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Circulation | 2011

Effectiveness-Based Guidelines for the Prevention of Cardiovascular Disease in Women—2011 Update: A Guideline From the American Heart Association

Lori Mosca; Emelia J. Benjamin; Kathy Berra; Judy L. Bezanson; Rowena J Dolor; Donald M. Lloyd-Jones; L. Kristin Newby; Ileana L. Piña; Véronique L. Roger; Leslee J. Shaw; Dong Zhao; Theresa M. Beckie; Cheryl Bushnell; Jeanine D'Armiento; Penny M. Kris-Etherton; Jing Fang; Theodore G. Ganiats; Antoinette S. Gomes; Clarisa R. Gracia; Constance K. Haan; Elizabeth A. Jackson; Debra R. Judelson; Ellie Kelepouris; Carl J. Lavie; Anne Moore; Nancy A. Nussmeier; Elizabeth Ofili; Suzanne Oparil; Pamela Ouyang; Vivian W. Pinn

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 “mans 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 Womens 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.nnDespite 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 womens 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 …


Circulation | 1998

Primary Prevention of Coronary Heart Disease: Guidance From Framingham A Statement for Healthcare Professionals From the AHA Task Force on Risk Reduction

Scott M. Grundy; Gary J. Balady; Michael H. Criqui; Gerald F. Fletcher; Philip Greenland; Loren F. Hiratzka; Nancy Houston-Miller; Penny M. Kris-Etherton; Harlan M. Krumholz; John C. LaRosa; Ira S. Ockene; Thomas A. Pearson; James Reed; Reginald L. Washington; Sidney C. Smith

The Framingham Heart Study has contributed importantly to understanding of the causes of coronary heart disease (CHD), stroke, and other cardiovascular diseases. Framingham research has helped define the quantitative and additive nature of these causes or, as they are now called, “cardiovascular risk factors.”1 The National Cholesterol Education Program (NCEP)2 3 has made extensive use of Framingham data in developing its strategy for preventing CHD by controlling high cholesterol levels. The NCEP guidelines2 3 adjust the intensity of cholesterol-lowering therapy with absolute risk as determined by summation of risk factors. The National High Blood Pressure Education Program (NHBPEP) has set forth a parallel approach for blood pressure control. In contrast to the NCEP,2 however, earlier NHBPEP reports issued through the Joint National Committee4 did not match the intensity of therapy to absolute risk for CHD. “Normalization” of blood pressure is the essential goal of therapy regardless of risk status. Blood pressure–lowering therapy is carried out as much for prevention of stroke and other cardiovascular complications as for reduction of CHD risk. Nonetheless, risk assessment could be important for making decisions about type and intensity of therapy for hypertension. Thus, the most recent Joint National Committee report5 gives more attention to risk stratification for adjustment of therapy for hypertension. Although Framingham data have already been influential in the development of national guidelines for risk factor management, the opportunity may exist for both cholesterol and blood pressure programs to draw more extensively from Framingham results when formulating improved risk assessment guidelines and recommending more specific strategies for risk factor modification.nnThe American Heart Association has previously used Framingham risk factor data to prepare charts for estimating CHD risk. Framingham investigators of the National Heart, Lung, and Blood Institute prepared the original charts and have now revised …


Journal of Cardiovascular Computed Tomography | 2010

ACCF/SCCT/ACR/AHA/ASE/ASNC/NASCI/SCAI/SCMR 2010 Appropriate Use Criteria for Cardiac Computed Tomography

Allen J. Taylor; Manuel D. Cerqueira; John McB. Hodgson; Daniel B. Mark; James K. Min; Patrick O'Gara; Geoffrey D. Rubin; Christopher M. Kramer; Daniel S. Berman; Alan S. Brown; Farooq A. Chaudhry; Ricardo C. Cury; Milind Y. Desai; Andrew J. Einstein; Antoinette S. Gomes; Robert A. Harrington; Udo Hoffmann; Rahul K. Khare; John R. Lesser; Christopher McGann; Alan Rosenberg; Robert S. Schwartz; Marc Shelton; Gerald W. Smetana; Sidney C. Smith; Michael J. Wolk; Joