiarrhythmia Devices: Summary Article Free AccessReview ArticlePDF/EPUBAboutView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toFree AccessReview ArticlePDF/EPUBACC/AHA/NASPE 2002 Guideline Update for Implantation of Cardiac Pacemakers and Antiarrhythmia Devices: Summary ArticleA Report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (ACC/AHA/NASPE Committee to Update the 1998 Pacemaker Guidelines) Committee Members Gabriel Gregoratos, Jonathan Abrams, Andrew E. Epstein, Roger A. Freedman, David L. Hayes, Mark A. Hlatky, Richard E. Kerber, Gerald V. Naccarelli, Mark H. Schoenfeld, Michael J. Silka, Stephen L. Winters, Raymond J. Gibbons, Elliott M. Antman, Joseph S. Alpert, Gabriel Gregoratos, Loren F. Hiratzka, David P. Faxon, Alice K. Jacobs, Valentin Fuster and Sidney C. SmithJr Committee Members , Gabriel GregoratosGabriel Gregoratos , Jonathan AbramsJonathan Abrams , Andrew E. EpsteinAndrew E. Epstein , Roger A. FreedmanRoger A. Freedman , David L. HayesDavid L. Hayes , Mark A. HlatkyMark A. Hlatky , Richard E. KerberRichard E. Kerber , Gerald V. NaccarelliGerald V. Naccarelli , Mark H. SchoenfeldMark H. Schoenfeld , Michael J. SilkaMichael J. Silka , Stephen L. WintersStephen L. Winters , Raymond J. GibbonsRaymond J. Gibbons , Elliott M. AntmanElliott M. Antman , Joseph S. AlpertJoseph S. Alpert , Gabriel GregoratosGabriel Gregoratos , Loren F. HiratzkaLoren F. Hiratzka , David P. FaxonDavid P. Faxon , Alice K. JacobsAlice K. Jacobs , Valentin FusterValentin Fuster and Sidney C. SmithJrSidney C. SmithJr Originally published15 Oct 2002https://doi.org/10.1161/01.CIR.0000035996.46455.09Circulation. 2002;106:2145–2161The current update of the ACC/AHA/NASPE Guidelines for Implantation of Cardiac Pacemakers and Antiarrhythmia Devices includes several significant changes in the recommendations and in the supporting narrative portion. In this summary, we list the updated recommendations along with the respective 1998 recommendations, each one accompanied by a brief comment outlining the rationale for the changes, additions, or deletions. All new or revised recommendations are listed in the second column and appear in boldface type. References that support either the 1998 recommendations that have not changed or the new or revised recommendations are noted in parentheses at the end of each recommendation. The reader is referred to the full-text version of the guidelines posted on the American College of Cardiology (ACC), American Heart Association (AHA), and North American Society for Pacing and Electrophysiology (NASPE) World Wide Web sites for a more detailed exposition of the rationale for these changes. In addition to the recommendation changes listed here, this update includes an expanded section on the selection of pacemakers and implantable cardioverter-defibrillators (ICDs) that reflects the technical advances that have taken place since 1998. A brief expanded summary of pacemaker follow-up procedures is also new to these guidelines. For both of these expanded sections, the reader is referred to the online full-text version.In preparing this update, the committee was guided by the following principles: Changes in recommendations and levels of evidence were made either because of new randomized trials or because of the accumulation of new clinical evidence and the development of clinical consensus.The committee is cognizant of the healthcare, logistic, and financial implications of recent trials and factored in these considerations in arriving at the class level of certain recommendations.Minor wording changes were made to render some recommendations more precise.The committee wishes to re-emphasize that the recommendations in the guideline apply to most patients but may require modification by existing situations that only the primary treating physician can evaluate properly.All of the listed recommendations for implantation of a device presume the absence of inciting causes that may be eliminated without detriment to the patient (eg, nonessential drug therapy).The committee endeavored to maintain consistency of recommendations in this and other previously published guidelines. In the section on atrioventricular (AV) block associated with acute myocardial infarction (AMI), the recommendations follow closely those in the ACC/AHA Guideline for the Management of Patients With Acute Myocardial Infarction.1 However, given the rapid evolution of pacemaker/ICD science, it has not always been possible to maintain consistency with other guidelines. An example of such a discrepancy can be found in Section I-H, in which the recommendation for biventricular pacing in selected patients with heart failure has been listed under Class IIa, whereas in the ACC/AHA Guideline for the Evaluation and Management of Chronic Heart Failure in the Adult,2 biventricular pacing is cited as an investigational procedure.The ACC/AHA classifications I, II, and III are used to summarize indications as follows:Class I: Conditions for which there is evidence and/or general agreement that a given procedure or treatment is useful and effective.Class II: Conditions for which there is conflicting evidence and/or a divergence of opinion about the usefulness/efficacy of a procedure or treatment.IIa: Weight of evidence/opinion is in favor of usefulness/efficacy.IIb: Usefulness/efficacy is less well established by evidence/opinion.Class III: Conditions for which there is evidence and/or general agreement that the procedure/treatment is not useful/effective and in some cases may be harmful.The weight of the evidence was ranked highest (A) if the data were derived from multiple randomized clinical trials that involved large numbers of patients and intermediate (B) if the data were derived from a limited number of randomized trials that involved small numbers of patients or from careful analyses of nonrandomized studies or observational registries. A lower rank (C) was given when expert consensus was the primary basis for the recommendation. 1998 Recommendation2002 New or Revised RecommendationsCommentsSECTION I-A: PACING FOR ACQUIRED ATRIOVENTRICULAR BLOCK IN ADULTSRecommendations for Permanent Pacing in Acquired Atrioventricular Block in AdultsClass IClass IClass I 1. Third-degree AV block at any anatomic level, associated with any one of the following conditions: 1. Third-degree and advanced second-degree AV block at any anatomic level, associated with any one of the following conditions: The changes emphasize the importance of the site of the block and introduce "advanced second-degree AV block" as a class I indication. This recommendation is based on several observational studies and is supported by a wealth of clinical experience. The narrative portion of this section also emphasizes that the site of origin of the escape rhythm in cases of advanced AV block is as important (or more important) than the escape rate itself. a. Bradycardia with symptoms presumed to be due to AV block. (Level of Evidence: C) a. Bradycardia with symptoms (including heart failure) presumed to be due to AV block. (Level of Evidence: C) b. Arrhythmias and other medical conditions that require drugs that result in symptomatic bradycardia. (Level of Evidence: C) b. (No change) c. Documented periods of asystole greater than or equal to 3.0 seconds or any escape rate less than 40 beats per minute (bpm) in awake, symptom-free patients. (Level of Evidence: B, C) c. Documented periods of asystole greater than or equal to 3.0 seconds (3) or any escape rate less than 40 beats per minute (bpm) in awake, symptom-free patients (4,5). (Levels of Evidence: B, C) In recommendation 1a, heart failure is specifically introduced as a major symptom that merits consideration when dealing with AV block–induced bradycardia. d. After catheter ablation of the AV junction. (Level of Evidence: B, C) There are no trials to assess outcome without pacing, and pacing is virtually always planned in this situation unless the operative procedure is AV junction modification. d. After catheter ablation of the AV junction. (Levels of Evidence: B, C) There are no trials to assess outcome without pacing, and pacing is virtually always planned in this situation unless the operative procedure is AV junction modification (6,7). In recommendation 1e, "cardiac surgery" was added to specifically define the situation(s) in which this recommendation applies. Recommendation 1f has been amplified to indicate that pacing therapy is recommended in patients with neuromuscular diseases and e. Postoperative AV block that is not expected to resolve. (Level of Evidence: C) e. Postoperative AV block that is not1998 Recommendation2002 New or Revised RecommendationsComments f. Neuromuscular diseases with AV block such as myotonic muscular dystrophy, Kearns-Sayre syndrome, Erb's dystrophy (limb-girdle), and peroneal muscular atrophy. (Level of Evidence: B)expected to resolve after cardiac surgery. (Level of Evidence: C) (8–10) f. Neuromuscular diseases with AV block, such as myotonic muscular dystrophy, Kearns-Sayre syndrome, Erb's dystrophy (limb-girdle), and peroneal muscular atrophy, with or without symptoms, because there may be unpredictable progression of AV conduction disease. (Level of Evidence: B) (11–17)third-degree AV block whether or not they are symptomatic, in view of the unpredictable progression of AV conduction in this group of diseases. 2. Second-degree AV block regardless of type or site of block, with associated symptomatic bradycardia. (Level of Evidence: B) (18) No changeClass IIaClass IIaClass IIa 1. Asymptomatic third-degree AV block at any anatomic site with average awake ventricular rates of 40 bpm or faster. (Level of Evidence: B, C) 1. Asymptomatic third-degree AV block at any anatomic site with average awake ventricular rates of 40 bpm or faster especially if cardiomegaly or left ventricular (LV) dysfunction is present. (Levels of Evidence: B, C) This change introduces the concept that cardiomegaly and LV dysfunction are important considerations in the decision-making process to implant a pacemaker in asymptomatic patients with third-degree AV block and otherwise "acceptable" heart rates. 2. Asymptomatic type II second-degree AV block. (Level of Evidence: B) 2. Asymptomatic type II second-degree AV block with a narrow QRS. When type II second-degree AV block occurs with a wide QRS, pacing becomes a Class I recommendation (see next section regarding Pacing for Chronic Bifascicular and Trifascicular Block). (Level of Evidence: B) (19,20) Based on reports and clinical experience, the change in this recommendation calls attention to the site of the block and emphasizes that a wide QRS complex in patients with type II second-degree AV block suggests the presence of diffuse conduction system disease and constitutes an indication for pacing therapy even in asymptomatic patients. 3. Asymptomatic type I second-degree AV block at intra- or infra-His levels found incidentally at electrophysiological study performed for other indications. (Level of Evidence: B) 3. Asymptomatic type I second-degree AV block at intra- or infra-His levels found at electrophysiological study performed for other indications. (Level of Evidence: B) (18–21) Minor wording change deleting an unnecessary word (incidentally) 4. First-degree AV block with symptoms suggestive of pacemaker syndrome and documented alleviation of symptoms with temporary AV pacing. (Level of Evidence: B) 4. First- or second-degree AV block with symptoms similar to those of pacemaker syndrome. (Level of Evidence: B) (22,23) Wording change to clarify that symptoms resulting from first- or second-degree AV block may be similar to those of the pacemaker syndrome rather than suggestive of this syndrome per se.Class IIbClass IIbClass IIb 1. Marked first-degree AV block (more than 0.30 seconds) in patients with LV dysfunction and symptoms of congestive heart failure in whom a shorter AV interval results in hemodynamic improvement, presumably by decreasing left atrial filling pressure. (Level of Evidence: C) (24) No change 2. Neuromuscular diseases such as myotonic muscular dystrophy, Kearns-Sayre syndrome, Erb's dystrophy (limb-girdle), and peroneal muscular atrophy with any degree of AV block (including first-degree AV block) with or without symptoms, because there may be unpredictable progression of AV conduction disease. (Level of Evidence: B) (11–17) New recommendation for pacemaker insertion in patients with neuromuscular diseases and second- or first-degree AV block, ie, lesser degrees of AV block than those listed under Class I recommendation 1f.1998 Recommendation2002 New or Revised RecommendationsCommentsClass IIIClass IIIClass III 1. Asymptomatic first-degree AV block. (Level of Evidence: B) (25) (See also "Pacing for Chronic Bifascicular and Trifascicular Block") No change 2. Asymptomatic type I second-degree AV block at the supra-His (AV node) level or not known to be intra- or infra-Hisian. (Level of Evidence: B, C) (18) No change 3. AV block expected to resolve and unlikely to recur (26) (eg, drug toxicity, Lyme disease). (Level of Evidence: B) 3. AV block expected to resolve and/or unlikely to recur (26) (eg, drug toxicity, Lyme disease, or during hypoxia in sleep apnea syndrome in absence of symptoms) (Level of Evidence: B) Addition of hypoxia occurring during periods of sleep apnea as a cause of transient AV block that is unlikely to recur once sleep apnea syndrome has been treated.SECTION I-B: PACING FOR CHRONIC BIFASCICULAR AND TRIFASCICULAR BLOCKRecommendations for Permanent Pacing in Chronic Bifascicular and Trifascicular BlockClass IClass IClass I 1. Intermittent third-degree AV block. (Level of Evidence: B) (27–33) No change 2. Type II second-degree AV block. (Level of Evidence: B) (34–36) No change 3. Alternating bundle-branch block. (Level of Evidence: C) (37) New Class I recommendation that adds alternating bundle branch block to the manifestations of fascicular block that indicate pacing therapy. This recommendation was not explicitly stated in the previous version.Class IIaClass IIaClass IIa 1. Syncope not proved to be due to AV block when other likely causes have been excluded, specifically ventricular tachycardia (VT). (Level of Evidence: B) 1. Syncope not demonstrated to be due to AV block when other likely causes have been excluded, specifically ventricular tachycardia (VT). (Level of Evidence: B) (38–55) Change of "proved" to "demonstrated" because it may be very difficult to prove the cause of syncope. 2. Incidental finding at electrophysiological study of markedly prolonged HV interval (greater than or equal to 100 milliseconds) in asymptomatic patients. (Level of Evidence: B) (47) No change 3. Incidental finding at electrophysiological study of pacing-induced infra-His block that is not physiological. (Level of Evidence: B) (54) No changeClass IIbClass IIbClass IIb1. Neuromuscular diseases such as myotonic muscular dystrophy, Kearns-Sayre syndrome, Erb's dystrophy (limb-girdle), and peroneal muscular atrophy with any degree of fascicular block with or without symptoms, because there may be unpredictable progression of AV conduction disease. (Level of Evidence: C) (11–17) New Class IIb recommendation for pacing therapy in patients with neuromuscular diseases and fascicular block. Clinical experience suggests that progression of AV conduction disturbance is unpredictable, and high-grade AV block can develop even in asymptomatic patients with these diseases.Class IIIClass IIIClass III 1. Fascicular block without AV block or symptoms. (Level of Evidence: B) (41,43,46,47) No change 2. Fascicular block with first-degree AV block without symptoms. (Level of Evidence: B) (41,43,46,47) No change1998 Recommendation2002 New or Revised RecommendationsCommentsSECTION I-C: PACING FOR ATRIOVENTRICULAR BLOCK ASSOCIATED WITH ACUTE MYOCARDIAL INFARCTIONRecommendations for Permanent Pacing After the Acute Phase of Myocardial InfarctionClass IClass IClass I 1. Persistent second-degree AV block in the His-Purkinje system with bilateral bundle-branch block or third-degree AV block within or below the His-Purkinje system after AMI. (Level of Evidence: B) (36,56–60) No change 2. Transient advanced (second- or third-degree) infranodal AV block and associated bundle-branch block. If the site of block is uncertain, an electrophysiological study may be necessary. (Level of Evidence: B) (56,57) No change 3. Persistent and symptomatic second- or third-degree AV block. (Level of Evidence: C) No changeClass IIbClass IIbClass IIb 1. Persistent second- or third-degree AV block at the AV node level. (Level of Evidence: B) (20) No changeClass IIIClass IIIClass III 1. Transient AV block in the absence of intraventricular conduction defects. (Level of Evidence: B) (56) No change 2. Transient AV block in the presence of isolated left anterior fascicular block. (Level of Evidence: B) (58) No change 3. Acquired left anterior fascicular block in the absence of AV block.(Level of Evidence: B) (56) No change 4. Persistent first-degree AV block in the presence of bundle-branch block that is old or age indeterminate. (Level of Evidence: B) (56) No change *These recommendations generally follow the ACC/AHA Guidelines for the Management of Patients With Acute Myocardial Infarction (61)SECTION I-D: PACING IN SINUS NODE DYSFUNCTIONRecommendations for Permanent Pacing in Sinus Node DysfunctionClass IClass IClass I 1. Sinus node dysfunction with documented symptomatic bradycardia, including frequent sinus pauses that produce symptoms. In some patients, bradycardia is iatrogenic and will occur as a consequence of essential long-term drug therapy of a type and dose for which there are no acceptable alternatives. (Level of Evidence: C) (5,62,63) No change 2. Symptomatic chronotropic incompetence. (Level of Evidence: C) (5,62–65) No changeClass IIaClass IIaClass IIa 1. Sinus node dysfunction occurring spontaneously or as a result of necessary drug therapy, with heart rate less than 40 bpm when a clear association between significant symptoms consistent with bradycardia and the actual presence of bradycardia has not been documented. (Level of Evidence: C) (4,5,62,63,66,67) No change1998 Recommendation2002 New or Revised RecommendationsComments 2. Syncope of unexplained origin when major abnormalities of sinus node function are discovered or provoked in electrophysiological studies (Level of Evidence: C) (68,69) New Class IIa recommendation for pacing therapy in patients with syncope, no other demonstrable cause, and who were found to have spontaneous or provocable sinus node dysfunction at electrophysiological study.Class IIbClass IIbClass IIb 1. In minimally symptomatic patients, chronic heart rate less than 30 bpm while awake. (Level of Evidence: C) 1. In minimally symptomatic patients, chronic heart rate less than 40 bpm while awake. (Level of Evidence: C) (4,5,62,63,66,67) The change of awake heart rate from 30 to 40 bpm was made on the basis of clinical experience and provides the clinician more flexibility to consider pacing in patients with suspected sinus node dysfunction, in whom a firm diagnosis cannot be made.Class IIIClass IIIClass III 1. Sinus node dysfunction in asymptomatic patients, including those in whom substantial sinus bradycardia (heart rate less than 40 bpm) is a consequence of long-term drug treatment. No change 2. Sinus node dysfunction in patients with symptoms suggestive of bradycardia that are clearly documented as not associated with a slow heart rate. No change 3. Sinus node dysfunction with symptomatic bradycardia due to nonessential drug therapy. No changeSECTION I-E: PREVENTION AND TERMINATION OF TACHYARRHYTHMIAS BY PACINGRecommendations for Permanent Pacemakers That Automatically Detect and Pace to Terminate TachycardiasClass IClass IClass I 1. Symptomatic recurrent supraventricular tachycardia that is reproducibly terminated by pacing after drugs and catheter ablation fail to control the arrhythmia or produce intolerable side effects. (Level of Evidence: C) This recommendation was downgraded from Class I to Class IIa. Committee consensus was that it is highly unlikely that treatment with drugs and/or ablation therapy would fail to control supraventricular tachycardia (SVT) (see below). 2. Symptomatic recurrent sustained VT as part of an automatic defibrillator system. (Level of Evidence: B) Deleted because this indication is dealt with in the ICD section.Class IIaClass IIaClass IIa1. Symptomatic recurrent SVT that is reproducibly terminated by pacing in the unlikely event that catheter ablation and/or drugs fail to control the arrhythmia or produce intolerable side effects. (Level of Evidence: C) (70–74) The rewording of this previously Class I recommendation is intended to convey that ablation and/or drugs are effective therapies for SVT, and it is unlikely that pacing therapy will be required.Class IIbClass IIbClass IIb 1. Recurrent SVT or atrial flutter that is reproducibly terminated by pacing as an alternative to drug therapy or ablation. (Level of Evidence: C) (70–75) No changeClass IIIClass IIIClass III 1. Tachycardias frequently accelerated or converted to fibrillation by pacing. No change 2. The presence of accessory pathways with the capacity for rapid anterograde conduction whether or not the pathways participate in the mechanism of the tachycardia. No change1998 Recommendation2002 New or Revised RecommendationsCommentsSECTION I-E: PREVENTION AND TERMINATION OF TACHYARRHYTHMIAS BY PACINGPacing Recommendations to Prevent TachycardiaClass IClass IClass I 1. Sustained pause-dependent VT, with or without prolonged QT, in which the efficacy of pacing is thoroughly documented. (Level of Evidence: C) (76,77) No changeClass IIaClass IIaClass IIa 1. High-risk patients with congenital long-QT syndrome. (Level of Evidence: C) (76,77) No changeClass IIbClass IIbClass IIb 1. AV re-entrant or AV node re-entrant supraventricular tachycardia not responsive to medical or ablative therapy. (Level of Evidence: C) (71,72,78) No change 2. Prevention of symptomatic, drug refractory, recurrent atrial fibrillation. (Level of Evidence: C)2. Prevention of symptomatic, drug-refractory, recurrent atrial fibrillation in patients with coexisting sinus node dysfunction. (Level of Evidence: B) (79–81) This recommendation was revised and the level of evidence upgraded to "B" to reflect the available information. Several studies suggest that in some patients with recurrent atrial fibrillation and coexisting sinus node dysfunction, atrial-based pacing reduces the recurrence rate of this arrhythmia.Class IIIClass IIIClass III 1. Frequent or complex ventricular ectopic activity without sustained VT in the absence of the long-QT syndrome. No change 2. Long-QT syndrome due to reversible causes. 2. Torsade de Pointes VT due to reversible causes. Wording change because the arrhythmia is the Torsade de Pointes VT and not the long-QT syndrome.SECTION I-F: PACING IN HYPERSENSITIVE CAROTID SINUS AND NEUROCARDIOGENIC SYNCOPERecommendations for Permanent Pacing in Hypersensitive Carotid Sinus Syndrome and Neurocardiogenic SyncopeClass IClass IClass I 1. Recurrent syncope caused by carotid sinus stimulation; minimal carotid sinus pressure induces ventricular asystole of more than 3-second duration in the absence of any medication that depresses the sinus node or AV conduction. (Level of Evidence: C) (82,83) No changeClass IIaClass IIaClass IIa 1. Recurrent syncope without clear, provocative events and with a hypersensitive cardioinhibitory response. (Level of Evidence: C) (82,83) No change 2. Syncope of unexplained origin when major abnormalities of sinus node function or AV conduction are discovered or provoked in electrophysiological studies. (Level of Evidence: C) Deleted from this section and more appropriately placed in the Sinus Node Dysfunction section as Recommendation #2, Class IIa. 3. Significantly symptomatic and recurrent neurocardiogenic syncope associated with bradycardia documented spontaneously or at the time of tilt-table testing. (Level of Evidence: B) (84–87) This recommendation was added to reflect the results of trials that have demonstrated that pacing therapy is effective in cases of vasovagal syncope associated with episodes of spontaneous or provoked bradycardia. The level of evidence was set to "B" to reflect published trials.1998 Recommendation2002 New or Revised RecommendationsCommentsClass IIbClass IIbClass IIb 1. Neurally mediated syncope with significant bradycardia reproduced by a head-up tilt with or without isoproterenol or other provocative maneuvers. (Level of Evidence: B) DeletedClass IIIClass IIIClass III 1. A hyperactive cardioinhibitory response to carotid sinus stimulation in the absence of symptoms.1. A hyperactive cardioinhibitory response to carotid sinus stimulation in the absence of symptoms or in the presence of vague symptoms such as dizziness, lightheadedness, or both. (Level of Evidence: C) This Class III recommendation replaces the prior recommendations #1 and #2 for the sake of simplicity. 2. A hyperactive cardioinhibitory response to carotid sinus stimulation in the presence of vague symptoms such as dizziness, lightheadedness, or both. Deleted 3. Recurrent syncope, lightheadedness, or dizziness in the absence of a hyperactive cardioinhibitory response. (Level of Evidence: C) This becomes #2. 4. Situational vasovagal syncope in which avoidance behavior is effective. (Level of Evidence: C) This becomes #3.SECTION I-G: PACING IN CHILDREN, ADOLESCENTS, AND PATIENTS WITH CONGENITAL HEART DISEASERecommendations for Permanent Pacing in Children, Adolescents, and Patients With Congenital Heart DiseaseClass IClass IClass I 1. Advanced second- or third-degree AV block associated with symptomatic bradycardia, congestive heart failure, or low cardiac output. (Level of Evidence: C)1. Advanced second- or third-degree AV block associated with symptomatic bradycardia, ventricular dysfunction, or low cardiac output. (Level of Evidence: C) This recommendation was reworded, substituting "ventricular dysfunction" for "congestive heart failure" to reflect accumulating clinical experience that ventricular dysfunction adversely affects the prognosis of patients with congenital third-degree AV block even in the absence of overt heart failure. 2. Sinus node dysfunction with correlation of symptoms during age-inappropriate bradycardia. The definition of bradycardia varies with the patient's age and expected heart rate. (Level of Evidence: B) (3,5,88) No change 3. Postoperative advanced second- or third-degree AV block that is not expected to resolve after cardiac surgery. (Level of Evidence: B, C)3. Postoperative advanced second- or third-degree AV block that is not expected to resolve or persists at least 7 days after cardiac surgery. (Level of Evidence: B, C (89,90) Reworded recommendation to specify that AV block that persists for more than 7 days after cardiac surgery is unlikely to resolve and is best treated with the implantation of a pacemaker. The change was made because of accumulating clinical experience and published studies demonstrating adverse prognosis in such patients who did not receive a permanent pacemaker for rate support. 4. Congenital third-degree AV block with a wide QRS escape rhythm or ventricular dysfunction. (Level of Evidence: B)4. Congenital third-degree AV block with a wide QRS escape rhythm, complex ventricular ectopy, or ventricular dysfunction. (Level of Evidence: B) (91–93) "Complex ventricular ectopy" was added to the other elements of this recommendation to reflect growing experience that in this setting, prognosis is adversely affected by such ectopy in the absence of rate support by a permanent pacemaker.1998 Recommendation2002 New or Revised RecommendationsComments 5. Congenital third-degree AV block in the infant with a ventricular rate less than 50 to 55 bpm or with congenital heart disease and a ventricular rate less than 70 bpm. (Level of Evidence: B, C) (92,94) No change 6. Sustained pause-dependent VT, with or without prolonged QT, in which the efficacy of pacing is thoroughly documented. (Level of Evidence: B) (76,77,95,96) No changeClass IIaClass IIaClass IIa 1. Bradycardia-tachycardia syndrome with the need for long-term antiarrhythmic treatment other than digitalis. (Level of Evidence: C) (97,98) No change 2. Congenital third-degree AV block beyond the first year of life with an average heart rate less than 50 bpm or abrupt pauses in ventricular rate that are two or three times the basic cycle length. (Level of Evidence: B)2. Congenital third-degree AV block beyond the first year of life with an average heart rate less than 50 bpm, abrupt pauses in ventricular rate that are two or three times the basic cycle length, or associated with symptoms due to chronotropic incompetence. (Level of Evidence: B) (99) Rewording of this recommendation to include symptoms due to chronotropic incompetence and abrupt pauses in ventricular rate in young patients with third-degree AV block after the first year of life. These events have been found to affect pro

Elliott M. Antman, MD, FACC, FAHA, Chair Daniel T. Anbe, MD, FACC, FAHA Paul W. Armstrong, MD, FACC, FAHA Eric R. Bates, MD, FACC, FAHA Lee A. Green, MD, MPH Mary Hand, MSPH, RN, FAHA Judith S. Hochman, MD, FACC, FAHA Harlan M. Krumholz, MD, FACC, FAHA Frederick G. Kushner, MD, FACC, FAHA

Grundy, Scott M. MD, PhD, Chair; Cleeman, James I. MD, Co-Chair; Daniels, Stephen R. MD, PhD; Donato, Karen A. MS, RD; Eckel, Robert H. MD; Franklin, Barry A. PhD; Gordon, David J. MD PhD, MPH; Krauss, Ronald M. MD; Savage, Peter J. MD; Smith, Sidney C. Jr MD; Spertus, John A. MD; Costa, Fernando MD Author Information

Since the 2006 update of the American Heart Association (AHA)/American College of Cardiology Foundation (ACCF) guidelines on secondary prevention ([1][1]), important evidence from clinical trials has emerged that further supports and broadens the merits of intensive risk-reduction therapies for

HomeCirculationVol. 117, No. 22007 Focused Update of the ACC/AHA/SCAI 2005 Guideline Update for Percutaneous Coronary Intervention Free AccessReview ArticlePDF/EPUBAboutView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toFree AccessReview ArticlePDF/EPUB2007 Focused Update of the ACC/AHA/SCAI 2005 Guideline Update for Percutaneous Coronary InterventionA Report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines: 2007 Writing Group to Review New Evidence and Update the ACC/AHA/SCAI 2005 Guideline Update for Percutaneous Coronary Intervention, Writing on Behalf of the 2005 Writing Committee Spencer B. KingIII, Sidney C. SmithJr, John W. HirshfeldJr, Alice K. Jacobs, Douglass A. Morrison, David O. Williams, 2005 WRITING COMMITTEE MEMBERS Sidney C. SmithJr, Ted E. Feldman, John W. HirshfeldJr, Alice K. Jacobs, Morton J. Kern, Spencer B. KingIII, Douglass A. Morrison, William W. O'Neill, Hartzell V. Schaff, Patrick L. Whitlow, David O. Williams, Sidney C. SmithJr, Alice K. Jacobs, Cynthia D. Adams, Jeffrey L. Anderson, Christopher E. Buller, Mark A. Creager, Steven M. Ettinger, Jonathan L. Halperin, Sharon A. Hunt, Harlan M. Krumholz, Frederick G. Kushner, Bruce W. Lytle, Rick Nishimura, Richard L. Page, Barbara Riegel, Lynn G. Tarkington and Clyde W. Yancy Spencer B. KingIIISpencer B. KingIII , Sidney C. SmithJrSidney C. SmithJr , John W. HirshfeldJrJohn W. HirshfeldJr , Alice K. JacobsAlice K. Jacobs , Douglass A. MorrisonDouglass A. Morrison , David O. WilliamsDavid O. Williams , 2005 WRITING COMMITTEE MEMBERS , Sidney C. SmithJrSidney C. SmithJr , Ted E. FeldmanTed E. Feldman , John W. HirshfeldJrJohn W. HirshfeldJr , Alice K. JacobsAlice K. Jacobs , Morton J. KernMorton J. Kern , Spencer B. KingIIISpencer B. KingIII , Douglass A. MorrisonDouglass A. Morrison , William W. O'NeillWilliam W. O'Neill , Hartzell V. SchaffHartzell V. Schaff , Patrick L. WhitlowPatrick L. Whitlow , David O. WilliamsDavid O. Williams , Sidney C. SmithJrSidney C. SmithJr , Alice K. JacobsAlice K. Jacobs , Cynthia D. AdamsCynthia D. Adams , Jeffrey L. AndersonJeffrey L. Anderson , Christopher E. BullerChristopher E. Buller , Mark A. CreagerMark A. Creager , Steven M. EttingerSteven M. Ettinger , Jonathan L. HalperinJonathan L. Halperin , Sharon A. HuntSharon A. Hunt , Harlan M. KrumholzHarlan M. Krumholz , Frederick G. KushnerFrederick G. Kushner , Bruce W. LytleBruce W. Lytle , Rick NishimuraRick Nishimura , Richard L. PageRichard L. Page , Barbara RiegelBarbara Riegel , Lynn G. TarkingtonLynn G. Tarkington and Clyde W. YancyClyde W. Yancy Originally published13 Dec 2007https://doi.org/10.1161/CIRCULATIONAHA.107.188208Circulation. 2008;117:261–295is corrected byCorrectionOther version(s) of this articleYou are viewing the most recent version of this article. Previous versions: December 13, 2007: Previous Version 1 Preamble…2621. Introduction…264 1.1. Evidence Review…264 1.2. Organization of Committee and Relationships With Industry…264 1.3. Review and Approval…2642. Patients With Unstable Angina/ Non–ST-Elevation Myocardial Infarction…264 2.1. Electrocardiogram…268 2.1.1. Comparison of Early Invasive and Initial Conservative Strategies for UA/NSTEMI…269 2.1.2. Selection for Coronary Angiography…271 2.1.3. Chronic Kidney Disease…2723. Facilitated PCI…2734. Rescue PCI…2755. PCI After Fibrinolysis or for Patients Not Undergoing Primary Reperfusion…2776. Ancillary Therapy for Patients Undergoing PCI for STEMI…2787. Antiplatelet Therapy…2788. Bare-Metal and Drug-Eluting Stents…281 8.1. Selection of a Bare-Metal or Drug-Eluting Stent…2819. Secondary Prevention…283References…288Appendix 1…293Appendix 2…293PreambleA primary challenge in the development of clinical practice guidelines is keeping pace with the stream of new data upon which recommendations are based. In an effort to respond more quickly to new evidence, the American College of Cardiology/American Heart Association (ACC/AHA) Task Force on Practice Guidelines has created a new "focused update" process to revise the existing guideline recommendations that are affected by evolving data or opinion. Before the initiation of this focused approach, periodic updates and revisions of existing guidelines required up to 3 years to complete. Now, however, new evidence will be reviewed in an ongoing fashion to more efficiently respond to important science and treatment trends that could have a major impact on patient outcomes and quality of care. Evidence will be reviewed at least twice a year, and updates will be initiated on an as needed basis as quickly as possible while maintaining the rigorous methodology that the ACC and AHA have developed during their more than 20 years of partnership.These updated guideline recommendations reflect a consensus of expert opinion following a thorough review primarily of late-breaking clinical trials identified through a broad-based vetting process as important to the relevant patient population and of other new data deemed to have an impact on patient care (see Section 1.1 for details regarding this focused update). It is important to note that this focused update is not intended to represent an update based on a full literature review from the date of the previous guideline publication. Specific criteria/considerations for inclusion of new data include: Publication in a peer-reviewed journalLarge, randomized, placebo-controlled trial(s)Nonrandomized data deemed important on the basis of results that impact current safety and efficacy assumptionsStrengths/weakness of research methodology and findingsLikelihood of additional studies influencing current findingsImpact on current performance measure(s) and/or likelihood of the need to develop new performance measure(s)Requests and requirements for review and update from the practice community, key stakeholders, regulatory agencies, and other sources free of relationships with industry or other potential biasNumber of previous trials showing consistent resultsNeed for consistency with other new guidelines or guideline revisionsIn analyzing the data and developing updated recommendations and supporting text, the focused update writing group used evidence-based methodologies developed by the ACC/AHA Task Force on Practice Guidelines, which are described elsewhere.1,2The schema for class of recommendation and level of evidence is summarized in Table 1, which also illustrates how the grading system provides estimates of the size of the treatment effect and the certainty of the treatment effect. Note that a recommendation with Level of Evidence B or C does not imply that the recommendation is weak. Many important clinical questions addressed in guidelines do not lend themselves to clinical trials. Although randomized trials may not be available, there may be a very clear clinical consensus that a particular test or therapy is useful and effective. Both the class of recommendation and level of evidence listed in the focused updates are based on consideration of the evidence reviewed in previous iterations of the guidelines as well as the focused update. Of note, the implications of older studies that have informed recommendations but have not been repeated in contemporary settings are carefully considered. Download figureDownload PowerPointTable 1. Applying Classification of Recommendations and Level of Evidence†*Data available from clinical trials or registries about the usefulness/efficacy in different subpopulations, such as gender, age, history of diabetes, history of prior myocardial infarction, history of heart failure, and prior aspirin use. A recommendation with Level of Evidence B or C does not imply that the recommendation is weak. Many important clinical questions addressed in the guidelines do not lend themselves to clinical trials. Even though randomized trials are not available, there may be a very clear clinical consensus that a particular test or therapy is useful or effective.†In 2003, the ACC/AHA Task Force on Practice Guidelines developed a list of suggested phrases to use when writing recommendations. All guideline recommendations have been written in full sentences that express a complete thought, such that a recommendation, even if separated and presented apart from the rest of the document (including headings above sets of recommendations), would still convey the full intent of the recommendation. It is hoped that this will increase readers' comprehension of the guidelines and will allow queries at the individual recommendation level.The ACC/AHA practice guidelines address patient populations (and health care providers) residing in North America. As such, drugs that are not currently available in North America are discussed in the text without a specific class of recommendation. For studies performed in large numbers of subjects outside of North America, each writing committee reviews the potential impact of different practice patterns and patient populations on the treatment effect and on the relevance to the ACC/AHA target population to determine whether the findings should form the basis of a specific recommendation.The ACC/AHA practice guidelines are intended to assist health care providers in clinical decision making by describing a range of generally acceptable approaches for the diagnosis, management, and prevention of specific diseases or conditions. The guidelines attempt to define practices that meet the needs of most patients in most circumstances. The ultimate judgment regarding care of a particular patient must be made by the health care provider and patient in light of all the circumstances presented by that patient. Thus, there are circumstances in which deviations from these guidelines may be appropriate. Clinical decision making should consider the quality and availability of expertise in the area where care is provided. These guidelines may be used as the basis for regulatory or payer decisions, but the ultimate goal is quality of care and serving the patient's best interests.Prescribed courses of treatment in accordance with these recommendations are only effective if they are followed by the patient. Because lack of patient adherence may adversely affect treatment outcomes, health care providers should make every effort to engage the patient in active participation with prescribed treatment.The ACC/AHA Task Force on Practice Guidelines makes every effort to avoid any actual, potential, or perceived conflict of interest arising from industry relationships or personal interests of a writing committee member. All writing committee members and peer reviewers were required to provide disclosure statements of all such relationships pertaining to the trials and other evidence under consideration (see Appendixes 1 and 2). Final recommendations were balloted to all writing committee members. Writing committee members with significant (greater than $10 000) relevant relationships with industry (RWI) were required to recuse themselves from voting on that recommendation. Writing committee members who did not participate are not listed as authors of this focused update.With the exception of the recommendations presented in this statement, the full guidelines remain current. Only the recommendations from the affected section(s) of the full guidelines are included in this focused update. For easy reference, all recommendations from any section of guidelines impacted by a change are presented with a notation as to whether they remain current, are new, or have been modified. When evidence impacts recommendations in more than 1 set of guidelines, those guidelines are updated concurrently.The recommendations in this focused update will be considered current until they are superseded by another focused update or the full-text guidelines are revised. This focused update is published in the January 15, 2008, issue of the Journal of the American College of Cardiology, the January 15, 2008, issue of Circulation, and e-published in Catheterization and Cardiovascular Interventions as an update to the full-text guidelines and is posted on the ACC (www.acc.org), AHA (my.americanheart.org), and Society for Angiography and Interventions (SCAI) (www.scai.org) Web sites. Copies of the focused update are available from all organizations.Sidney C. Smith, Jr., MD, FACC, FAHAChair, ACC/AHA Task Force on Practice GuidelinesAlice K. Jacobs, MD, FACC, FAHAVice-Chair, ACC/AHA Task Force on Practice Guidelines1. Introduction1.1. Evidence ReviewSelected late-breaking clinical trials presented at the 2005 and 2006 annual scientific meetings of the ACC, AHA, and European Society of Cardiology, as well as selected other data, were reviewed by the standing guideline writing committee along with the parent Task Force and other experts to identify those trials and other key data that might impact guideline recommendations. On the basis of the criteria/considerations noted above, recent trial data and other clinical information were considered important enough to prompt a focused update of the ACC/AHA/SCAI 2005 Guideline Update for Percutaneous Coronary Intervention.3–13To provide clinicians with a comprehensive set of data, whenever possible, the exact event rates in various treatment arms of clinical trials are presented to permit calculation of the absolute risk difference (ARD) and number needed to treat (NNT) or harm (NNH); the relative treatment effects are described either as odds ratio (OR), relative risk (RR), or hazard ratio (HR), depending on the format in the original publication.Consult the full-text version or executive summary of the ACC/AHA/SCAI 2005 Guideline Update for Percutaneous Coronary Intervention for policy on clinical areas not covered by the focused update.13a Individual recommendations updated in this focused update will be incorporated into future revisions and/or updates of the full-text guidelines.1.2. Organization of Committee and Relationships With IndustryFor this focused update, all members of the 2005 PCI writing committee were invited to participate; those who agreed (referred to as the 2007 focused update writing group) were required to disclose all RWI relevant to the data under consideration.2 Focused update writing group members who had no significant relevant RWI wrote the first draft of the focused update; the draft was then reviewed and revised by the full writing group. Each recommendation required a confidential vote by the writing group members before external review of the document. Any writing committee member with a significant (greater than $10 000) RWI relevant to the recommendation was recused from voting on that recommendation.1.3. Review and ApprovalThis document was reviewed by 2 outside reviewers nominated by each cosponsoring organization (ACC, AHA, and SCAI) and 24 individual content reviewers. All reviewer RWI information was collected and distributed to the writing committee and is published in this document (see Appendix 2 for details).This document was approved for publication by the governing bodies of the American College of Cardiology Foundation, AHA, and SCAI.2. Patients With Unstable Angina/Non–ST-Elevation Myocardial InfarctionThis 2007 PCI Focused Update section regarding patients with unstable angina (UA)/non–ST-elevation myocardial infarction (NSTEMI) is based on recommendations from the ACC/AHA 2007 Guidelines for the Management of Patients With Unstable Angina/Non–ST-Elevation Myocardial Infarction,14 which emphasize the importance of assessing risk of cardiovascular events as a guide to therapeutic decision making and the need for interventional therapy (see Table 2). Table 2. Updates to Section 5.3: Initial Conservative Versus Initial Invasive Strategies (Patients With UA/NSTEMI)2005 PCI Guideline Update Recommendation2007 PCI Focused Update RecommendationCommentsClass IAn early invasive PCI strategy is indicated for patients with UA/NSTEMI who have no serious comorbidity† and coronary lesions amenable to PCI. Patients must have any of the following high-risk features:1. An early invasive PCI strategy is indicated for patients with UA/NSTEMI who have no serious comorbidity† and who have coronary lesions amenable to PCI and who have characteristics for invasive therapy (see Table 3 and Section 3.3 of the ACC/AHA 2007 UA/NSTEMI Guidelines).14(Level of Evidence: A)Modified recommendation*a. Recurrent ischemia despite intensive anti-ischemic therapy. (Level of Evidence: A)b. Elevated troponin level. (Level of Evidence: A)c. New ST-segment depression. (Level of Evidence: A)d. HF symptoms or new or worsening MR. (Level of Evidence: A)e. Depressed LV systolic function. (Level of Evidence: A)f. Hemodynamic instability. (Level of Evidence: A)g. Sustained ventricular tachycardia. (Level of Evidence: A)h. PCI within 6 months. (Level of Evidence: A)i. Prior CABG. (Level of Evidence: A) j. High risk score (e.g., TIMI, GRACE). (Level of Evidence: A)k. High risk findings from non-invasive testing. (Level of Evidence: A)2. Percutaneous coronary intervention (or CABG) is recommended for UA/NSTEMI patients with 1- or 2-vessel CAD with or without significant proximal left anterior descending CAD but with a large area of viable myocardium and high-risk criteria on noninvasive testing. (Level of Evidence: B)New recommendation*3. Percutaneous coronary intervention (or CABG) is recommended for UA/NSTEMI patients with multivessel coronary disease with suitable coronary anatomy, with normal LV function, and without diabetes mellitus. (Level of Evidence: A)New recommendation*4. An intravenous platelet GP IIb/IIIa inhibitor is useful in UA/NSTEMI patients undergoing PCI. (Level of Evidence: A) See Section 3.2.3 and Table 13 of the 2007 ACC/AHA 2007 UA/NSTEMI Guidelines.14New recommendation*5. An early invasive strategy (i.e., diagnostic angiography with intent to perform revascularization) is indicated in UA/NSTEMI patients who have refractory angina or hemodynamic or electrical instability (without serious comorbidities or contraindications to such procedures). (Level of Evidence: B)New recommendation*Table 2. Continued2005 PCI Guideline Update Recommendation2007 PCI Focused Update RecommendationCommentsClass IIaIt is reasonable that PCI be performed in patients with UA/NSTEMI and single-vessel or multivessel CAD who are undergoing medical therapy with focal saphenous vein graft lesions or multiple stenoses who are poor candidates for reoperative surgery. (Level of Evidence: C)1. Percutaneous coronary intervention is reasonable for focal saphenous vein graft lesions or multiple stenoses in UA/NSTEMI patients who are undergoing medical therapy and who are poor candidates for reoperative surgery. (Level of Evidence: C)Modified recommendation*In the absence of high-risk features associated with UA/NSTEMI, it is reasonable to perform PCI in patients with amenable lesions and no contraindication for PCI with either an early invasive or early conservative strategy. (Level of Evidence: B)Deleted recommendation*2. Percutaneous coronary intervention (or CABG) is reasonable for UA/NSTEMI patients with 1- or 2-vessel CAD with or without significant proximal left anterior descending CAD but with a moderate area of viable myocardium and ischemia on noninvasive testing. (Level of Evidence: B)New recommendation*3. Percutaneous coronary intervention (or CABG) can be beneficial compared with medical therapy for UA/NSTEMI patients with 1-vessel disease with significant proximal left anterior descending CAD. (Level of Evidence: B)New recommendation*Use of PCI is reasonable in patients with UA/NSTEMI with significant left main CAD (greater than 50% diameter stenosis) who are candidates for revascularization but are not eligible for CABG. (Level of Evidence: B)4. Use of PCI is reasonable in patients with UA/NSTEMI with significant left main CAD (greater than 50% diameter stenosis) who are candidates for revascularization but are not eligible for CABG or who require emergency intervention at angiography for hemodynamic instability. (Level of Evidence: B)2005 recommendation remains current in 2007 PCI Update but receives additional wording.Class IIbIn the absence of high-risk features associated with UA/NSTEMI, PCI may be considered in patients with single-vessel or multivessel CAD who are undergoing medical therapy and who have 1 or more lesions to be dilated with a less than optimal likelihood of success. (Level of Evidence: B)1. In the absence of high-risk features associated with UA/NSTEMI, PCI may be considered in patients with single-vessel or multivessel CAD who are undergoing medical therapy and who have 1 or more lesions to be dilated with a reduced likelihood of success. (Level of Evidence: B)Modified recommendation*PCI may be considered in patients with UA/NSTEMI who are undergoing medical therapy who have 2- or 3-vessel disease, significant proximal LAD CAD, and treated diabetes or abnormal LV function. (Level of Evidence: B)2. PCI may be considered in patients with UA/NSTEMI who are undergoing medical therapy who have 2- or 3-vessel disease, significant proximal left anterior descending CAD, and treated diabetes or abnormal LV function, with anatomy suitable for catheter-based therapy. (Level of Evidence: B)2005 recommendation remains current in 2007 PCI Update but receives additional wording.3. In initially stabilized patients, an initially conservative (i.e., a selectively invasive) strategy may be considered as a treatment strategy for UA/NSTEMI patients (without serious comorbidities or contraindications to such procedures†) who have an elevated risk for clinical events (see Table 3) including those who are troponin positive. (Level of Evidence: B). The decision to implement an initial conservative (versus initial invasive) strategy‡ in these patients may be made by considering physician and patient preference. (Level of Evidence: C)New recommendation*4. An invasive strategy may be reasonable in patients with chronic renal insufficiency. (Level of Evidence: C)New recommendation*Class III1. Percutaneous coronary intervention (or CABG) is not recommended for patients with 1- or 2-vessel CAD without significant proximal left anterior descending CAD with no current symptoms or symptoms that are unlikely to be due to myocardial ischemia and who have no ischemia on noninvasive testing. (Level of Evidence: C)New recommendation*Table 2. Continued2005 PCI Guideline Update Recommendation2007 PCI Focused Update RecommendationComments*Based on the ACC/AHA 2007 UA/NSTEMI Guidelines.14†For example, severe hepatic, pulmonary, or renal failure, or active/inoperable cancer. Clinical judgment is required in such cases.‡Diagnostic angiography with intent to perform revascularization.CABG indicates coronary artery bypass graft; CAD, coronary artery disease; GP, glycoprotein; GRACE, Global Registry of Acute Coronary Events; HF, heart failure; IV, intravenous; LAD, left anterior descending; LV, left ventricular; MR, mitral regurgitation; PCI, percutaneous coronary intervention; SVG, saphenous vein graft; TIMI, Thrombolysis in Myocardial Infarction; and UA/NSTEMI, unstable angina/non–ST-elevation myocardial infarction.In the absence of high-risk features associated with UA/NSTEMI, PCI is not recommended for patients with UA/NSTEMI who have single-vessel or multivessel CAD and no trial of medical therapy, or who have 1 or more of the following:2. In the absence of high-risk features associated with UA/NSTEMI, PCI is not recommended for patients with UA/NSTEMI who have single-vessel or multivessel CAD and no trial of medical therapy, or who have 1 or more of the following:2005 recommendation remains current in 2007 PCI Update a. Only a small area of myocardium at risk. (Level of Evidence: C) a. Only a small area of myocardium at risk. (Level of Evidence: C) b. All lesions or the culprit lesion to be dilated with morphology that conveys a low likelihood of success. (Level of Evidence: C) b. All lesions or the culprit lesion to be dilated with morphology that conveys a low likelihood of success. (Level of Evidence: C) c. A high risk of procedure-related morbidity or mortality. (Level of Evidence: C) d. Insignificant disease (less than 50% coronary stenosis). (Level of Evidence: C) c. A high risk of procedure-related morbidity or mortality. (Level of Evidence: C) e. Significant left main CAD and candidacy for CABG. (Level of Evidence: B) d. Insignificant disease (less than 50% coronary stenosis). (Level of Evidence: C) e. Significant left main CAD and candidacy for CABG. (Level of Evidence: B)3. A PCI strategy in stable patients (see Table 12 Class III No. 1 for specific recommendations) with persistently occluded infarct related coronary arteries after STEMI/NSTEMI is not indicated. (Level of Evidence: B)New recommendation*Because of the importance of several new changes in the ACC/AHA 2007 UA/NSTEMI Guidelines, selected text from the guidelines is included in the following paragraphs and summarized in Table 2.A number of risk-assessment tools have been developed to assist in assessing risk of death and ischemic events in patients with UA/NSTEMI, thereby providing a basis for therapeutic decision making. It should be recognized that the predictive ability of these commonly used risk assessment scores for risk of nonfatal coronary heart disease (CHD) is only moderate.The Thrombolysis in Myocardial Infarction (TIMI) risk score15 is a simple tool composed of 7 (1-point) risk indicators rated on presentation (Table 4). The composite end points (all-cause mortality, new or recurrent myocardial infarction [MI], or severe recurrent ischemia prompting urgent revascularization within 14 days) increase as the TIMI risk score increases. The TIMI risk score has been validated internally within the TIMI IIB trial and 2 separate cohorts of patients from the ESSENCE (Efficacy and Safety of Subcutaneous Enoxaparin in Unstable Angina and Non–Q-Wave Myocardial Infarction) trial.16 The model remained a significant predictor of events and appeared relatively insensitive to missing information, such as knowledge of previously documented coronary stenosis of 50% or greater. The model's predictive ability remained intact, with a cutoff of 65 years of age. The TIMI risk score was recently studied in an unselected emergency department population with chest pain syndrome; its performance was similar to that in the acute coronary syndrome (ACS) population from which it was derived and validated.17 The TIMI risk calculator is available at www.timi.org. The TIMI risk index, a modification of the TIMI risk score that uses the variables age, systolic blood pressure, and heart rate, has not only been shown to predict short-term mortality in ST-elevation myocardial infarction (STEMI) but also has been useful in prediction of 30-day and 1-year mortality rates across the spectrum of patients with ACS, including UA/NSTEMI.18Table 4. TIMI Risk Score for Unstable Angina/Non–ST-Elevation Myocardial InfarctionTIMI Risk ScoreAll-Cause Mortality, New or Recurrent MI, or Severe Recurrent Ischemia Requiring Urgent Revascularization Through 14 Days After Randomization, %The TIMI risk score is determined by the sum of the presence of 7 variables at admission; 1 point is given for each of the following variables: age 65 years or older; at least 3 risk factors for CAD; prior coronary stenosis of 50% or more; ST-segment deviation on ECG presentation; at least 2 anginal events in prior 24 hours; use of aspirin in prior 7 days; and elevated serum cardiac biomarkers. Prior coronary stenosis of 50% or more remained relatively insensitive to missing information and remained a significant predictor of events. Reprinted with permission from Antman EM, Cohen M, Bernink PJ, et al. The TIMI risk score for unstable angina/non-ST elevation MI: a method for prognostication and therapeutic decision making. JAMA. 2000;284:835–42.15 Copyright © 2000 American Medical Association.CAD indicates coronary artery disease; ECG, electrocardiogram; MI, myocardial infarction; and TIMI, Thrombolysis in Myocardial Infarction.0–14.728.3313.2419.9526.26–740.9The PURSUIT (Platelet Glycoprotein IIb-IIIa in Unstable Angina: Receptor Suppression Using Integrilin Therapy) trial risk model,19 based on patients enrolled in the PURSUIT trial, is another useful tool to guide the clinical decision-making process when the patient is admitted to the hospital. In the PURSUIT risk model, critical clinical features associated with an increased 30-day incidence of death and the composite of death or myocardial (re)infarction were (in order of strength) age, heart rate, systolic blood pressure, ST-segment depression, signs of heart failure (HF), and cardiac enzymes.19The GRACE (Global Registry of Acute Coronary Events) study risk model, which predicts in-hospital mortality (and death or MI), can be useful to clinicians to guide treatment type and intensity.20,21 The GRACE risk tool was developed on the basis of 11 389 patients in GRACE and validated in subsequent GRACE and GUSTO (Global Utilization of Streptokinase and TPA for Occluded Coronary Arteries) IIb cohorts and predicts in-hospital death in patients with STEMI, NSTEMI, or UA (C statistic=0.83). The 8 variables used in the GRACE risk model are older age (OR 1.7 per 10 years), Killip class (OR 2.0 per class), systolic blood pressure (OR 1.4 per 20 mm Hg decrease), ST-segment deviation (OR 2.4), cardiac arrest during presentation (OR 4.3), serum creatinine level (OR 1.2 per 1 mg per dL increase), positive initial cardiac markers (OR 1.6), and heart rate (OR 1.3 per 30-bpm increase). The sum of scores is applied to a reference nonog

HomeCirculationVol. 109, No. 5Evidence-Based Guidelines for Cardiovascular Disease Prevention in Women

With Acute Myocardial Infarction have been reviewed over the past 2.5 years

HomeCirculationVol. 106, No. 14ACC/AHA Guideline Update for the Management of Patients With Unstable Angina and Non–ST-Segment Elevation Myocardial Infarction—2002: Summary Article Free AccessReview ArticlePDF/EPUBAboutView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toFree AccessReview ArticlePDF/EPUBACC/AHA Guideline Update for the Management of Patients With Unstable Angina and Non–ST-Segment Elevation Myocardial Infarction—2002: Summary ArticleA Report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Committee on the Management of Patients With Unstable Angina) Committee Members Eugene Braunwald, Elliott M. Antman, John W. Beasley, Robert M. Califf, Melvin D. Cheitlin, Judith S. Hochman, Robert H. Jones, Dean Kereiakes, Joel Kupersmith, Thomas N. Levin, Carl J. Pepine, John W. Schaeffer, Earl E. SmithIII, David E. Steward, Pierre Theroux, Raymond J. Gibbons, Elliott M. Antman, Joseph S. Alpert, David P. Faxon, Valentin Fuster, Gabriel Gregoratos, Loren F. Hiratzka, Alice K. Jacobs and Sidney C. SmithJr Committee Members , Eugene BraunwaldEugene Braunwald , Elliott M. AntmanElliott M. Antman , John W. BeasleyJohn W. Beasley , Robert M. CaliffRobert M. Califf , Melvin D. CheitlinMelvin D. Cheitlin , Judith S. HochmanJudith S. Hochman , Robert H. JonesRobert H. Jones , Dean KereiakesDean Kereiakes , Joel KupersmithJoel Kupersmith , Thomas N. LevinThomas N. Levin , Carl J. PepineCarl J. Pepine , John W. SchaefferJohn W. Schaeffer , Earl E. SmithIIIEarl E. SmithIII , David E. StewardDavid E. Steward , Pierre TherouxPierre Theroux , Raymond J. GibbonsRaymond J. Gibbons , Elliott M. AntmanElliott M. Antman , Joseph S. AlpertJoseph S. Alpert , David P. FaxonDavid P. Faxon , Valentin FusterValentin Fuster , Gabriel GregoratosGabriel Gregoratos , Loren F. HiratzkaLoren F. Hiratzka , Alice K. JacobsAlice K. Jacobs and Sidney C. SmithJrSidney C. SmithJr Originally published1 Oct 2002https://doi.org/10.1161/01.CIR.0000037106.76139.53Circulation. 2002;106:1893–1900The American College of Cardiology (ACC)/American Heart Association (AHA) guidelines for the management of unstable angina and non–ST-segment elevation myocardial infarction (UA/NSTEMI) were published in September 2000.1 Since then, a number of clinical trials and observational studies have been published or presented that, when taken together, alter significantly the recommendations made in that document. Therefore, the ACC/AHA Committee on the Management of Patients With Unstable Angina, with the concurrence of the ACC/AHA Task Force on Practice Guidelines, revised these guidelines. These revisions were prepared in December 2001, reviewed and approved, and then published on the ACC World Wide Web site (www.acc.org) and AHA World Wide Web site (www.americanheart.org) on March 15, 2002. The present article describes these revisions and provides further updates in this rapidly moving field. Minor clarifications in the wording of three recommendations that now appear differently from those that were previously published on the ACC and AHA Web sites are noted in footnotes.The ACC/AHA classifications I, II, and III are used to summarize indications as follows:Class I: Conditions for which there is evidence and/or general agreement that a given procedure or treatment is useful and effective.Class II: Conditions for which there is conflicting evidence and/or a divergence of opinion about the usefulness/efficacy of a procedure or treatment.IIa: Weight of evidence/opinion is in favor of usefulness/efficacy.IIb: Usefulness/efficacy is less well established by evidence/opinion.Class III: Conditions for which there is evidence and/or general agreement that the procedure/treatment is not useful/effective and in some cases may be harmful.The weight of the evidence was ranked highest (A) if the data were derived from multiple randomized clinical trials that involved large numbers of patients and intermediate (B) if the data were derived from a limited number of randomized trials that involved small numbers of patients or from careful analyses of nonrandomized studies or observational registries. A lower rank (C) was given when expert consensus was the primary basis for the recommendation.Risk AssessmentClinical FeaturesUnstable angina and NSTEMI are heterogeneous disorders in which patients have widely varying risks. Risk is an important "driver" of management decisions, and accurate yet simple methods of risk assessment are important for patient care.Risk was assessed by multivariable regression techniques in patients presenting with UA/NSTEMI in several large clinical trials. Boersma et al analyzed the relation between baseline characteristics and the incidence of death and the composite of death or myocardial (re)infarction at 30 days in patients who entered the PURSUIT (Platelet IIb/IIIa in Unstable angina: Receptor Suppression Using Integrilin Therapy) trial.2 The most important baseline features associated with death were age, heart rate, systolic blood pressure, ST-segment depression, signs of heart failure, and elevation of cardiac biomarkers. From this analysis, a simple risk estimation score was developed.Antman et al developed a 7-point risk score, the "TIMI Risk Score," (age greater than or equal to 65 years, more than 3 coronary risk factors, prior angiographic coronary obstruction, ST-segment deviation, more than 2 angina events within 24 hours, use of aspirin (ASA) within 7 days, and elevated cardiac markers).3 The score was defined as the simple sum of these individual prognostic variables. The risk of developing an adverse outcome—death, (re)infarction, or recurrent severe ischemia that required revascularization—ranged from 5% with a score of 0 or 1 to 41% with a score of 6 or 7. The score was derived from data in the TIMI 11B (Thrombolysis In Myocardial Infarction 11B) trial4 and then validated in 3 additional trials—ESSENCE (Efficacy and Safety of Subcutaneous Enoxaparin in Non–Q-wave Coronary Events study),5 and PRISM-PLUS (Platelet Receptor inhibition for Ischemic Syndrome Management in Patients Limited by Unstable Signs and symptoms)6 and prospectively in one TACTICS-TIMI 18 (Treat angina with Aggrastat and determine Cost of Therapy with an Invasive or Conservative Strategy–Thrombolysis In Myocardial Infarction) 18.7 A progressively greater benefit from newer therapies such as low-molecular-weight heparin (LMWH),4,5 platelet glycoprotein (GP) IIb/IIIa receptor antagonists,6 and an invasive strategy7 with increasing risk score have been reported.BiomarkersThe Joint European Society of Cardiology/American College of Cardiology Committee for the Redefinition of Myocardial Infarction8 emphasized the use of troponins as critical markers of the presence of myocardial necrosis. Although troponins are accurate in identifying myocardial necrosis, the latter is not always secondary to atherosclerotic coronary artery disease. Therefore, in establishing the diagnosis of NSTEMI, cardiac troponins should be used in conjunction with appropriate clinical features and electrocardiographic changes. Myocardial injury of diverse origins (eg, myocarditis, trauma, or cardioversion) may cause necrosis and release of troponins. Although these may be considered instances of NSTEMI, they should be distinguished on clinical grounds from the more common form of NSTEMI secondary to coronary atherosclerosis.Antiplatelet TherapyAntiplatelet therapy is a cornerstone in the management of UA/NSTEMI. Three classes of antiplatelet drugs (ASA, thienopyridines, and GP IIb/IIIa antagonists) have been found useful in the management of these patients and are the subject of continued intensive investigation and analysis.ClopidogrelGiven its more rapid onset of action9,10 and better safety profile compared with ticlopidine, clopidogrel is now the preferred thienopyridine. The CURE (Clopidogrel in Unstable angina to prevent Recurrent ischemic Events) trial11 randomized 12 562 patients with UA/STEMI who presented within 24 hours to placebo or clopidogrel (loading dose of 300 mg followed by 75 mg daily) and followed them for 3 to 12 months; all patients were given aspirin. Cardiovascular death, myocardial infarction (MI), or stroke occurred in 11.5% of patients assigned to placebo and 9.3% of those assigned to clopidogrel (relative risk [RR] 0.80; P less than 0.001). Looking at the individual components of the primary composite and end point, there was a trend in favor of clopidogrel for cardiovascular death and stroke (5.5% and 1.4%, respectively, for placebo vs 5.1% and 1.2% for clopidogrel), and there was a significant reduction in MI (6.7% vs 5.2% RR = 0.77, P less than 0.001). However, there was no significant difference in the incidence of non–Q-wave MI (3.8% vs 3.5%). A reduction in recurrent ischemia was noted within the first few hours after randomization. These salutary results were observed across all subgroups of patients. There was, however, a significant excess of major bleeding (2.7% in the placebo group versus 3.7% in the clopidogrel group; P= 0.003) and of minor bleeding, as well as a (nonsignificant) trend for an increase in life-threatening bleeding. The risk of bleeding was increased in patients who underwent coronary artery bypass grafting (CABG) within the first 5 days after clopidogrel was discontinued.The CURE trial was performed in hospitals in which there was no routine policy of early invasive procedures, and therefore, revascularization was performed during the initial admission in only 23% of the patients, a substantially lower percentage than currently receive this therapy at most US hospitals. Although the addition of a GP IIb/IIIa antagonist appeared to be well tolerated in patients who were given ASA, clopidogrel, and heparin in CURE, fewer than 10% of patients received this combination. Therefore, additional information on the safety of "quadruple therapy" (heparin [unfractionated or low molecular weight], ASA, clopidogrel, and a GP IIb/IIIa antagonist) should be obtained.The CURE trial provides strong support for the addition of clopidogrel to ASA on admission in the management of patients with UA and NSTEMI. Clopidogrel appears to be especially useful in hospitals that do not have a routine policy of early invasive procedures and in patients who are not candidates or who do not wish to be considered for revascularization. The optimal duration of therapy with clopidogrel has not been determined. The major benefits in CURE were observed at 30 days, with small additional benefits observed over the subsequent treatment period, which averaged 8 months.In PCI-CURE, a substudy of CURE, 2658 patients who underwent percutaneous coronary intervention (PCI) had been randomly assigned to double-blind treatment with clopidogrel (n=1313) or placebo (n= 1345)12; all patients also received ASA. Patients were pretreated with placebo or study drug for a median of 10 days before PCI. After the procedure, most patients received open-label thienopyridine (clopidogrel or ticlopidine) for approximately 4 weeks, after which the study drug (placebo or clopidogrel) was again administered for an average of 8 months. The primary end point, a composite of cardiovascular death, MI, or urgent target-vessel revascularization within 30 days of PCI, occurred in 86 patients (6.4%) in the placebo group compared with 59 (4.5%) in the clopidogrel group (RR 0.70; P= 0.03). When events that occurred before and after PCI were considered, there was a 31% reduction in cardiovascular death or MI with assignment to clopidogrel (P=0.002). Thus, in patients with UA and NSTEMI who are given ASA and are undergoing PCI, a strategy of clopidogrel pretreatment followed by at least 1 month and probably longer-term therapy is beneficial in reducing major cardiovascular events.12There now appears to be an important role for clopidogrel in patients with UA/NSTEMI, both those who are managed conservatively and those who undergo PCI, especially stenting. However, it is not entirely clear how long therapy should be maintained. Because clopidogrel, when added to ASA, increases the risk of bleeding during major surgery in patients who are scheduled for CABG, if possible, clopidogrel should be withheld for at least 5 days11 and preferably for 7 days before surgery.13 In many hospitals in which patients with UA/NSTEMI undergo diagnostic catheterization within 24 to 36 hours of admission, clopidogrel is not started until it is clear that CABG will not be scheduled within the next several days. A loading dose of clopidogrel can be given to a patient on the catheterization table if a PCI is to be performed immediately. If PCI is not performed, clopidogrel can be begun after the catheterization.Glycoprotein IIb/IIIa Antagonists in PCIThe introduction of platelet GP IIb/IIIa antagonists represents an important advance in the treatment of patients with UA/NSTEMI who are undergoing PCI. These drugs take advantage of the fact that platelets play an important role in the development of ischemic complications that may occur in patients with UA/NSTEMI during coronary revascularization procedures. The September 2000 guidelines emphasized the value of GP IIb/IIIa antagonists in patients with UA/NSTEMI who were undergoing PCI.1Two trials of GP IIb/IIIa inhibitors have been published since September 2000. The ESPRIT trial (Enhanced Suppression of the Platelet IIb/IIIa Receptor with Integrilin Therapy) was a placebo-controlled trial designed to assess whether eptifibatide improved outcome in patients undergoing stenting.14 Fourteen percent of the 2064 patients enrolled in ESPRIT had UA/NSTEMI. The primary end point (the composite of death, MI, target-vessel revascularization, and "bailout" GP IIb/IIIa antagonist therapy) was reduced from 10.5% to 6.6% with treatment (P=0.0015). There was consistency in the reduction of events in all components of the end point and in all major subgroups, including patients with UA/NSTEMI. Major bleeding occurred more frequently in patients who received eptifibatide (1.3%) than in those who received placebo (0.4%; P=0.027); however, no significant difference in the transfusion rate occurred. At 1 year of follow-up, death or MI occurred in 12.4% of patients assigned to placebo and 8.0% of eptifibatide-treated patients (hazard ratio 0.63; 95% confidence interval [CI] 0.48 to 0.83; P=0.001).15In the only head-to-head comparison of GP IIb/IIIa antagonists, the TARGET trial (Do Tirofiban and ReoPro Give similar Efficacy? Trial) randomized 5308 patients to tirofiban or abciximab before PCI with the intent to perform stenting.16 The primary end point, a composite of death, nonfatal MI, and urgent target-vessel revascularization at 30 days, occurred less frequently in those given abciximab than in those given tirofiban (6.0% versus 7.6%; P=0.038). There was a similar direction and magnitude for each component of the end point. The difference in outcome between the 2 treatment groups may be related to a suboptimal dose of tirofiban resulting in inadequate platelet inhibition. However, by six months, the primary end point occurred in a similar percentage of patients in each group (14.9% tirofiban versus 14.3% abciximab, NS). Mortality was also similar (1.9% versus 1.7%, NS).17Glycoprotein IIb/IIIa Antagonists Without Scheduled PCIThe Global Utilization of Strategies to Open Occluded Coronary Arteries IV-Acute Coronary Syndromes (GUSTO IV-ACS) trial18 enrolled 7800 patients with UA/NSTEMI who were admitted to the hospital with more than 5 minutes of chest pain and ST-segment depression and/or elevated troponin T or I concentration and in whom early (less than 48 hours) revascularization was not intended to be conducted. All received ASA and either unfractionated heparin (UFH) or LMWH. They were randomized to placebo, an abciximab bolus and 24-hour infusion, or an abciximab bolus and 48-hour infusion. The primary end point, death or MI at 30 days, occurred in 8.0% of patients given placebo, 8.2% given 24-hour abciximab, and 9.1% given 48-hour abciximab, differences that were not statistically significant. At 48 hours, death occurred in 0.3%, 0.7%, and 0.9% in these groups, respectively (placebo versus abciximab 48 hours, P=0.008). The lack of benefit of abciximab was observed in most subgroups, including patients with elevated concentrations of troponin who were at higher risk. Although the explanation for these results is not clear, they indicate that abciximab, at least at the dosing regimen used in GUSTO IV-ACS, is not indicated in the management of patients with UA or NSTEMI in whom an early invasive management strategy is not planned.In the PRISM-PLUS trial, 1069 patients did not undergo early PCI. Although tirofiban treatment was associated with a lower incidence of death, MI or death, and MI or refractory ischemia at 30 days, these reductions were not statistically significant.19 In a high-risk subgroup of these patients not undergoing PCI (TIMI risk score greater than or equal to 4),3 tirofiban appeared to be beneficial whether they underwent PCI (odds ratio [OR] 0.60, 95% CI 0.35 to 1.01) or not (OR 0.69, 95% CI 0.49 to 0.99). However, no benefit was observed in the patients at lower risk.6 In the PURSUIT trial, eptifibatide reduced the incidence of death or MI from 15.7% to 14.2% (RR 0.91; 95% CI 0.79 to 1.00; P=0.032).20Boersma et al performed a meta-analysis of GP IIb/IIIa antagonists in all 6 large, randomized, placebo-controlled trials (including GUSTO IV-ACS, 18 which involved 31 402 patients with UA/NSTEMI who were not routinely scheduled to undergo coronary revascularization.21 A small reduction in the odds of death or MI in the active treatment arm (11.8% versus 10.8%; OR 0.91, 95% CI 0.84 to 0.98; P=0.015) was observed. Unexpectedly, no benefit was observed in women (test for interaction between treatment assignment and gender, P less than 0.0001). However, women with positive troponins derived a treatment benefit that was similar to men. In the meta-analysis, reductions in the end points of death or nonfatal MI considered individually did not achieve statistical significance.Although not scheduled for coronary revascularization procedures, 11 965 of the 31 402 patients (38%) actually underwent PCI or CABG within 30 days, and in this subgroup, the OR for death or MI in patients assigned to GP IIb/IIIa antagonists was 0.89 (95% CI 0.80 to 0.98). In the other 19 416 patients who did not undergo coronary revascularization, the OR for death or MI in the GP IIb/IIIa group was 0.95 (95% CI 0.86 to 1.05, P=NS). Major bleeding complications were increased in the GP IIb/IIIa antagonist-treated group compared with those who received placebo (1.4% versus 2.4%, P less than 0.0001). The authors concluded that in patients with UA/NSTEMI who were not routinely scheduled for early revascularization and who were at high risk of thrombotic complications, "treatment with a GP IIb/IIIa inhibitor might therefore be considered." Thus, GP IIb/IIIa inhibitors are of benefit in high-risk patients with UA/NSTEMI, and their administration, in addition to ASA and heparin, to patients in whom catheterization and PCI are planned received a Class I recommendation. These agents are of questionable benefit in patients who do not undergo PCI. However, the revised guidelines recommend broader indications for a routine invasive strategy (see following text).Thus, clopidogrel (in addition to aspirin and heparin or low molecular weight heparin) is recommended for patients with UA/NSTEMI in whom a noninterventional approach is planned (Class I recommendation). In patients in whom an interventional approach is planned, a GP IIb/IIIa inhibitor (in addition to aspirin and heparin or low molecular weight heparin) is recommended (Class I recommendation). No head-to-head comparison of clopidogrel, a GP IIb/IIIa inhibitor, and their combination has been reported. The addition of a GP IIb/IIIa inhibitor to a subset of patients in the CURE trial who were receiving aspirin, clopidogrel, and heparin appeared to be well tolerated, and current practice frequently involves the use of this combination of drugs. However, until further information on the safety and efficacy of such quadruple therapy becomes available, a Class IIa recommendation is made for the addition of a GP IIb/IIIa inhibitor for patients with UA/NSTEMI who are receiving aspirin, clopidogrel, and unfractionated or low molecular weight heparin and who are referred for an invasive strategy. A Class I recommendation is made for a GP IIb/IIIa inhibitor at the time of PCI in patients receiving heparin and aspirin. Specific updated recommendations for the use of antiplatelet regimens in the revised guidelines are as follows:Class I1. Antiplatelet therapy should be initiated promptly. ASA should be administered as soon as possible after presentation and continued indefinitely. (Level of Evidence: A)2. Clopidogrel should be administered to hospitalized patients who are unable to take ASA because of hypersensitivity or major gastrointestinal intolerance. (Level of Evidence: A)*3. In hospitalized patients in whom an early noninterventional approach is planned, clopidogrel should be added to ASA as soon as possible on admission and administered for at least 1 month (Level of Evidence: A), and for up to 9 months. (Level of Evidence: B)*4. A platelet GP IIb/IIIa antagonist should be administered, in addition to ASA and heparin, to patients in whom catheterization and PCI are planned. The GP IIb/IIIa antagonist may also be administered just prior to PCI. (Level of Evidence: A)*†5. In patients for whom a PCI is planned and who are not at high risk for bleeding, clopidogrel should be started and continued for at least 1 month (Level of Evidence: A) and for up to 9 months. (Level of Evidence: B)*6. In patients taking clopidogrel in whom elective CABG is planned, the drug should be withheld for 5 to 7 days. (Level of Evidence: B)Class IIa*1. Eptifibatide or tirofiban should be administered, in addition to ASA and LMWH or UFH, to patients with continuing ischemia, an elevated troponin, or with other high-risk features in whom an invasive management strategy is not planned. (Level of Evidence: A)*2. A platelet GP IIb/IIIa antagonist should be administered to patients already receiving heparin, ASA, and clopidogrel in whom catheterization and PCI are planned. The GP IIb/IIIa antagonist may also be administered just prior to PCI. (Level of Evidence: B)Class IIb*1. ptifibatide or tirofiban, in addition to ASA and LMWH or UFH, to patients without continuing ischemia who have no other high-risk features and in whom PCI is not planned. (Level of Evidence: A)Class III1.Intravenous fibrinolytic therapy in patients without acute ST-segment elevation, a true posterior MI, or a presumed new left bundle-branch block. (Level of Evidence: A)*2.Abciximab administration in patients in whom PCI is not planned. (Level of Evidence: A)*New indication, not included in September 2000 guidelines.†Minor clarification different from full-text version on web site.Anticoagulant TherapyThe September 2000 guidelines1 reviewed the evidence regarding the use of intravenous UFH or subcutaneous LMWH. It provided the following Class I recommendation:"Parenteral anticoagulation with intravenous UFH or subcutaneous LMWH should be added to antiplatelet therapy with ASA or a thienopyridine. (Level of Evidence: B)"In the interim, a number of studies have appeared that support the use of enoxaparin. In the EVET trial (Enoxaparin VErsus Tinzaparin in the management of unstable coronary artery disease), 2 LMWHs, enoxaparin and tinzaparin, administered for 7 days, were compared in 438 patients with UA/NSTEMI. A preliminary report stated that both the recurrence of unstable angina and the need for revascularization were significantly lower in the enoxaparin group.22 Because the level of anticoagulant activity cannot be easily measured in patients given LMWH (eg, activated partial thromboplastin time or activated clotting time), interventional cardiologists have expressed concern about the substitution of LMWH for UFH in patients scheduled for catheterization with possible PCI. However, Collet et al23 have shown in a small nonrandomized observation study in 293 patients that PCI can be performed safely with UA/NSTEMI patients who received the usual dose of enoxaparin. In NICE-1 (National Investigators Collaborating on Enoxaparin), an observational study, intravenous enoxaparin (1.0 mg/kg) was used in 828 patients undergoing elective PCI without an intravenous GP IIb/IIIa antagonist.24 The rates of bleeding (1.1% major bleeding and 6.2% minor bleeding in 30 days) were comparable to those observed in historical controls with UFH.An alternative approach is to use LMWH during the period of initial stabilization and to withhold the dose on the morning of the procedure. If an intervention is required and more than 8 hours has elapsed since the last dose of LMWH, UFH can be used for PCI according to usual practice patterns. Because the anticoagulant effect of UFH can be more readily reversed than that of LMWH, UFH is preferred in patients likely to undergo CABG within 24 hours.The September 2000 guidelines reflected concern regarding the combined use of LMWH and GP IIb/IIIa antagonists. Although the data are not definitive, it now appears that GP IIb/IIIa antagonists can be used with LMWH. In the ACUTE II (Anti-thrombotic Combination Using Tirofiban and Enoxaparin II) study,25 UFH and enoxaparin were compared in patients with UA/NSTEMI who were given tirofiban. The frequencies of both major and minor bleeding were similar, and there was a trend to fewer adverse events in the patients given enoxaparin. A number of other open-label studies have examined the safety of combining enoxaparin, with abciximab, eptifibatide, or tirofiban in patients with UA/NSTEMI who are treated with PCI or conservatively; of combining enoxaparin with abciximab in patients undergoing elective PCI26; and of combining dalteparin with abciximab in patients with UA/NSTEMI who are treated conservatively and during PCI.27 Although the majority of these studies relied on historical controls, none suggested that the combination of enoxaparin and a GP IIb/IIIa antagonist was associated with excess bleeding, whether or not the patient also underwent PCI.Specific recommendations for the use of heparins in the revised guidelines are as follows:Class I*1. Anticoagulation with subcutaneous LMWH or intravenous UFH should be added to antiplatelet therapy with ASA and/or clopidogrel. (Level of Evidence: A)Class IIa*†1. Enoxaparin is preferable to UFH as an anticoagulant in patients with UA/NSTEMI, in the absence of renal failure and unless CABG is planned within 24 hours. (Level of Evidence: A)*New indication, not included in the September 2000 guidelines.†Minor clarification different from full-text version on web site.Early Conservative vs Early Invasive StrategiesThe September 2000 guidelines indicated that 2 different treatment strategies, termed "early conservative" and "early invasive, " may be used in patients with UA/NSTEMI.1 In the early conservative strategy, coronary angiography is reserved for patients with evidence of recurrent ischemia (angina at rest or with minimal activity or dynamic ST-segment changes) or a strongly positive stress test despite vigorous medical therapy. In the early invasive strategy, patients without clinically obvious contraindications to coronary revascularization are routinely recommended for coronary angiography and angiographically directed revascularization, if possible.Several trials comparing these 2 strategies were reviewed, but greatest attention was paid to the then-most-recent trial, FRISC II (Fragmin and Fast Revascularization during InStability in Coronary artery disease II).28 At 1 year, the mortality rate in the invasive strategy group was 2.2% compared with 3.9% in the noninvasive strategy group (P=0.016).29 However, in FRISC II, the invasive strategy involved treatment for an average of 6 days in the hospital with LMWH, ASA, nitrates, and beta-blockers before coronary angiography, an approach that would be difficult to adopt in US hospitals.In the interim, the TACTICS-TIMI 18 trial was reported.7 In this trial, 2220 patients with UA or NSTEMI were treated with ASA, heparin, and the GP IIb/IIIa antagonist tirofiban. They were then randomized to an early invasive strategy with routine coronary angiography within 48 hours followed by revascularization if the coronary anatomy was deemed suitable, or to a more conservative strategy. In the latter, catheterization was performed only if the patient had recurrent ischemia or a strongly positive stress test. Death, myocardial (re)infarction, or rehospitalization for an acute coronary syndrome at 6 months occurred in 19.4% of patients assigned to the conservative strategy versus 15.9% assigned to the invasive strategy (OR 0.78; 95% CI 0.62 to 0.97; P=0.025). Occurrence of death or MI was also reduced at 6 months (9.5% versus 7.3%; P less than 0.05). The beneficial effects on outcome were particularly evident in medium- and high-risk patients, as defined by an elevation of troponin T greater than 0.01 ng/mL or of troponin I greater than 0.1 ng/mL, the presence of ST-segment deviation, or a TIMI risk score greater than or equal to 3.7,30 In the absence of these high-risk features, outcomes in patients assigned to the 2 strategies were similar. Rates of major bleeding were similar, and lengths of hospital stay were reduced in patients assigned to the invasive strategy. The benefits of the invasive strategy were achieved at no significant increase in the cost of care over the 6-mo

2007;50;e159-e242; originally published online Sep 27, 2007; J. Am. Coll. Cardiol. Tarkington, and Clyde W. Yancy Lytle, Rick Nishimura, Joseph P. Ornato, Richard L. Page, Barbara Riegel, Lynn G. W. Valentin Fuster, Jonathan L. Halperin, Loren F. Hiratzka, Sharon A. Hunt, Bruce Christopher E. Buller, Mark A. Creager, Steven M. Ettinger, David P. Faxon, Alice K. Jacobs, Cynthia D. Adams, Jeffrey L. Anderson, Elliott M. Antman, K. Kasper, Judy R. Kersten, Barbara Riegel, John F. Robb, Sidney C. Smith, Jr, Chaikof, Kirsten E. Fleischmann, William K. Freeman, James B. Froehlich, Edward Lee A. Fleisher, Joshua A. Beckman, Kenneth A. Brown, Hugh Calkins, Elliott L. Vascular Surgery Interventions, Society for Vascular Medicine and Biology, and Society for and Cardiovascular Anesthesiologists, Society for Cardiovascular Angiography Society of Nuclear Cardiology, Heart Rhythm Society, Society of Collaboration With the American Society of Echocardiography, American Developed in Cardiovascular Evaluation for Noncardiac Surgery) (Writing Committee to Revise the 2002 Guidelines on Perioperative Cardiology/American Heart Association Task Force on Practice Guidelines Care for Noncardiac Surgery: A Report of the American College of ACC/AHA 2007 Guidelines on Perioperative Cardiovascular Evaluation and This information is current as of March 25, 2009 http://content.onlinejacc.org/cgi/content/full/50/17/e159 located on the World Wide Web at: The online version of this article, along with updated information and services, is

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The ACC/AHA Task Force on Practice Guidelines makes every effort to avoid any actual or potential conflicts of interest that might arise as a result of an outside relationship or personal interest of a member of the writing panel.Specifically, all members of the writing panel are asked to provide disclosure statements of all such relationships that might be perceived

The ACC/AHA Task Force on Practice Guidelines makes every effort to avoid any actual or potential conflicts of interest that might arise as a result of an outside relationship or personal interest of a member of the writing panel.Specifically, all members of the writing panel are asked to provide disclosure statements of all such relationships that might be perceived as real or potential conflicts of interest.These statements are reviewed by the parent task force, reported orally to all members of the writing panel at the first meeting, and updated as changes occur.The

<h3>Context</h3>Clinicians and trialists have difficulty with identifying which patients are highest risk for cardiovascular events. Prior ischemic events, polyvascular disease, and diabetes mellitus have all been identified as predictors of ischemic events, but their comparative contributions to future risk remain unclear.<h3>Objective</h3>To categorize the risk of cardiovascular events in stable outpatients with various initial manifestations of atherothrombosis using simple clinical descriptors.<h3>Design, Setting, and Patients</h3>Outpatients with coronary artery disease, cerebrovascular disease, or peripheral arterial disease or with multiple risk factors for atherothrombosis were enrolled in the global Reduction of Atherothrombosis for Continued Health (REACH) Registry and were followed up for as long as 4 years. Patients from 3647 centers in 29 countries were enrolled between 2003 and 2004 and followed up until 2008. Final database lock was in April 2009.<h3>Main Outcome Measures</h3>Rates of cardiovascular death, myocardial infarction, and stroke.<h3>Results</h3>A total of 45 227 patients with baseline data were included in this 4-year analysis. During the follow-up period, a total of 5481 patients experienced at least 1 event, including 2315 with cardiovascular death, 1228 with myocardial infarction, 1898 with stroke, and 40 with both a myocardial infarction and stroke on the same day. Among patients with atherothrombosis, those with a prior history of ischemic events at baseline (n = 21 890) had the highest rate of subsequent ischemic events (18.3%; 95% confidence interval [CI], 17.4%-19.1%); patients with stable coronary, cerebrovascular, or peripheral artery disease (n = 15 264) had a lower risk (12.2%; 95% CI, 11.4%-12.9%); and patients without established atherothrombosis but with risk factors only (n = 8073) had the lowest risk (9.1%; 95% CI, 8.3%-9.9%) (P &lt; .001 for all comparisons). In addition, in multivariable modeling, the presence of diabetes (hazard ratio [HR], 1.44; 95% CI, 1.36-1.53; P &lt; .001), an ischemic event in the previous year (HR, 1.71; 95% CI, 1.57-1.85; P &lt; .001), and polyvascular disease (HR, 1.99; 95% CI, 1.78-2.24; P &lt; .001) each were associated with a significantly higher risk of the primary end point.<h3>Conclusion</h3>Clinical descriptors can assist clinicians in identifying high-risk patients within the broad range of risk for outpatients with atherothrombosis.

Abdominal adiposity is a growing clinical and public health problem. It is not known whether it is similarly associated with cardiovascular disease (CVD) and diabetes mellitus in different regions around the world, and thus whether measurement of waist circumference (WC) in addition to body mass index (BMI) is useful in primary care practice.Randomly chosen primary care physicians in 63 countries recruited consecutive patients aged 18 to 80 years on 2 prespecified half days. WC and BMI were measured and the presence of CVD and diabetes mellitus recorded. Of the patients who consulted the primary care physicians, 97% agreed to participate in the present study. Overall, 24% of 69,409 men and 27% of 98,750 women were obese (BMI > or = 30 kg/m2). A further 40% and 30% of men and women, respectively, were overweight (BMI 25 to 30 kg/m2). Increased WC (> 102 for men and > 88 cm for women) was recorded in 29% and 48%, CVD in 16% and 13%, and diabetes mellitus in 13% and 11% of men and women, respectively. A statistically significant graded increase existed in the frequency of CVD and diabetes mellitus with both BMI and WC, with a stronger relationship for WC than for BMI across regions for both genders. This relationship between WC, CVD, and particularly diabetes mellitus was seen even in lean patients (BMI < 25 kg/m2).Among men and women who consulted primary care physicians, BMI and particularly WC were both strongly linked to CVD and especially to diabetes mellitus. Strategies to address this global problem are required to prevent an epidemic of these major causes of morbidity and mortality.

Selected care processes are increasingly being used to measure hospital quality; however, data regarding the association between hospital process performance and outcomes are limited.To evaluate contemporary care practices consistent with the American College of Cardiology/American Heart Association (ACC/AHA) guideline recommendations, to examine how hospital performance varied among centers, to identify characteristics predictive of higher guideline adherence, and to assess whether hospitals' overall composite guideline adherence was associated with observed and risk-adjusted in-hospital mortality rates.An observational analysis of hospital care in 350 academic and nonacademic US centers of 64,775 patients enrolled in the CRUSADE (Can Rapid Risk Stratification of Unstable Angina Patients Suppress Adverse Outcomes With Early Implementation of the ACC/AHA Guidelines) National Quality Improvement Initiative between January 1, 2001, and September 30, 2003, presenting with chest pain and positive electrocardiographic changes or cardiac biomarkers consistent with non-ST-segment elevation acute coronary syndrome (ACS).Use of 9 ACC/AHA class I guideline-recommended treatments and the correlation among hospitals' use of individual care processes as well as overall composite adherence rates.Overall, the 9 ACC/AHA guideline-recommended treatments were adhered to in 74% of eligible instances. There was modest correlation in hospital performance among the individual ACS process metrics. However, composite adherence performance varied widely (median [interquartile range] composite adherence scores from lowest to highest hospital quartiles, 63% [59%-66%] vs 82% [80%-84%]). Composite guideline adherence rate was significantly associated with in-hospital mortality, with observed mortality rates decreasing from 6.31% for the lowest adherence quartile to 4.15% for the highest adherence quartile (P<.001). After risk adjustment, every 10% increase in composite adherence at a hospital was associated with an analogous 10% decrease in its patients' likelihood of in-hospital mortality (adjusted odds ratio, 0.90; 95% confidence interval, 0.84-0.97; P<.001).A significant association between care process and outcomes was found, supporting the use of broad, guideline-based performance metrics as a means of assessing and helping improve hospital quality.

HomeCirculationVol. 108, No. 15ACC/AHA/ESC Guidelines for the Management of Patients With Supraventricular Arrhythmias*—Executive Summary Free AccessReview ArticlePDF/EPUBAboutView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toFree AccessReview ArticlePDF/EPUBACC/AHA/ESC Guidelines for the Management of Patients With Supraventricular Arrhythmias*—Executive SummaryA Report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines and the European Society of Cardiology Committee for Practice Guidelines (Writing Committee to Develop Guidelines for the Management of Patients With Supraventricular Arrhythmias) Committee Members Carina Blomström-Lundqvist, MD, PhD, FACC, FESC, Co-chair, Melvin M. Scheinman, MD, FACC, Co-chair, Etienne M. Aliot, MD, FACC, FESC, Joseph S. Alpert, MD, FACC, FAHA, FESC, Hugh Calkins, MD, FACC, FAHA, A. John Camm, MD, FACC, FAHA, FESC, W. Barton Campbell, MD, FACC, FAHA, David E. Haines, MD, FACC, Karl H. Kuck, MD, FACC, FESC, Bruce B. Lerman, MD, FACC, D. Douglas Miller, MD, CM, FACC, Charlie Willard ShaefferJr, MD, FACC, William G. Stevenson, MD, FACC, Gordon F. Tomaselli, MD, FACC, FAHA, Elliott M. Antman, Task Force Members:, MD, FACC, FAHA, Chair, Sidney C. SmithJr, MD, FACC, FAHA, FESC, Vice-Chair, Joseph S. Alpert, MD, FACC, FAHA, FESC, David P. Faxon, MD, FACC, FAHA, Valentin Fuster, MD, PhD, FACC, FAHA, FESC, Raymond J. Gibbons, MD, FACC, FAHA, Gabriel Gregoratos, MD, FACC, FAHA, Loren F. Hiratzka, MD, FACC, FAHA, Sharon Ann Hunt, MD, FACC, FAHA, Alice K. Jacobs, MD, FACC, FAHA, Richard O. RussellJr, MD, FACC, FAHA, ESC Committee for Practice Guidelines Members Silvia G. Priori, MD, PhD, FESC, Chair, Jean-Jacques Blanc, MD, PhD, FESC, Andzrej Budaj, MD, FESC, Enrique Fernandez Burgos, MD, Martin Cowie, MD, PhD, FESC, Jaap Willem Deckers, MD, PhD, FESC, Maria Angeles Alonso Garcia, MD, FESC, Werner W. Klein, MD, FACC, FESC, John Lekakis, MD, FESC, Bertil Lindahl, MD, Gianfranco Mazzotta, MD, FESC, João Carlos Araujo Morais, MD, FESC, Ali Oto, MD, FACC, FESC, Otto Smiseth, MD, PhD, FESC and Hans-Joachim Trappe, MD, PhD, FESC Committee Members , Carina Blomström-LundqvistCarina Blomström-Lundqvist , Melvin M. ScheinmanMelvin M. Scheinman , Etienne M. AliotEtienne M. Aliot , Joseph S. AlpertJoseph S. Alpert , Hugh CalkinsHugh Calkins , A. John CammA. John Camm , W. Barton CampbellW. Barton Campbell , David E. HainesDavid E. Haines , Karl H. KuckKarl H. Kuck , Bruce B. LermanBruce B. Lerman , D. Douglas MillerD. Douglas Miller , Charlie Willard ShaefferJrCharlie Willard ShaefferJr , William G. StevensonWilliam G. Stevenson , Gordon F. TomaselliGordon F. Tomaselli , Elliott M. AntmanElliott M. Antman , Sidney C. SmithJrSidney C. SmithJr , Joseph S. AlpertJoseph S. Alpert , David P. FaxonDavid P. Faxon , Valentin FusterValentin Fuster , Raymond J. GibbonsRaymond J. Gibbons , Gabriel GregoratosGabriel Gregoratos , Loren F. HiratzkaLoren F. Hiratzka , Sharon Ann HuntSharon Ann Hunt , Alice K. JacobsAlice K. Jacobs , Richard O. RussellJrRichard O. RussellJr , ESC Committee for Practice Guidelines Members , Silvia G. PrioriSilvia G. Priori , Jean-Jacques BlancJean-Jacques Blanc , Andzrej BudajAndzrej Budaj , Enrique Fernandez BurgosEnrique Fernandez Burgos , Martin CowieMartin Cowie , Jaap Willem DeckersJaap Willem Deckers , Maria Angeles Alonso GarciaMaria Angeles Alonso Garcia , Werner W. KleinWerner W. Klein , John LekakisJohn Lekakis , Bertil LindahlBertil Lindahl , Gianfranco MazzottaGianfranco Mazzotta , João Carlos Araujo MoraisJoão Carlos Araujo Morais , Ali OtoAli Oto , Otto SmisethOtto Smiseth and Hans-Joachim TrappeHans-Joachim Trappe Originally published14 Oct 2003https://doi.org/10.1161/01.CIR.0000091380.04100.84Circulation. 2003;108:1871–1909Preamble 1872 I. Introduction 1872 A. Organization of Committee and Evidence Review 1872 B. Contents of These Guidelines—Scope 1873 II. Public Health Considerations and Epidemiology 1873 III. General Mechanisms of Supraventricular Arrhythmia 1874 A. Specialized Atrial Tissue 1874 B. General Mechanisms 1874 IV. Clinical Presentation, General Evaluation, and Management of Patients With Supraventricular Arrhythmia 1874 A. General Evaluation of Patients Without Documented Arrhythmia 1874 Clinical History and Physical Examination 1874 Diagnostic Investigations 1875 Management 1876 B. General Evaluation of Patients With Documented Arrhythmia 1876 Diagnostic Evaluation 1876 Management 1878 V. Specific Arrhythmias 1880 A. Sinus Tachyarrhythmias 1880 Physiological Sinus Tachycardia 1880 Inappropriate Sinus Tachycardia 1881 Postural Orthostatic Tachycardia Syndrome 1883 Sinus Node Re-entry Tachycardia 1883 B. Atrioventricular Nodal Reciprocating Tachycardia 1884 Definitions and Clinical Features 1884 Acute Treatment 1884 Long-Term Pharmacologic Therapy 1884 Catheter Ablation 1885 C. Focal and Nonparoxysmal Junctional Tachycardia 1886 Focal Junctional Tachycardia 1886 Nonparoxysmal Junctional Tachycardia 1887 D. Atrioventricular Reciprocating Tachycardia (Extra Nodal Accessory Pathways) 1888 Sudden Death in WPW Syndrome and Risk Stratification 1888 Acute Treatment 1889 Long-Term Pharmacologic Therapy 1889 Catheter Ablation 1890 Management of Patients With Asymptomatic Accessory Pathways 1891 Summary of Management 1891 E. Focal Atrial Tachycardias 1891 Definition and Clinical Presentation 1891 Diagnosis 1891 Site of Origin and Mechanisms 1892 Treatment 1892 Multifocal Atrial Tachycardia 1894 F. Macro–Re-entrant Atrial Tachycardia 1894 Isthmus-Dependent Atrial Flutter 1894 Non–Cavotricuspid Isthmus–Dependent Atrial Flutter 1898 VI. Special Circumstances 1899 A. Pregnancy 1899 Acute Conversion of Atrioventricular Node– Dependent Tachycardias 1901 Prophylactic Antiarrhythmic Drug Therapy 1901 B. Supraventricular Tachycardias in Adult Patients With Congenital Heart Disease 1901 Introduction 1902 Specific Disorders 1902 C. Quality-of-Life and Cost Considerations 1903References 1904PreambleThese practice guidelines are intended to assist physicians in clinical decision making by describing a range of generally acceptable approaches for the diagnosis and management of supraventricular arrhythmias. These guidelines attempt to define practices that meet the needs of most patients in most circumstances. The ultimate judgment regarding care of a particular patient must be made by the physician and the patient in light of all of the circumstances presented by that patient. There are situations in which deviations from these guidelines are appropriate.I. IntroductionA. Organization of Committee and Evidence ReviewSupraventricular arrhythmias are a group of common rhythm disturbances. The most common treatment strategies include antiarrhythmic drug therapy and catheter ablation. Over the past decade, the latter has been shown to be a highly successful and often curative intervention. To facilitate and optimize the management of patients with supraventricular arrhythmias, the American College of Cardiology Foundation (ACCF), the American Heart Association (AHA), and the European Society of Cardiology (ESC) created a committee to establish guidelines for better management of these heterogeneous tachyarrhythmias. This document summarizes the management of patients with supraventricular arrhythmias with recommendations for diagnostic procedures as well as indications for antiarrhythmic drugs and/or nonpharmacologic treatments.Writing groups are specifically charged to perform a formal literature review, weigh the strength of evidence for or against a particular treatment or procedure, and include estimates of expected health outcomes where data exist. Patient-specific modifiers, comorbidities, and issues of patient preference that might influence the choice of particular tests or therapies are considered, as are frequency of follow-up and cost effectiveness. In controversial areas, or with regard to issues without evidence other than usual clinical practice, a consensus was achieved by agreement of the expert panel after thorough deliberations.This document was peer reviewed by two official external reviewers representing the American College of Cardiology Foundation, two official external reviewers representing the American Heart Association, and two official external reviewers representing the European Society of Cardiology. The North American Society for Pacing and Electrophysiology—Heart Rhythm Society assigned one organizational reviewer to the guideline. In addition, 37 external content reviewers participated in the review representing the ACC/AHA Task Force on Practice Guidelines, the ESC Committee for Practice Guidelines, the ACCF Electrophysiology Committee, the AHA ECG/Arrhythmias Committee, the ESC Working Group on Arrhythmias, and the ESC Task Force on Grown-Up Congenital Heart Disease. Please see Appendix 2 in the full-text guideline for the names of all reviewers.The document was approved for publication by the governing bodies of the ACCF, AHA, and ESC. These guidelines will be reviewed annually by the ESC and the ACC/AHA Task Force on Practice Guidelines and will be considered current unless they are revised or withdrawn from distribution.Recommendations are evidence-based and derived primarily from published data. The level of evidence was ranked as follows:Level A (highest): derived from multiple randomized clinical trials;Level B (intermediate): data are on the basis of a limited number of randomized trials, nonrandomized studies, or observational registries;Level C (lowest): primary basis for the recommendation was expert consensus.Recommendations follow the format of previous ACC/AHA guidelines for classifying indications, summarizing both the evidence and expert opinion.Class I: Conditions for which there is evidence for and/or general agreement that the procedure or treatment is useful and effective.Class II: Conditions for which there is conflicting evidence and/or a divergence of opinion about the usefulness/efficacy of a procedure or treatment. Class IIa: The weight of evidence or opinion is in favor of the procedure or treatment. Class IIb: Usefulness/efficacy is less well established by evidence or opinion.Class III: Conditions for which there is evidence and/or general agreement that the procedure or treatment is not useful/effective and in some cases may be harmful.B. Contents of these Guidelines—ScopeThe purpose of this joint ACC/AHA/ESC document is to provide clinicians with practical and authoritative guidelines for the management and treatment of patients with supraventricular arrhythmias (SVA). These include rhythms emanating from the sinus node, from atrial tissue (atrial flutter), and from junctional as well as reciprocating or accessory pathway–mediated tachycardia. This document does not include recommendations for patients with either atrial fibrillation (AF) (see ACC/AHA/ESC Guidelines for the Management of Patients With Atrial Fibrillation1) or for pediatric patients with supraventricular arrhythmias. For our purposes, the term "supraventricular arrhythmia" refers to all types of supraventricular arrhythmias, excluding AF, as opposed to SVT, which includes atrioventricular nodal reciprocating tachycardia (AVNRT), atrioventricular reciprocating tachycardia (AVRT), and atrial tachycardia (AT).Overall, this is a consensus document that includes evidence and expert opinions from several countries. The pharmacologic and nonpharmacologic antiarrhythmic approaches discussed may, therefore, include some drugs and devices that do not have the approval of governmental regulatory agencies. Because antiarrhythmic drug dosages and drug half-lives are detailed in the ACC/AHA/ESC Guidelines for the Management of Patients With Atrial Fibrillation,1 they are not repeated in this document.II. Public Health Considerations and EpidemiologySupraventricular arrhythmias are relatively common, often repetitive, occasionally persistent, and rarely life threatening. The precipitants of supraventricular arrhythmias vary with age, sex, and associated comorbidity.2Failure to discriminate among AF, atrial flutter, and other supraventricular arrhythmias has complicated the precise definition of this arrhythmia in the general population. The estimated prevalence of paroxysmal supraventricular tachycardia (PSVT) in a 3.5% sample of medical records in the Marshfield (Wisconsin) Epidemiologic Study Area (MESA) was 2.25 per 1000.3 The incidence of PSVT in this survey was 35 per 100 000 person-years.3Age exerts an influence on the occurrence of SVT. The mean age at the time of PSVT onset in the MESA cohort was 57 years (ranging from infancy to more than 90 years old).3 In the MESA population, compared with those with other cardiovascular disease, "lone" (no cardiac structural disease) PSVT patients were younger (mean age equals 37 versus 69 years), had faster heart rates (186 versus 155 beats per minute [bpm]), and were more likely to present first to an emergency room (69% versus 30%).3 The age of tachycardia onset is higher for AVNRT (32 plus or minus 18 years) than for AVRT (23 plus or minus 14 years).Gender plays a role in the epidemiology of SVT. Female residents in the MESA population had a twofold greater relative risk (RR) of PSVT (RR equals 2.0; 95% confidence interval equals 1.0 to 4.2) compared with males.3The only reported epidemiologic study of patients with atrial flutter4 involved a selected sample of individuals treated in the Marshfield Clinic in predominantly white, rural mid-Wisconsin. More than 75% of the 58 820 residents and virtually all health events were included in this population database. In approximately 60% of cases, atrial flutter occurred for the first time in association with a specific precipitating event (ie, major surgery, pneumonia, or acute myocardial infarction). In the remaining patients, atrial flutter was associated with chronic comorbid conditions (ie, heart failure, hypertension, and chronic lung disease). Only 1.7% of cases had no structural cardiac disease or precipitating causes (lone atrial flutter). The overall incidence of atrial flutter was 0.088%; 58% of these patients also had AF. Atrial flutter alone was seen in 0.037%. The incidence of atrial flutter increased markedly with age, from 5 per 100 000 of those more than 50 years old to 587 per 100 000 over age 80. Atrial flutter was 2.5 times more common in men and was diagnosed twice as often as PSVT.III. General Mechanisms of SVAA. Specialized Atrial TissueThe sinoatrial node, atria, and atrioventricular (AV) node are heterogeneous structures. There is distinct electrophysiological specialization of tissues and cells within these structures. In the case of the nodes, cellular heterogeneity is a prominent feature.The sinoatrial node is a collection of morphologically and electrically distinct cells.5,6 The central portion of the sinus node, which houses the dominant pacemaking function, contains cells with longer action potentials and faster rates of phase 4 diastolic depolarization than other cardiac cells.6,7Cellular recordings support the existence of distinct populations of cells in the mammalian AV node. Differences in ion channel expression underlie the differences in the electrophysiological behavior of each of the cell types.B. General MechanismsAll cardiac tachyarrhythmias are produced by one or more mechanisms, including disorders of impulse initiation and abnormalities of impulse conduction. The former are often referred to as automatic, and the latter as re-entrant. Tissues exhibiting abnormal automaticity that underlie SVT can reside in the atria, the AV junction, or vessels that communicate directly with the atria, such as the vena cava or pulmonary veins.8,9 The cells with enhanced automaticity exhibit enhanced diastolic phase 4 depolarization and, therefore, an increase in firing rate compared with pacemaker cells. If the firing rate of the ectopic focus exceeds that of the sinus node, then the sinus node can be overdriven and the ectopic focus will become the predominant pacemaker of the heart. The rapid firing rate may be incessant (ie, more than 50% of the day) or episodic.Triggered activity is a tachycardia mechanism associated with disturbances of recovery or repolarization. Triggered rhythms are generated by interruptions in repolarization of a heart cell called afterdepolarizations. An afterdepolarization of sufficient magnitude may reach "threshold" and trigger an early action potential during repolarization.The most common arrhythmia mechanism is re-entry, which may occur in different forms. In its simplest form, it occurs as repetitive excitation of a region of the heart and is a result of conduction of an electrical impulse around a fixed obstacle in a defined circuit. This is referred to as re-entrant tachycardia. There are several requirements for the initiation and maintenance of this type of re-entry. Initiation of a circus movement tachycardia requires unidirectional conduction block in one limb of a circuit. Unidirectional block may occur as a result of acceleration of the heart rate or block of a premature impulse that impinges on the refractory period of the pathway. Slow conduction is usually required for both initiation and maintenance of a circus movement tachycardia. In the case of orthodromic AV re-entry (ie, anterograde conduction across the AV node with retrograde conduction over an accessory pathway), slowed conduction through the AV node allows for recovery of, and retrograde activation over, the accessory pathway.Re-entry is the mechanism of tachycardia in SVTs such as AVRT, AVNRT and atrial flutter; however, a fixed obstacle and predetermined circuit are not essential requirements for all forms of re-entry. In functionally determined re-entry, propagation occurs through relatively refractory tissue and there is an absence of a fully excitable gap. Specific mechanisms are considered in the following sections.IV. Clinical Presentation, General Evaluation, and Management of Patients With SVAA. General Evaluation of Patients Without Documented Arrhythmia1. Clinical History and Physical ExaminationPatients with paroxysmal arrhythmias are most often asymptomatic at the time of evaluation. Arrhythmia-related symptoms include palpitations; fatigue; lightheadedness; chest discomfort; dyspnea; presyncope; or, more rarely, syncope.A history of arrhythmia-related symptoms may yield important clues to the type of arrhythmia. Premature beats are commonly described as pauses or nonconducted beats followed by a sensation of a strong heart beat, or they are described as irregularities in heart rhythm. Supraventricular tachycardias occur in all age groups and may be associated with minimal symptoms, such as palpitations, or they may present with syncope. The clinician should distinguish whether the palpitations are regular or irregular. Irregular palpitations may be due to premature depolarizations, AF, or multifocal atrial tachycardia (MAT). The latter are most commonly encountered in patients with pulmonary disease. If the arrhythmia is recurrent and has abrupt onset and termination, then it is designated paroxysmal. Sinus tachycardia is, conversely, nonparoxysmal and accelerates and terminates gradually. Patients with sinus tachycardia may require evaluation for stressors, such as infection or volume loss. Episodes of regular and paroxysmal palpitations with a sudden onset and termination (also referred to as PSVT) most commonly result from AVRT or AVNRT. Termination by vagal maneuvers further suggests a re-entrant tachycardia involving AV nodal tissue (eg, AVNRT, AVRT). Polyuria is caused by release of atrial natriuretic peptide in response to increased atrial pressures from contraction of atria against a closed AV valve, which is supportive of a sustained supraventricular arrhythmia.With SVT, syncope is observed in approximately 15% of patients, usually just after initiation of rapid SVT or with a prolonged pause after abrupt termination of the tachycardia. Syncope may be associated with AF with rapid conduction over an accessory AV pathway or may suggest concomitant structural abnormalities, such as valvular aortic stenosis, hypertrophic cardiomyopathy, or cerebrovascular disease. Symptoms vary with the ventricular rate, underlying heart disease, duration of SVT, and individual patient perceptions. Supraventricular tachycardia that is persistent for weeks to months and associated with a fast ventricular response may lead to a tachycardia-mediated cardiomyopathy.10,11Of crucial importance in clinical decision making is a clinical history describing the pattern in terms of the number of episodes, duration, frequency, mode of onset, and possible triggers.Supraventricular tachycardia has a heterogeneous clinical presentation, most often occurring in the absence of detectable heart disease in younger individuals. The presence of associated heart disease should nevertheless always be sought, and an echocardiogram may be helpful. While a physical examination during tachycardia is standard, it usually does not lead to a definitive diagnosis. If irregular cannon A waves and/or irregular variation in S1 intensity is present, then a ventricular origin of a regular tachycardia is strongly suggested.2. Diagnostic InvestigationsA resting 12-lead echocardiogram (ECG) should be recorded. The presence of pre-excitation on the resting ECG in a patient with a history of paroxysmal regular palpitations is sufficient for the presumptive diagnosis of AVRT, and attempts to record spontaneous episodes are not required before referral to an arrhythmia specialist for therapy (Figure 1). Specific therapy is discussed in Section V. A clinical history of irregular and paroxysmal palpitations in a patient with baseline pre-excitation strongly suggests episodes of AF, which requires immediate electrophysiological evaluation because these patients are at risk for significant morbidity and possibly sudden death (see Section V-D). The diagnosis is otherwise made by careful analysis of the 12-lead ECG during tachycardia (see Section IV). Therefore, patients with a history of sustained arrhythmia should always be encouraged to have at least one 12-lead ECG taken during the arrhythmia. Automatic analysis systems of 12-lead ECGs are unreliable and commonly suggest an incorrect arrhythmia diagnosis. Download figureDownload PowerPointFigure 1. Initial evaluation of patients with suspected tachycardia. AVRT indicates atrioventricular reciprocating tachycardia.Indications for referral to a cardiac arrhythmia specialist include presence of a wide complex tachycardia of unknown origin. For those with narrow complex tachycardias, referral is indicated for those with drug resistance or intolerance as well as for patients desiring to be free of drug therapy. Because of the potential for lethal arrhythmias, all patients with the Wolff-Parkinson-White (WPW) syndrome (ie, pre-excitation combined with arrhythmias) should be referred for further evaluation. All patients with severe symptoms, such as syncope or dyspnea, during palpitations should also be referred for prompt evaluation by an arrhythmia specialist. An echocardiographic examination should be considered in patients with documented sustained SVT to exclude the possibility of structural heart disease, which usually cannot be detected by physical examination or 12-lead ECG.An ambulatory 24-hour Holter recording can be used in patients with frequent (ie, several episodes per week) but transient tachycardias.12 An event or wearable loop recorder is often more useful than a 24-hour recording in patients with less frequent arrhythmias. Implantable loop recorders may be helpful in selected cases with rare symptoms (ie, fewer than two episodes per month) associated with severe symptoms of hemodynamic instability.13 Exercise testing is less often useful for diagnosis unless the arrhythmia is clearly triggered by exertion.Transesophageal atrial recordings and stimulation may be used in selected cases for diagnosis or to provoke paroxysmal tachyarrhythmias if the clinical history is insufficient or if other measures have failed to document an arrhythmia. Esophageal stimulation is not indicated if invasive electrophysiological investigation is planned. Invasive electrophysiological investigation with subsequent catheter ablation may be used for diagnoses and therapy in cases with a clear history of paroxysmal regular palpitations. It may also be used empirically in the presence of pre-excitation or disabling symptoms (Figure 1).3. ManagementThe management of patients with symptoms suggestive of an arrhythmia but without ECG documentation depends on the nature of the symptoms. If the surface ECG is normal and the patient reports a history consistent with premature extra beats, then precipitating factors, such as excessive caffeine, alcohol, nicotine intake, recreational drugs, or hyperthyroidism, should be reviewed and eliminated. Benign extrasystoles are often manifest at rest and tend to become less common with exercise.If symptoms and the clinical history indicate that the arrhythmia is paroxysmal in nature and the resting 12-lead ECG gives no clue for the arrhythmia mechanism, then further diagnostic tests for documentation may not be necessary before referral for an invasive electrophysiological study and/or catheter ablation. Patients should be taught to perform vagal maneuvers. A beta-blocking agent may be prescribed empirically provided that significant bradycardia (less than 50 bpm) have been excluded. Due to the risk of proarrhythmia, antiarrhythmic treatment with class I or class III drugs should not be initiated without a documented arrhythmia.B. General Evaluation of Patients With Documented Arrhythmia1. Diagnostic EvaluationWhenever possible, a 12-lead ECG should be taken during tachycardia but should not delay immediate therapy to terminate the arrhythmia if there is hemodynamic instability. At a minimum, a monitor strip should be obtained from the defibrillator, even in cases with cardiogenic shock or cardiac arrest, before direct current (DC) cardioversion is applied to terminate the arrhythmia.a. Differential Diagnosis for Narrow QRS-Complex TachycardiaIf ventricular action (QRS) is narrow (less than 120 ms), then the tachycardia is almost always supraventricular and the differential diagnosis relates to its mechanism (Figure 2). If no P waves or evidence of atrial activity is apparent and the RR interval is regular, then AVNRT is most commonly the mechanism. P-wave activity in AVNRT may be only partially hidden within the QRS complex and may deform the QRS to give a pseudo–R wave in lead V1 and/or a pseudo–S wave in inferior leads (Figure 3). If a P wave is present in the ST segment and separated from the QRS by 70 ms, then AVRT is most likely. In tachycardias with RP longer than PR, the most likely diagnosis is atypical AVNRT, permanent form of junctional reciprocating tachycardia (PJRT) (ie, AVRT via a slowly conducting accessory pathway), or AT (see Section V-B, D, and E). Responses of narrow QRS-complex tachycardias to adenosine or carotid massage may aid in the differential diagnosis (Figure 4).14,15 A 12-lead ECG recording is desirable during use of adenosine or carotid massage. If P waves are not visible, then the use of esophageal pill electrodes can also be helpful. Download figureDownload PowerPointFigure 2. Differential diagnosis for narrow QRS tachycardia. Patients with focal junctional tachycardia may mimic the pattern of slow–fast AVNRT and may show AV dissociation and/or marked irregularity in the junctional rate. AV indicates atrioventricular; AVNRT, atrioventricular nodal reciprocating tachycardia; AVRT, atrioventricular reciprocating tachycardia; MAT, multifocal atrial tachycardia; ms, milliseconds; PJRT, permanent form of junctional reciprocating tachycardia; QRS, ventricular activation on ECG.Download figureDownload PowerPointFigure 3. ECG pattern of typical AVNRT. Panel A: 12-Lead ECG shows a regular SVT recorded at an ECG paper speed of 25 mm/sec. Panel B: After conversion to sinus rhythm, the 12-lead ECG shows sinus rhythm with narrow QRS complexes. In comparison with Panel A: Note the pseudo r' in V1 (arrow) and accentuated S waves in 2, 3, aVF (arrow). These findings are pathognomonic for AVNRT. AVNRT indicates atrioventricular nodal reciprocating tachycardia; mm/sec, millimeters per second; QRS, ventricular activation on ECG; SVT, supraventricular tachycardia; VF, ventricular fibrillation.Download figureDownload PowerPointFigure 4. Responses of narrow complex tachycardias to adenosine. AT indicates atrial tachycardia; AV, atrioventricular; AVNRT, atrioventricular nodal reciprocating tachycardia; AVRT, atrioventricular reciprocating tachycardia; IV, intravenous; QRS, ventricular activation on ECG; VT, ventricular tachycardia.b. Differential Diagnosis for Wide QRS-Complex TachycardiaIf the QRS is wide (more than 120 ms), then it is important to differentiate between SVT and ventricular tachycardia (VT) (Figure 5). Intravenous medications given for the treatment of SVT, particularly verapamil or diltiazem, may be deleterious because they may precipitate hemodyna

Substantial progress has been made in the awareness, treatment, and prevention of cardiovascular disease (CVD) in women since the first women-specific clinical recommendations for the prevention of CVD were published by the American Heart Association (AHA) in 1999.1 The myth that heart disease is a “man's disease” has been debunked; the rate of public awareness of CVD as the leading cause of death among US women has increased from 30% in 1997 to 54% in 2009.2 The age-adjusted death rate resulting from coronary heart disease (CHD) in females, which accounts for about half of all CVD deaths in women, was 95.7 per 100 000 females in 2007, a third of what it was in 1980.3,4 Approximately 50% of this decline in CHD deaths has been attributed to reducing major risk factors and the other half to treatment of CHD including secondary preventive therapies.4 Major randomized controlled clinical trials such as the Women's Health Initiative have changed the practice of CVD prevention in women over the past decade.5 The investment in combating this major public health issue for women has been significant, as have the scientific and medical achievements. Despite the gains that have been made, considerable challenges remain. In 2007, CVD still caused ≈1 death per minute among women in the United States.6 These represent 421 918 deaths, more women's lives than were claimed by cancer, chronic lower respiratory disease, Alzheimer disease, and accidents combined.6 Reversing a trend of the past 4 decades, CHD death rates in US women 35 to 54 years of age now actually appear to be increasing, likely because of the effects of the obesity epidemic.4 CVD rates in the United States are significantly higher for black females compared with their white counterparts (286.1/100 000 versus …

### Table of contents It is important that the medical profession play a significant role in critically evaluating the use of diagnostic procedures and therapies in the management or prevention of disease states. Rigorous and expert analysis of the available data documenting relative benefits and

These practice guidelines are intended to assist physicians in clinical decision making by describing a range of generally acceptable approaches for the diagnosis and management of supraventricular arrhythmias. These guidelines attempt to define practices that meet the needs of most patients in most

Background Mitral regurgitation (MR) may complicate acute myocardial infarction (MI). However, it is not known whether mild MR is an independent predictor of post-MI outcome. Methods and Results The study cohort consisted of 727 Survival and Ventricular Enlargement Study patients who underwent cardiac catheterization, including left ventriculography, up to 16 days after MI. Left ventriculograms were analyzed for diastolic and systolic volumes, global left ventricular sphericity, extent of wall motion abnormality, and endocardial curvature. The presence of MR was related to the risk of developing a cardiovascular event during 3.5 years of follow-up. MR was present in 141 patients (19.4%). Severe (3+) MR was present in only 2 patients. Patients with MR were more likely to have a persistently occluded infarct artery (MR versus no MR, 27.3% versus 15.2%; P =.001). Although the ejection fractions were similar, MR patients had larger end-systolic and end-diastolic volumes and more spherical ventricles than patients without MR. Sphericity change from diastole to systole was also significantly reduced in MR patients. Patients with MR were more likely to experience cardiovascular mortality (29% versus 12%; P &lt;.001), severe heart failure (24% versus 16%; P =.0153), and the combined end point of cardiovascular mortality, severe heart failure, or recurrent myocardial infarction (47% versus 29%; P &lt;.001). The presence of MR was an independent predictor of cardiovascular mortality (relative risk, 2.00; 95% CI, 1.28 to 3.04). Conclusions Mild MR is an independent predictor of post-MI mortality. As such, it adds important information for risk stratification of post-MI patients.

HomeArteriosclerosis, Thrombosis, and Vascular BiologyVol. 24, No. 2Definition of Metabolic Syndrome

IntroductionAtrial fibrillation (AF), the most common sustained cardiac rhythm disturbance, is increasing in prevalence as the popu-lation ages.Although it is often associated with heart disease, AF occurs in many patients with no detectable disease.Hemodynamic impairment and thromboembolic events result This document was

The American College of Cardiology/American Heart Association (ACC/AHA) Task Force on Practice Guidelines was formed to gather information and make recommendations about appropriate use of technology for the diagnosis and treatment of patients with cardiovascular disease. Percutaneous coronary interventions (PCI) are an important group of technologies in this regard. Although initially limited to PTCA, and termed percutaneous transluminal coronary angioplasty (PTCA), PCI now includes other new techniques capable of relieving coronary narrowing. Accordingly, in this document, rotational atherectomy, directional atherectomy, extraction atherectomy, laser angioplasty, implantation of intracoronary stents and other catheter devices for treating coronary atherosclerosis are considered components of PCI. In this context PTCA will be used to refer to those studies using primarily PTCA while PCI will refer to the broader group of percutaneous techniques. These new technologies have impacted the effectiveness and safety profile initially established for PTCA. Moreover, important advances have occurred in the use of adjunctive medical therapies such as glycoprotein (GP) IIb/IIIa receptor blockers. In addition, since publication of the previous Guidelines in 1993, greater experience in the performance of PCI in patients with acute coronary syndromes and in community hospital settings has been gained. In view of these developments, further review and revision of the guidelines is warranted. This document reflects the opinion of the third ACC/AHA committee charged with revising the guidelines for PTCA to include the broader group of technologies now termed PCI. Several issues relevant to the Committee’s process and the interpretation of the Guidelines have been noted previously and are worthy of restatement. First, PCI is a technique that has been continually refined and modified; hence continued, periodic Guideline revision is anticipated. Second, these guidelines are to be viewed as broad recommendations to aid in the appropriate application of PCI. Under unique circumstances, exceptions may exist. These Guidelines are …

HomeCirculationVol. 108, No. 11ACC/AHA/ASNC Guidelines for the Clinical Use of Cardiac Radionuclide Imaging—Executive Summary Free AccessReview ArticlePDF/EPUBAboutView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toFree AccessReview ArticlePDF/EPUBACC/AHA/ASNC Guidelines for the Clinical Use of Cardiac Radionuclide Imaging—Executive SummaryA Report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (ACC/AHA/ASNC Committee to Revise the 1995 Guidelines for the Clinical Use of Cardiac Radionuclide Imaging) Committee Members Francis J. Klocke, Michael G. Baird, Beverly H. Lorell, Timothy M. Bateman, Joseph V. Messer, Daniel S. Berman, Patrick T. O’Gara, Blase A. Carabello, Richard O. RussellJr, Manuel D. Cerqueira, Martin G. St. John Sutton, Anthony N. DeMaria, James E. Udelson, J. Ward Kennedy, Mario S. Verani, Kim Allan Williams, Elliott M. Antman, Sidney C. SmithJr, Joseph S. Alpert, Gabriel Gregoratos, Jeffrey L. Anderson, Loren F. Hiratzka, David P. Faxon, Sharon Ann Hunt, Valentin Fuster, Alice K. Jacobs, Raymond J. Gibbons and Richard O. Russell Committee Members , Francis J. KlockeFrancis J. Klocke , Michael G. BairdMichael G. Baird , Beverly H. LorellBeverly H. Lorell , Timothy M. BatemanTimothy M. Bateman , Joseph V. MesserJoseph V. Messer , Daniel S. BermanDaniel S. Berman , Patrick T. O’GaraPatrick T. O’Gara , Blase A. CarabelloBlase A. Carabello , Richard O. RussellJrRichard O. RussellJr , Manuel D. CerqueiraManuel D. Cerqueira , Martin G. St. John SuttonMartin G. St. John Sutton , Anthony N. DeMariaAnthony N. DeMaria , James E. UdelsonJames E. Udelson , J. Ward KennedyJ. Ward Kennedy , Mario S. VeraniMario S. Verani , Kim Allan WilliamsKim Allan Williams , Elliott M. AntmanElliott M. Antman , Sidney C. SmithJrSidney C. SmithJr , Joseph S. AlpertJoseph S. Alpert , Gabriel GregoratosGabriel Gregoratos , Jeffrey L. AndersonJeffrey L. Anderson , Loren F. HiratzkaLoren F. Hiratzka , David P. FaxonDavid P. Faxon , Sharon Ann HuntSharon Ann Hunt , Valentin FusterValentin Fuster , Alice K. JacobsAlice K. Jacobs , Raymond J. GibbonsRaymond J. Gibbons and Richard O. RussellRichard O. Russell Originally published16 Sep 2003https://doi.org/10.1161/01.CIR.0000080946.42225.4DCirculation. 2003;108:1404–1418I. Introduction 1405II. Acute Syndromes 1406 A. Myocardial Perfusion Imaging in the Assessment of Patients Presenting With Chest Pain to the Emergency Department 1406 B. Detection of AMI When Conventional Measures Are Nondiagnostic 1406 C. Radionuclide Testing in Risk Assessment: Prognosis and Assessment of Therapy After STEMI 1406D. Radionuclide Testing in Risk Assessment: Prognosis and Assessment of Therapy After NSTEMI or UA 1406III. Chronic Syndromes 1407 A. Detection (Diagnosis) of CAD 1407 Sensitivity and Specificity 1407 Effect of Referral Bias 1407 Quantitative Analysis 1408 ECG-Gated SPECT 1408 Attenuation Correction 1408 Positron Emission Tomography 1408 B. Management of Patients With Known or Suspected Chronic CAD: Assessment of Disease Severity, Risk Stratification, Prognosis 1408 Nongated Myocardial Perfusion Imaging 1408 Gated SPECT 1408 Radionuclide Angiography 1408 Cost Effectiveness 1408 Frequency of Testing 1408 Evaluation of the Effects of Medical Therapy 1408 C. Specific Patient Populations 1408 African Americans 1408 Women 1408 Normal Resting ECG, Able to Exercise 1409 Intermediate-Risk Duke Treadmill Score 1409 Normal Resting ECG, Unable to Exercise 1409 LBBB/Pacemakers 1409 Left Ventricular Hypertrophy 1409 Patients With Nonspecific ST-T-Wave Changes 1409 Elderly 1409 Asymptomatic Patients 1409 Obese Patients 1409 Diabetes 1409 After Coronary Calcium Screening 1410 Before and After Revascularization 1410 Radionuclide Imaging Before Noncardiac Surgery 1410 D. Recommendations 1410IV. Heart Failure 1412 A. Introduction 1412 B. Assessment of LV Function 1413 Assessment of LV Systolic Dysfunction 1413 Assessment of LV Diastolic Dysfunction 1413 C. Assessment of CAD 1413 Importance of Detecting CAD in Heart Failure Patients 1413 Myocardial Perfusion Imaging to Detect CAD in Heart Failure Patients 1413 D. Assessment of Myocardial Viability 1413 Goals of Assessing Myocardial Viability 1413 General Principles of Assessing Myocardial Viability by Radionuclide Techniques 1414 Techniques and Protocols for Assessing Myocardial Viability 1414 Image Interpretation for Myocardial Viability: Quantitative Versus Visual Analysis of Tracer Activities 1414 Comparison of Techniques 1414 E. Etiologies of Heart Failure 1415 Dilated Cardiomyopathy 1415 Dilated Cardiomyopathy Due to Doxorubicin/Anthracycline Cardiotoxicity 1415 Dilated Cardiomyopathy Due to Myocarditis 1415 Posttransplantation Rejection and Allograft Vasculopathy 1415 Chagas Myocarditis and/or Cardiomyopathy 1416 Sarcoid Heart Disease 1416 Cardiac Amyloidosis 1416 RV Dysplasia 1416 Hypertrophic Cardiomyopathy 1416 Hypertensive Heart Disease 1416 Valvular Heart Disease 1416 Adults With Congenital Heart Disease 1417 References 1417I. IntroductionThe American College of Cardiology (ACC)/American Heart Association (AHA) Task Force on Practice Guidelines regularly reviews existing guidelines to determine when an update or full revision is needed. Guidelines for the Clinical Use of Cardiac Radionuclide Imaging were originally published in 1986 and updated in 1995. Important new developments have continued to occur since 1995, particularly in the areas of acute and chronic ischemic syndromes and heart failure. The Task Force therefore believed the topic should be revisited de novo and invited the American Society for Nuclear Cardiology (ASNC) to cosponsor the undertaking, which represents a joint effort of the 3 organizations.The full-text guideline is available on the Internet (www.acc.org, www.americanheart.org, and www.asnc.org). It discusses the usefulness of nuclear cardiological techniques in 3 broad areas: acute ischemic syndromes, chronic syndromes, and heart failure. Utility is considered for diagnosis, severity of disease/risk assessment/prognosis, and assessment of therapy. An appendix provides descriptions of individual techniques. This Executive Summary includes recommended indications for the use of specific techniques and summary evaluations of topics addressed in the full-text document. Additional supporting evidence and a complete reference list are presented in the full-text document.The current guideline overlaps with several previously published ACC/AHA guidelines for patient treatment that potentially involve cardiac radionuclide imaging. These include published guidelines for chronic stable angina (SA; 2002), unstable angina and non–ST-elevation myocardial infarction (UA/NSTEMI; 2002), heart failure (2001), perioperative cardiovascular evaluation for noncardiac surgery (2002), exercise testing (2002), valvular heart disease (1998), and acute myocardial infarction (AMI; 1999). The present report is not intended to include information previously covered in these guidelines or to provide a comprehensive treatment of the topics addressed in these guidelines.The ACC/AHA classifications I, II, and III are used to summarize indications as follows:Class I: Conditions for which there is evidence and/or general agreement that a given procedure or treatment is useful and effectiveClass II: Conditions for which there is conflicting evidence and/or a divergence of opinion about the usefulness/efficacy of a procedure or treatment IIa: Weight of evidence/opinion is in favor of usefulness/efficacy IIb: Usefulness/efficacy is less well established by evidence/opinionClass III: Conditions for which there is evidence and/or general agreement that the procedure/treatment is not useful/effective and in some cases may be harmfulLevels of evidence for individual class assignments are designated as follows:A: Data derived from multiple randomized clinical trialsB: Data derived from a single randomized trial or from nonrandomized studiesC: Consensus opinion of expertsThese guidelines will be reviewed annually by the Task Force and will be considered current unless the Task Force revises or withdraws them from distribution.II. Acute SyndromesA. Myocardial Perfusion Imaging in the Assessment of Patients Presenting With Chest Pain to the Emergency DepartmentOptimal decision-making in patients seen in the emergency department with chest pain requires triage into risk categories on the basis of the probability of AMI, UA, or both and the subsequent risk and potential interventional options. Within such an algorithm, radionuclide imaging provides clinically useful information for diagnosis and management. The UA guidelines use 4 risk levels for chest pain: noncardiac, chronic SA, possible acute coronary syndrome (ACS), and definite ACS (http://www.acc.org/clinical/guidelines/unstable/unstable.pdf).1 Radionuclide imaging is most appropriate in patients with possible ACS. After initial triage on the basis of symptoms, ECG, and history, rest single-photon emission CT (SPECT) imaging appears to be useful for identifying patients at high risk (those with perfusion defects), who should be admitted, and patients with low risk (those with normal scans), who in general may be discharged home with a low risk for subsequent ischemic events. Randomized clinical trials2,3 now support several observational studies (see Table 1 in the full-text guideline) indicating a high negative predictive value for excluding ACS. Table 1 lists recommendations for emergency department imaging for suspected ACS. TABLE 1. Recommendations for Emergency Department Imaging for Suspected ACSIndicationTestClassLevel of EvidenceSee Figure 6 of ACC/AHA 2002 Guideline Update for the Management of Patients With Unstable Angina and Non–ST-Segment Elevation Myocardial Infarction at http://www.acc.org/clinical/guidelines/unstable/incorporated/figure6.htm and Figure 1 of ACC/AHA Guidelines for the Management of Patients with Acute Myocardial Infarction at www.acc.org/clinical/guidelines/nov96/1999/jac1716f01.htm.ACS indicates acute coronary syndromes; CAD, coronary artery disease; ECG, electrocardiogram; MPI, myocardial perfusion imaging.1. Assessment of myocardial risk in possible ACS patients with nondiagnostic ECG and initial serum markers and enzymes, if available.Rest MPIIA2. Diagnosis of CAD in possible ACS patients with chest pain with nondiagnostic ECG and negative serum markers and enzymes or normal resting scan.Same day rest/stress perfusion imagingIB3. Routine imaging of patients with myocardial ischemia/necrosis already documented clinically, by ECG and/or serum markers or enzymesRest MPIIIICB. Detection of AMI When Conventional Measures Are NondiagnosticRest myocardial perfusion imaging with 99mTc tracers has a high sensitivity for diagnosing AMI. Because there is minimal redistribution of the radiopharmaceutical over time, imaging can be delayed for a few hours after the injection and still provide accurate information about myocardial perfusion at the time of injection, which reflects the area of myocardium at risk. Perfusion defects, however, do not distinguish among acute ischemia, acute infarction, or previous infarction.C. Radionuclide Testing in Risk Assessment: Prognosis and Assessment of Therapy After STEMIAs discussed in the ACC/AHA Guidelines for the Management of Patients with Acute Myocardial Infarction: 1999 Update4 (http://www.acc.org/clinical/guidelines/nov96/1999/index.htm), the prognosis of STEMI is primarily a function of ejection fraction (EF), infarct size, and residual myocardium at risk. Thus, acute or late measurement of EF, infarct size, and myocardium at risk provides important prognostic management information. Radionuclide techniques are also useful for assessing the presence and extent of stress-induced myocardial ischemia—information that is useful for immediate and long-term patient management.5–9Table 2 lists recommendations for radionuclide testing in diagnosis, risk assessment, prognosis, and assessment of therapy after acute STEMI. TABLE 2. Recommendations for Use of Radionuclide Testing in Diagnosis, Risk Assessment, Prognosis, and Assessment of Therapy After Acute STEMIPatient Subgroup(s)IndicationTestClassLevel of EvidenceECG indicates electrocardiography; FPRNA, first-pass radionuclide angiography; LV, left ventricular; MPI, myocardial perfusion imaging; RNA, radionuclide angiography; RV, right ventricular; SPECT, single-photon emission computed tomography; STEMI, ST-segment elevation myocardial infarction.All1. Rest LV functionRest RNA or ECG-gated SPECTIBThrombolytic therapy without catheterization2. Detection of inducible ischemia and myocardium at riskStress MPI with ECG-gated SPECT whenever possibleIBAcute STEMI3. Assessment of infarct size and residual viable myocardiumMPI at rest or with stress using gated SPECTIB4. Assessment of RV function with suspected RV infarctionEquilibrium or FPRNAIIaBD. Radionuclide Testing in Risk Assessment: Prognosis and Assessment of Therapy After NSTEMI or UAThe ACC/AHA 2002 Guideline Update for the Management of Patients with UA/NSTEMI1 recommends an early invasive strategy in patients with any of several high-risk indicators and no serious comorbidities. High-risk findings on noninvasive stress testing (eg, myocardial perfusion imaging) are one such indication. In the absence of high-risk findings, the guidelines endorse either an early conservative or early invasive strategy in patients without contraindications for revascularization. Myocardial perfusion imaging is particularly useful in the predischarge risk stratification of patients with UA. The presence and extent of reversible perfusion defects on stress testing after the patient is stabilized are highly predictive of future events.10–14Table 3 lists recommendations for radionuclide testing for risk assessment/prognosis in patients with NSTEMI or UA. TABLE 3. Recommendations for Use of Radionuclide Testing for Risk Assessment/Prognosis in Patients With NSTEMI and UAIndicationTestClassLevel of EvidenceECG indicates electrocardiography; LV, left ventricular; MPI, myocardial perfusion imaging; RNA, radionuclide angiography; SPECT, single-photon emission computed tomography.1. Identification of inducible ischemia in the distribution of the “culprit lesion” or in remote areas in patients at intermediate or low risk for major adverse cardiac events.Stress MPI with ECG gating whenever possibleIB2. Identification of the severity/extent of inducible ischemia in patients whose angina is satisfactorily stabilized with medical therapy or in whom diagnosis is uncertain.Stress MPI with ECG gating whenever possibleIA3. Identification of hemodynamic significance of coronary stenosis after coronary arteriography.Stress MPIIB4. Measurement of baseline LV function.RNA or gated SPECTIB5. Identification of the severity/extent of disease in patients with ongoing suspected ischemia symptoms when ECG changes are not diagnostic.Rest MPIIIaBIII. Chronic SyndromesA. Detection (Diagnosis) of Coronary Artery DiseaseA thorough discussion of the concepts of likelihood of coronary artery disease (CAD) is provided in the ACC/AHA 2002 Guideline Update for the Management of Patients With Chronic Stable Angina15 (http://www.acc.org/clinical/guidelines/stable/stable_clean.pdf), accompanied by a simplified table for estimating pretest probability ranges. Myocardial perfusion imaging is most useful in patients with an intermediate likelihood of angiographically significant CAD on the basis of age, sex, symptoms, risk factors, and the results of stress testing (for patients who have undergone prior stress testing).1. Sensitivity and SpecificityTables 5 and 6 in the full-text guideline summarize studies reporting sensitivities and specificities of exercise and vasodilator stress perfusion SPECT for the detection of angiographically significant (more than 50% stenosis) CAD. Sensitivities (generally uncorrected for referral bias) average 87% and 89%, respectively; specificities (also uncorrected) average 73% and 75%. TABLE 5. Recommendations for the Use of Radionuclide Techniques to Assess Myocardial ViabilityIndicationTestClassLevel of EvidenceFDG indicates flurodeoxyglucose; PET, positron emission tomography; RNA, radionuclide angiography; SPECT, single-photon emission computed tomography; 201Tl, thallium-201.1. Predicting improvement in regional and global LV function after revascularizationStress/redistribution/reinjection 201TlIBRest-redistribution imagingIBPerfusion plus PET FDG imagingIBResting sestamibi imagingIBGated SPECT sestamibi imagingIIaBLate 201Tl redistribution imaging (after stress)IIbBDobutamine RNAIIbCPostexercise RNAIIbCPostnitroglycerin RNAIIbC2. Predicting improvement in heart failure symptoms after revascularization.Perfusion plus PET FDG imagingIIaB3. Predicting improvement in natural history after revascularization201Tl imaging (rest-redistribution and stress/redistribution/reinjection)IBPerfusion plus PET FDG imagingIBTABLE 6. Recommendations for the Use of Radionuclide Imaging to Diagnose Specific Causes of Dilated CardiomyopathyIndicationTestClassLevel of Evidence67Ga indicates gallium-67; 99mTc-pyrophosphate, Tc-99m-pyrophosphate; 111In, indium-111; CAD, coronary artery disease; LV, left ventricular; RNA, radionuclide angiography; RV, right ventricular.1. Baseline and serial monitoring of LV function during therapy with cardiotoxic drugs (eg, doxorubicin)Rest RNAIA2. RV dysplasiaRest RNAIIaB3. Assessment of posttransplant obstructive CADExercise perfusion imagingIIbB4. Diagnosis and serial monitoring of Chagas diseaseExercise perfusion imagingIIbB5. Diagnosis of amyloid heart disease99mTc-pyrophosphate imagingIIbB6. Diagnosis and serial monitoring of sarcoidRest perfusion imagingIIbBheart diseaseRest 67Ga imagingIIbB7. Detection of myocarditisRest 67Ga imagingIIbB111In antimyosin antibody imagingIIbC2. Effect of Referral BiasIn estimating the true sensitivity and specificity of noninvasive testing, referral or work-up bias needs to be taken into account. Table 7 in the full-text guideline summarizes studies in which effects of referral bias have been estimated. Because of the profound impact of referral bias on specificity, the concept of the normalcy rate has been developed. The term normalcy rate is used to describe the frequency of normal test results in patients with a low likelihood of CAD, to differentiate it from specificity. TABLE 7. Recommendations for the Use of Radionuclide Imaging to Evaluate Hypertrophic Heart DiseaseIndicationTestClassLevel of EvidenceCAD indicates coronary artery disease; RNA, radionuclide angiography.1. Diagnosis of CAD in hypertrophic cardiomyopathyRest and exercise perfusion imagingIIbB2. Diagnosis and serial monitoring of hypertensive hypertrophic heart diseaseRest RNAIIbB3. Diagnosis and serial monitoring of hypertrophic cardiomyopathy, with and without outflow obstructionRest RNAIIIB3. Quantitative AnalysisQuantitative analysis of myocardial perfusion SPECT has been developed using a variety of approaches and, in general, has similar sensitivities and specificities compared with those of expert visual analysis.4. ECG-Gated SPECTThe current state of the art is ECG-gated myocardial perfusion SPECT (gated SPECT). The ability to observe myocardial contraction in segments with apparent fixed perfusion defects permits the nuclear test reader to discern attenuation artifacts from true perfusion abnormalities. The ability of gated SPECT to provide measurement of left ventricular (LV) EF (LVEF), segmental wall motion, and absolute LV volumes also adds to the prognostic information that can be derived from a SPECT study.5. Attenuation CorrectionThe field of attenuation correction continues to evolve rapidly, with some available systems having undergone more detailed and successful clinical validation than others. On the basis of current information and the rate of technology improvement, the Society of Nuclear Medicine and the American Society of Nuclear Cardiology have concluded that attenuation correction has become a method for which the weight of evidence/opinion is in favor of its usefulness.166. Positron Emission TomographyStudies involving several hundred patients (see Table 10 in the full-text guideline) indicate that perfusion imaging with positron emission tomography (PET) using dipyridamole and either 82Rb or 13N ammonia is also a sensitive and specific clinical means to diagnose CAD.B. Management of Patients With Known or Suspected Chronic CAD: Assessment of Disease Severity, Risk Stratification, PrognosisNuclear tests are best applied for risk stratification in patients with a clinically intermediate risk of a subsequent cardiac event, analogous to the optimal diagnostic application of nuclear testing to patients with an intermediate likelihood of having CAD. Many of the major determinants of prognosis in CAD can be assessed by measurements of stress-induced perfusion and function. Studies including large patient samples have now demonstrated that factors estimating the extent of LV dysfunction (LVEF, the extent of infarcted myocardium, transient ischemic dilation of the LV, and increased lung uptake) are excellent predictors of cardiac mortality. In contrast, markers of provocative ischemia (exertional symptoms, electrocardiographic changes, the extent of reversible perfusion defects, and stress-induced ventricular dyssynergy) are better predictors of the subsequent development of acute ischemic syndromes.171. Nongated Myocardial Perfusion ImagingNot withstanding the now well-demonstrated advantages of gated imaging, nongated perfusion scintigraphy has played a major role in risk stratification of CAD patients. The full-text guideline summarizes studies of stress myocardial perfusion imaging in definite or suspected CAD (see Table 12 in the full-text guideline). Normal stress perfusion SPECT results are consistently predictive of a less than 1% annual risk of cardiac death or myocardial infarction.2. Gated SPECTThe information contained in the combined assessment of perfusion and function with gated myocardial perfusion SPECT is likely to enhance its prognostic and diagnostic content. The most common current approach combines poststress and/or rest LV function by gated SPECT with rest/stress perfusion measurements.3. Radionuclide AngiographyRest LVEF is universally recognized as one of the most important determinants of long-term prognosis in patients with chronic stable CAD. Radionuclide angiography (RNA) can also be helpful in evaluating dyspnea by establishing the state of right ventricular (RV) and LV performance. LV function during exercise reflects disease severity and provides prognostic information.4. Cost EffectivenessAs indicated in the ACC/AHA 2002 Guideline Update for the Management of Patients With Chronic Stable Angina,15 cardiac imaging can serve as a gatekeeper to cardiac catheterization to minimize the rate of normal catheterizations and to enrich the angiographic population with a greater proportion of patients with significant, yet treatable, disease.5. Frequency of TestingConsiderations for follow-up testing are also summarized in the ACC/AHA 2002 Guideline Update for the Management of Patients With Chronic Stable Angina.15 If patients develop new signs or symptoms suggesting a worsened clinical state, repeat testing at the time of worsening would be appropriate. In the absence of a change in clinical state, the estimated patient risk after initial testing (high, intermediate, or low, as defined earlier) should play an important role in individual recommendations.186. Evaluation of the Effects of Medical TherapyAlthough the available evidence suggests that the efficacy of therapy can be assessed with repeat SPECT procedures while the patient is under the effects of the medical treatment, information about the effects of medical therapy on outcomes is limited.C. Specific Patient Populations1. African AmericansThe role of noninvasive imaging has been studied infrequently in African Americans or other minorities. Normal rest and stress SPECT perfusion studies have been associated with higher rates of AMI and/or cardiac death in African Americans than in other populations,19,20 but included higher than usual cardiac risk patients and did not account for the incidence of LV hypertrophy (LVH).212. WomenAs discussed in the ACC/AHA 2002 Guideline Update for Exercise Testing22 (http://www.acc.org/clinical/guidelines/exercise/exercise_clean.pdf), the use of radionuclide testing in women is influenced importantly by the later presentation of CAD in women than in men and by sex-related limitations in exercise stress testing. These issues have provoked interest in the potential additive benefit of stress perfusion imaging in women, particularly those with at least an intermediate likelihood of coronary disease.23–263. Normal Resting ECG, Able to ExercisePatients with a normal resting ECG constitute a large and important subgroup. Most patients who present with multiple risk factors with or without cardiac symptoms have a normal resting ECG. Such patients are likely to have normal LV function and an excellent prognosis. For these reasons, a stepwise strategy is generally recommended in which an exercise ECG, and not a stress imaging procedure, is performed as the initial test in patients with an intermediate pretest likelihood of CAD who are not taking digoxin, have a normal resting ECG, and are able to exercise. A stress imaging technique should be used for patients with widespread rest ST depression (more than 1 mm), complete left bundle-branch block (LBBB), ventricular-paced rhythm, pre-excitation, or LVH with repolarization changes.154. Intermediate-Risk Duke Treadmill ScoreThe Duke treadmill score combines various forms of information from stress testing and provides a simple way to calculate risk.27 Annual mortality rates according to risk groups are presented in the ACC/AHA 2002 Chronic Stable Angina Guideline Update.15 The score has been reported to work well for both inpatients and outpatients and equally well for men and women. Only a small number of elderly patients, however, have been studied. Several studies have demonstrated value of myocardial perfusion scintigraphy in further risk assessment of patients with an intermediate score associated with an intermediate risk of cardiac death.28–305. Normal Resting ECG, Unable to ExerciseIn patients with an intermediate to high likelihood of CAD who have a normal resting ECG but are unable to exercise, pharmacologic myocardial perfusion SPECT with adenosine or dipyridamole has been shown to be highly effective in diagnosis and risk stratification.6. LBBB/PacemakersPharmacologic stress perfusion imaging is preferable to exercise perfusion imaging for purposes of both diagnosis and risk stratification.31,32 Several studies have observed an increased prevalence of myocardial perfusion defects during exercise imaging, in the absence of angiographic coronary disease, in patients with LBBB. Given that ECG testing is nondiagnostic in patients with ventricular pacing in a manner similar to that observed with LBBB, it is likely that the considerations with regard to the use of radionuclide techniques for diagnostic and risk stratification purposes in patients with ventricular pacemakers are the same as those applied to patients with LBBB.7. Left Ventricular HypertrophyIn patients with LVH, with or without resting ST-segment abnormality, ST depression during exercise is frequently present in the absence of significant CAD. In these patients, stress nuclear techniques have similar diagnostic sensitivity and specificity to those observed in patients without LVH. The diagnostic value of myocardial perfusion SPECT is not generally degraded by the presence of hypertension without evidence of LVH,33 although an increased frequency of false-positive studies has been reported in athletes.34 Similarly, although the number of reports is small, the prognostic value of myocardial perfusion SPECT in patients with LVH appears to be equal to that observed in patients without LVH.358. Patients With Nonspecific ST-T-Wave ChangesPatients with nonspecific ST-T-wave changes, such as might occur with digoxin, Wolff-Parkinson-White syndrome (WPW), or other conditions, are considered to have nondiagnostic stress ECG responses with regard to ST-segment depression. Although there are limited data on the diagnostic and prognostic information for myocardial perfusion SPECT in these patients, those with intermediate to high likelihood of coronary disease can perhaps be effectively assessed for detection and risk stratification with myocardial perfusion SPECT.9. ElderlyPrognostic value of perfusion scintigraphy in elderly patients has been reported.3610. Asymptomatic PatientsThe relatively low prevalence of CAD and risk of future events will affect the performance of any diagnostic test in a manner predictable by Bayesian principles (ie, positive predictive value will usually be low). It is not clear that detecting asymptomatic preclinical CAD will lead to therapeutic intervention that will reduce risk beyond that indicated by risk factor profiling and currently recommended strategies to reduce risk.37Persons whose occupations may affect public safety (eg, airline pilots, truckers, bus drivers) or who are professional or high-profile athletes co

HomeCirculationVol. 126, No. 252012 ACCF/AHA/ACP/AATS/PCNA/SCAI/STS Guideline for the Diagnosis and Management of Patients With Stable Ischemic Heart Disease Free AccessResearch ArticlePDF/EPUBAboutView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissionsDownload Articles + Supplements ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toSupplemental MaterialFree AccessResearch ArticlePDF/EPUB2012 ACCF/AHA/ACP/AATS/PCNA/SCAI/STS Guideline for the Diagnosis and Management of Patients With Stable Ischemic Heart DiseaseA Report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines, and the American College of Physicians, American Association for Thoracic Surgery, Preventive Cardiovascular Nurses Association, Society for Cardiovascular Angiography and Interventions, and Society of Thoracic Surgeons Stephan D. Fihn, MD, MPH, Julius M. Gardin, MD, Jonathan Abrams, MD, Kathleen Berra, MSN, ANP, James C. Blankenship, MD, Apostolos P. Dallas, MD, Pamela S. Douglas, MD, JoAnne M. Foody, MD, Thomas C. Gerber, MD, PhD, Alan L. Hinderliter, MD, Spencer B. KingIII, MD, Paul D. Kligfield, MD, Harlan M. Krumholz, MD, Raymond Y.K. Kwong, MD, Michael J. Lim, MD, Jane A. Linderbaum, MS, CNP-BC, Michael J. Mack, MD, Mark A. Munger, PharmD, Richard L. Prager, MD, Joseph F. Sabik, MD, Leslee J. Shaw, PhD, Joanna D. Sikkema, MSN, ANP-BC, Craig R. SmithJr, MD, Sidney C. SmithJr, MD, John A. Spertus, MD, MPH and Sankey V. Williams, MD Stephan D. FihnStephan D. Fihn †ACP Representative. Search for more papers by this author , Julius M. GardinJulius M. Gardin *Writing committee members are required to recuse themselves from voting on sections to which their specific relationship could apply; see Appendix 1 for detailed information. Search for more papers by this author , Jonathan AbramsJonathan Abrams ‡ACCF/AHA Representative. Search for more papers by this author , Kathleen BerraKathleen Berra *Writing committee members are required to recuse themselves from voting on sections to which their specific relationship could apply; see Appendix 1 for detailed information. Search for more papers by this author , James C. BlankenshipJames C. Blankenship *Writing committee members are required to recuse themselves from voting on sections to which their specific relationship could apply; see Appendix 1 for detailed information. Search for more papers by this author , Apostolos P. DallasApostolos P. Dallas *Writing committee members are required to recuse themselves from voting on sections to which their specific relationship could apply; see Appendix 1 for detailed information. Search for more papers by this author , Pamela S. DouglasPamela S. Douglas *Writing committee members are required to recuse themselves from voting on sections to which their specific relationship could apply; see Appendix 1 for detailed information. Search for more papers by this author , JoAnne M. FoodyJoAnne M. Foody *Writing committee members are required to recuse themselves from voting on sections to which their specific relationship could apply; see Appendix 1 for detailed information. Search for more papers by this author , Thomas C. GerberThomas C. Gerber ‡ACCF/AHA Representative. Search for more papers by this author , Alan L. HinderliterAlan L. Hinderliter ‡ACCF/AHA Representative. Search for more papers by this author , Spencer B. KingIIISpencer B. KingIII *Writing committee members are required to recuse themselves from voting on sections to which their specific relationship could apply; see Appendix 1 for detailed information. Search for more papers by this author , Paul D. KligfieldPaul D. Kligfield ‡ACCF/AHA Representative. Search for more papers by this author , Harlan M. KrumholzHarlan M. Krumholz ‡ACCF/AHA Representative. Search for more papers by this author , Raymond Y.K. KwongRaymond Y.K. Kwong ‡ACCF/AHA Representative. Search for more papers by this author , Michael J. LimMichael J. Lim *Writing committee members are required to recuse themselves from voting on sections to which their specific relationship could apply; see Appendix 1 for detailed information. Search for more papers by this author , Jane A. LinderbaumJane A. Linderbaum ¶Critical care nursing expertise. Search for more papers by this author , Michael J. MackMichael J. Mack *Writing committee members are required to recuse themselves from voting on sections to which their specific relationship could apply; see Appendix 1 for detailed information. Search for more papers by this author , Mark A. MungerMark A. Munger *Writing committee members are required to recuse themselves from voting on sections to which their specific relationship could apply; see Appendix 1 for detailed information. Search for more papers by this author , Richard L. PragerRichard L. Prager #STS Representative. Search for more papers by this author , Joseph F. SabikJoseph F. Sabik *Writing committee members are required to recuse themselves from voting on sections to which their specific relationship could apply; see Appendix 1 for detailed information. Search for more papers by this author , Leslee J. ShawLeslee J. Shaw *Writing committee members are required to recuse themselves from voting on sections to which their specific relationship could apply; see Appendix 1 for detailed information. Search for more papers by this author , Joanna D. SikkemaJoanna D. Sikkema *Writing committee members are required to recuse themselves from voting on sections to which their specific relationship could apply; see Appendix 1 for detailed information. Search for more papers by this author , Craig R. SmithJrCraig R. SmithJr **AATS Representative. Search for more papers by this author , Sidney C. SmithJrSidney C. SmithJr *Writing committee members are required to recuse themselves from voting on sections to which their specific relationship could apply; see Appendix 1 for detailed information. Search for more papers by this author , John A. SpertusJohn A. Spertus *Writing committee members are required to recuse themselves from voting on sections to which their specific relationship could apply; see Appendix 1 for detailed information. Search for more papers by this author and Sankey V. WilliamsSankey V. Williams *Writing committee members are required to recuse themselves from voting on sections to which their specific relationship could apply; see Appendix 1 for detailed information. Search for more papers by this author Originally published19 Nov 2012https://doi.org/10.1161/CIR.0b013e318277d6a0Circulation. 2012;126:e354–e471is corrected byCorrectionsOther version(s) of this articleYou are viewing the most recent version of this article. Previous versions: January 1, 2012: Previous Version 1 Table of ContentsPreamble. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .e3571. Introduction. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .e3591.1. Methodology and Evidence Overview. . . . . . .e3591.2. Organization of the Writing Committee. . . . . .e3601.3. Document Review and Approval. . . . . . . . . . .e3601.4. Scope of the Guideline. . . . . . . . . . . . . . . . . . .e3601.5. General Approach and Overlap With Other Guidelines or Statements. . . . . . . . . . . . . . . . .e3621.6. Magnitude of the Problem. . . . . . . . . . . . . . . .e3631.7. Organization of the Guideline. . . . . . . . . . . . . .e3641.8. Vital Importance of Involvement by an Informed Patient: Recommendation. . . . . . . . .e3642. Diagnosis of SIHD. . . . . . . . . . . . . . . . . . . . . . . . . .e3672.1. Clinical Evaluation of Patients With Chest Pain. . . . . . . . . . . . . . . . . . . . . . . . . . . . .e3672.1.1. Clinical Evaluation in the Initial Diagnosis of SIHD in Patients With Chest Pain: Recommendations. . . . . . . .e3672.1.2. History. . . . . . . . . . . . . . . . . . . . . . . . . .e3672.1.3. Physical Examination. . . . . . . . . . . . . . .e3682.1.4. Electrocardiography. . . . . . . . . . . . . . . .e3682.1.4.1. Resting Electrocardiography to Assess Risk: Recommendation. . . . . . . . . . .e3692.1.5. Differential Diagnosis. . . . . . . . . . . . . .e3702.1.6. Developing the Probability Estimate. . .e3702.2. Noninvasive Testing for Diagnosis of IHD. . . .e3712.2.1. Approach to the Selection of Diagnostic Tests to Diagnose SIHD. . . .e3712.2.1.1. Assessing Diagnostic Test Characteristics. . . . . . . . . .e3722.2.1.2. Safety and Other Considerations Potentially Affecting Test Selection. . . . . .e3732.2.1.3. Exercise Versus Pharmacological Testing. . . . . .e3742.2.1.4. Concomitant Diagnosis of SIHD and Assessment of Risk. . . . . . . . . . . . . . . . . . .e3742.2.1.5. Cost-Effectiveness. . . . . . . . . . .e3752.2.2. Stress Testing and Advanced Imaging for Initial Diagnosis in Patients With Suspected SIHD Who Require Noninvasive Testing: Recommendations. . . . . . . . . . . . . . . . .e3752.2.2.1. Able to Exercise. . . . . . . . . . . .e3752.2.2.2. Unable to Exercise. . . . . . . . . .e3762.2.2.3. Other. . . . . . . . . . . . . . . . . . . . .e3772.2.3. Diagnostic Accuracy of Nonimaging and Imaging Stress Testing for the Initial Diagnosis of Suspected SIHD. . . . . . . .e3772.2.3.1. Exercise ECG . . . . . . . . . . . . . .e3772.2.3.2. Exercise and Pharmacological Stress Echocardiography. . . . . . . . . . .e3772.2.3.3. Exercise and Pharmacological Stress Nuclear Myocardial Perfusion SPECT and Myocardial Perfusion PET. . . .e3782.2.3.4. Pharmacological Stress CMR Wall Motion/Perfusion. . . . . . .e3782.2.3.5. Hybrid Imaging. . . . . . . . . . . . .e3782.2.4. Diagnostic Accuracy of Anatomic Testing for the Initial Diagnosis of SIHD. . . . . . . . . . . . . . . . . . . . . . . . .e3792.2.4.1. Coronary CT Angiography. . . .e3792.2.4.2. CAC Scoring. . . . . . . . . . . . . .e3792.2.4.3. CMR Angiography. . . . . . . . . .e3793. Risk Assessment. . . . . . . . . . . . . . . . . . . . . . . . . . . .e3803.1. Clinical Assessment. . . . . . . . . . . . . . . . . . . . .e3803.1.1. Prognosis of IHD for Death or Nonfatal MI: General Considerations. . . . . . . . . .e3803.1.2. Risk Assessment Using Clinical Parameters. . . . . . . . . . . . . . . . . . . . . . .e3803.2. Advanced Testing: Resting and Stress Noninvasive Testing. . . . . . . . . . . . . . . . . . . . .e3813.2.1. Resting Imaging to Assess Cardiac Structure and Function: Recommendations. . . . . . . . . . . . . . . . .e3813.2.2. Stress Testing and Advanced Imaging in Patients With Known SIHD Who Require Noninvasive Testing for Risk Assessment: Recommendations. . . . . . .e3833.2.2.1. Risk Assessment in Patients Able to Exercise. . . . . . . . . . . .e3833.2.2.2. Risk Assessment in Patients Unable to Exercise. . . . . . . . . .e3833.2.2.3. Risk Assessment Regardless of Patients' Ability to Exercise. . . . . . . . . . . . . . . .e3843.2.2.4. Exercise ECG. . . . . . . . . . . . . .e3853.2.2.5. Exercise Echocardiography and Exercise Nuclear MPI. . . .e3853.2.2.6. Dobutamine Stress Echocardiography and Pharmacological Stress Nuclear MPI. . . . . . . . . . . . . . .e3863.2.2.7. Pharmacological Stress CMR Imaging. . . . . . . . . . . . . .e3863.2.2.8. Special Patient Group: Risk Assessment in Patients Who Have an Uninterpretable ECG Because of LBBB or Ventricular Pacing. . . . . . . . . . . . . . . . . . . .e3863.2.3. Prognostic Accuracy of Anatomic Testing to Assess Risk in Patients With Known CAD. . . . . . . . . . . . . . . . . . . . .e3873.2.3.1. Coronary CT Angiography. . . .e3873.3. Coronary Angiography. . . . . . . . . . . . . . . . . . .e3873.3.1. Coronary Angiography as an Initial Testing Strategy to Assess Risk: Recommendations. . . . . . . . . . . . . . . . .e3873.3.2. Coronary Angiography to Assess Risk After Initial Workup With Noninvasive Testing: Recommendations. . . . . . . . . . .e3874. Treatment. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .e3894.1. Definition of Successful Treatment. . . . . . . . . .e3894.2. General Approach to Therapy. . . . . . . . . . . . . .e3904.2.1. Factors That Should Not Influence Treatment Decisions. . . . . . . . . . . . . . . .e3924.2.2. Assessing Patients' Quality of Life. . . .e3934.3. Patient Education: Recommendations. . . . . . . .e3934.4. Guideline-Directed Medical Therapy. . . . . . . .e3954.4.1. Risk Factor Modification: Recommendations. . . . . . . . . . . . . . . . .e3954.4.1.1. Lipid Management. . . . . . . . . .e3954.4.1.2. Blood Pressure Management. . .e3974.4.1.3. Diabetes Management. . . . . . . .e3984.4.1.4. Physical Activity. . . . . . . . . . . .e3994.4.1.5. Weight Management. . . . . . . . .e4004.4.1.6. Smoking Cessation Counseling. . . . . . . . . . . . . . . .e4014.4.1.7. Management of Psychological Factors. . . . . . . .e4014.4.1.8. Alcohol Consumption. . . . . . . .e4024.4.1.9. Avoiding Exposure to Air Pollution. . . . . . . . . . . . . . .e4034.4.2. Additional Medical Therapy to Prevent MI and Death: Recommendations. . . . .e4034.4.2.1. Antiplatelet Therapy. . . . . . . . .e4034.4.2.2. Beta-Blocker Therapy. . . . . . . .e4044.4.2.3. Renin-Angiotensin-Aldosterone Blocker Therapy. . . . . . . . . . . . . . . . . . .e4054.4.2.4. Influenza Vaccination. . . . . . . .e4064.4.2.5. Additional Therapy to Reduce Risk of MI and Death. . . . . . . . . . . . . . . . . . . .e4074.4.3. Medical Therapy for Relief of Symptoms. . . . . . . . . . . . . . . . . . . . . . .e4084.4.3.1. Use of Anti-ischemic Medications: Recommendations. . . . . . . . . . .e4084.4.4. Alternative Therapies for Relief of Symptoms in Patients With Refractory Angina: Recommendations. . . . . . . . . . .e4114.4.4.1. Enhanced External Counterpulsation. . . . . . . . . . . .e4124.4.4.2. Spinal Cord Stimulation. . . . . .e4124.4.4.3. Acupuncture. . . . . . . . . . . . . . .e4135. CAD Revascularization. . . . . . . . . . . . . . . . . . . . . .e4135.1. Heart Team Approach to Revascularization Decisions: Recommendations. . . . . . . . . . . . .e4135.2. Revascularization to Improve Survival: Recommendations. . . . . . . . . . . . . . . . . . . . . .e4165.3. Revascularization to Improve Symptoms: Recommendations. . . . . . . . . . . . . . . . . . . . . .e4175.4. CABG Versus Contemporaneous Medical Therapy. . . . . . . . . . . . . . . . . . . . . . . . . . . . . .e4175.5. PCI Versus Medical Therapy. . . . . . . . . . . . .e4175.6. CABG Versus PCI. . . . . . . . . . . . . . . . . . . . .e4185.6.1. CABG Versus Balloon Angioplasty or BMS. . . . . . . . . . . . . . . . . . . . . . .e4185.6.2. CABG Versus DES. . . . . . . . . . . . . .e4185.7. Left Main CAD. . . . . . . . . . . . . . . . . . . . . . .e4195.7.1. CABG or PCI Versus Medical Therapy for Left Main CAD. . . . . . . . . . . . . .e4195.7.2. Studies Comparing PCI Versus CABG for Left Main CAD. . . . . . . . . . . . . .e4195.7.3. Revascularization Considerations for Left Main CAD. . . . . . . . . . . . . .e4195.8. Proximal LAD Artery Disease. . . . . . . . . . . .e4205.9. Clinical Factors That May Influence the Choice of Revascularization. . . . . . . . . . .e4205.9.1. Completeness of Revascularization. . .e4205.9.2. LV Systolic Dysfunction. . . . . . . . . .e4205.9.3. Previous CABG. . . . . . . . . . . . . . . . .e4215.9.4. Unstable Angina/Non–ST-Elevation Myocardial Infarction. . . . . . . . . . . . .e4215.9.5. DAPT Compliance and Stent Thrombosis: Recommendation. . . . . .e4215.10. Transmyocardial Revascularization. . . . . . . . .e4215.11. Hybrid Coronary Revascularization: Recommendations. . . . . . . . . . . . . . . . . . . . . .e4215.12. Special Considerations. . . . . . . . . . . . . . . . . .e4225.12.1. Women. . . . . . . . . . . . . . . . . . . . . . . .e4225.12.2. Older Adults. . . . . . . . . . . . . . . . . . . .e4235.12.3. Diabetes Mellitus. . . . . . . . . . . . . . . .e4245.12.4. Obesity. . . . . . . . . . . . . . . . . . . . . . . .e4255.12.5. Chronic Kidney Disease. . . . . . . . . . .e4255.12.6. HIV Infection and SIHD. . . . . . . . . .e4265.12.7. Autoimmune Disorders. . . . . . . . . . . .e4265.12.8. Socioeconomic Factors. . . . . . . . . . . .e4265.12.9. Special Occupations. . . . . . . . . . . . . .e4266. Patient Follow-Up: Monitoring of Symptoms and Antianginal Therapy. . . . . . . . . . . . . . . . . . . . . . . . .e4266.1. Clinical Evaluation, Echocardiography During Routine, Periodic Follow-Up: Recommendations. . . . . . . . . . . . . . . . . . . . . . .e4276.2. Follow-Up of Patients With SIHD. . . . . . . . . .e4276.2.1. Focused Follow-Up Visit: Frequency. . .e4286.2.2. Focused Follow-Up Visit: Interval History and Coexisting Conditions. . . . .e4286.2.3. Focused Follow-Up Visit: Physical Examination. . . . . . . . . . . . . . .e4296.2.4. Focused Follow-Up Visit: Resting 12-Lead ECG. . . . . . . . . . . . . . . . . . . . .e4296.2.5. Focused Follow-Up Visit: Laboratory Examination. . . . . . . . . . . . . . . . . . . . . .e4296.3. Noninvasive Testing in Known SIHD. . . . . . . .e4296.3.1. Follow-Up Noninvasive Testing in Patients With Known SIHD: New, Recurrent, or Worsening Symptoms Not Consistent With Unstable Angina: Recommendations. . . . . . . . . . . . . . . . .e4296.3.1.1. Patients Able to Exercise. . . . .e4296.3.1.2. Patients Unable to Exercise. . .e4306.3.1.3. Irrespective of Ability to Exercise. . . . . . . . . . . . . . . . . .e4306.3.2. Noninvasive Testing in Known SIHD—Asymptomatic (or Stable Symptoms): Recommendations. . . . . . . .e4316.3.3. Factors Influencing the Use of Follow-Up Testing. . . . . . . . . . . . . . . . .e4326.3.4. Patient Risk and Testing. . . . . . . . . . . .e4326.3.5. Stability of Results After Normal Stress Testing in Patients With Known SIHD. . . . . . . . . . . . . . . .e4336.3.6. Utility of Repeat Stress Testing in Patients With Known CAD. . . . . . . . . .e4336.3.7. Future Developments. . . . . . . . . . . . . . .e434Appendix 1. Author Relationships With Industry and Other Entities (Relevant). . . . . . . . . . . . .e464Appendix 2. Reviewer Relationships With Industry and Other Entities (Relevant). . . . . . . . . .e467Appendix 3. Abbreviations List. . . . . . . . . . . . . . . . . .e470Appendix 4. Nomogram for Estimating–Year CAD Event-Free Survival. . . . . . . . . . . . . . . . .e471Anderson Jeffrey L., MD, FACC, FAHAPreambleThe medical profession should play a central role in evaluating the evidence related to drugs, devices, and procedures for the detection, management, and prevention of disease. When properly applied, expert analysis of available data on the benefits and risks of these therapies and procedures can improve the quality of care, optimize patient outcomes, and favorably affect costs by focusing resources on the most effective strategies. An organized and directed approach to a thorough review of evidence has resulted in the production of clinical practice guidelines that assist physicians in selecting the best management strategy for an individual patient. Moreover, clinical practice guidelines can provide a foundation for other applications, such as performance measures, appropriate use criteria, and both quality improvement and clinical decision support tools.The American College of Cardiology Foundation (ACCF) and the American Heart Association (AHA) have jointly produced guidelines in the area of cardiovascular disease since 1980. The ACCF/AHA Task Force on Practice Guidelines (Task Force), charged with developing, updating, and revising practice guidelines for cardiovascular diseases and procedures, directs and oversees this effort. Writing committees are charged with regularly reviewing and evaluating all available evidence to develop balanced, patient-centric recommendations for clinical practice.Experts in the subject under consideration are selected by the ACCF and AHA to examine subject-specific data and write guidelines in partnership with representatives from other medical organizations and specialty groups. Writing committees are asked to perform a literature review; weigh the strength of evidence for or against particular tests, treatments, or procedures; and include estimates of expected outcomes where such data exist. Patient-specific modifiers, comorbidities, and issues of patient preference that may influence the choice of tests or therapies are considered. When available, information from studies on cost is considered, but data on efficacy and outcomes constitute the primary basis for the recommendations contained herein.In analyzing the data and developing recommendations and supporting text, the writing committee uses evidence-based methodologies developed by the Task Force.1 The Class of Recommendation (COR) is an estimate of the size of the treatment effect, with consideration given to risks versus benefits as well as evidence and/or agreement that a given treatment or procedure is or is not useful/effective or in some situations may cause harm. The Level of Evidence (LOE) is an estimate of the certainty or precision of the treatment effect. The writing committee reviews and ranks evidence supporting each recommendation, with the weight of evidence ranked as LOE A, B, or C according to specific definitions that are included in Table 1. Studies are identified as observational, retrospective, prospective, or randomized as appropriate. For certain conditions for which inadequate data are available, recommendations are based on expert consensus and clinical experience and are ranked as LOE C. When recommendations at LOE C are supported by historical clinical data, appropriate references (including clinical reviews) are cited if available. For issues for which sparse data are available, a survey of current practice among the clinicians on the writing committee is the basis for LOE C recommendations, and no references are cited. The schema for COR and LOE is summarized in Table 1, which also provides suggested phrases for writing recommendations within each COR. A new addition to this methodology is separation of the Class III recommendations to delineate whether the recommendation is determined to be of “no benefit” or is associated with “harm” to the patient. In addition, in view of the increasing number of comparative effectiveness studies, comparator verbs and suggested phrases for writing recommendations for the comparative effectiveness of one treatment or strategy versus another have been added for COR I and IIa, LOE A or B only.Table 1. Applying Classification of Recommendations and Level of EvidenceTable 1. Applying Classification of Recommendations and Level of EvidenceA recommendation with Level of Evidence B or C does not imply that the recommendation is weak. Many important clinical questions addressed in the guidelines do not lend themselves to clinical trials. Although randomized trials are unavailable, there may be a very clear clinical consensus that a particular test or therapy is useful or effective.*Data available from clinical trials or registries about the usefulness/efficacy in different subpopulations, such as sex, age, history of diabetes, history of prior myocardial infarction, history of heart failure, and prior aspirin use.†For comparative effectiveness recommendations (Class I and IIa; Level of Evidence A and B only), studies that support the use of comparator verbs should involve direct comparisons of the treatments or strategies being evaluated.In view of the advances in medical therapy across the spectrum of cardiovascular diseases, the Task Force has designated the term guideline-directed medical therapy (GDMT) to represent optimal medical therapy as defined by ACCF/AHA guideline (primarily Class I)–recommended therapies. This new term, GDMT, will be used herein and throughout all future guidelines.Because the ACCF/AHA practice guidelines address patient populations (and healthcare providers) residing in North America, drugs that are not currently available in North America are discussed in the text without a specific COR. For studies performed in large numbers of subjects outside North America, each writing committee reviews the potential influence of different practice patterns and patient populations on the treatment effect and relevance to the ACCF/AHA target population to determine whether the findings should inform a specific recommendation.The ACCF/AHA practice guidelines are intended to assist healthcare providers in clinical decision making by describing a range of generally acceptable approaches to the diagnosis, management, and prevention of specific diseases or conditions. The guidelines attempt to define practices that meet the needs of most patients in most circumstances. The ultimate judgment about care of a particular patient must be made by the healthcare provider and patient in light of all the circumstances presented by that patient. As a result, situations may arise in which deviations from these guidelines might be appropriate. Clinical decision making should involve consideration of the quality and availability of expertise in the area where care is provided. When these guidelines are used as the basis for regulatory or payer decisions, the goal should be improvement in quality of care. The Task Force recognizes that situations arise in which additional data are needed to inform patient care more effectively; these areas will be identified within each respective guideline when appropriate.Prescribed courses of treatment in accordance with these recommendations are effective only if followed. Because lack of patient understanding and adherence may adversely affect outcomes, physicians and other healthcare providers should make every effort to engage the patient's active participation in prescribed medical regimens and lifestyles. In addition, patients should be informed of the risks, benefits, and alternatives to a particular treatment and should be involved in shared decision making whenever feasible, particularly for COR IIa and IIb, for which the benefit-to-risk ratio may be lower.The Task Force makes every effort to avoid actual, potential, or perceived conflicts of interest that may arise as a result of industry relationships or personal interests among the members of the writing committee. All writing committee members and peer reviewers of this guideline were required to disclose all such current health care-related relationships, including those existing 24 months (from 2005) before initiation of the writing effort. The writing committee chair may not have any relevant relationships with industry or other entities (RWI); however, RWI are permitted for the vice chair position. In December 2009, the ACCF and AHA implemented a new policy that requires a minimum of 50% of the writing committee to have no relevant RWI; in addition, the disclosure term was changed to 12 months before writing committee initiation. The present guideline was developed during the transition in RWI policy and occurred over an extended period of time. In the interest of transparency, we provide full information on RWI existing over the entire period of guideline development, including delineation of relationships that expired more than 24 months before the guideline was finalized. This information is included in Appendix 1. These statements are reviewed by the Task Force and all members during each conference call and meeting of the writing committee and are updated as changes occur. All guideline recommendations require a confidential vote by the writing committee and must be approved by a consensus of the voting members. Members who recused themselves from voting are indicated in the list of writing committee members, and specific section recusals are noted in Appendix 1. Authors' and peer reviewers' RWI pertinent to this guideline are disclosed in Appendixes 1 and 2, respectively. Comprehensive disclosure information for the Task Force is also available online at http://www.cardiosource.org/ACC/About-ACC/Who-We-Are/Leadership/Guidelines-and-Documents-Task-Forces.aspx. The work of the writing committee is supported exclusively by the ACCF, AHA, American College of Physicians (ACP), American Association for Thoracic Surgery (AATS), Preventive Cardiovascular Nurses Association (PCNA), Society for Cardiovascular Angiography and Interventions (SCAI), and Society of Thoracic Surgeons (STS), without commercial support. Writing committee members volunteered their time for this activity.The recommendations in this guideline are considered current until they are superseded by a focused update or the full-text guideline is revised. Guidelines are official policy of both the ACCF and AHA.Jeffrey L. Anderson, MD, FACC, FAHA Chair, ACCF/AHA Task Force on Practice Guidelines1. Introduction1.1. Methodology and Evidence OverviewThe recommendations listed in this document are, whenever possible, evidence based. An extensive evidence review was conducted as the document was compiled through December 2008. Repeated literature searches were performed by the guideline development staff and writing committee members as new issues were considered. New clinical trials published in peer-reviewed journals and articles through December 2011 were also reviewed and incorporated when relevant. Furthermore, because of the extended development time period for this guideline, peer review comments indicated that the sections focused on imaging technologies required additional updating, which occurred during 2011. Therefore, the evidence review for the imaging sections includes published literature through December 2011.Searches were limited to studies, reviews, and other evidence in human subjects and that were published in English. Key search words included but were not limited to the following: accuracy, angina, asymptomatic patients, cardiac magnetic resonance (CMR), cardiac rehabilitation, chest pain, chronic angina, chronic coronary occlusions, chronic

HomeCirculationVol. 97, No. 18Primary Prevention of Coronary Heart Disease: Guidance From Framingham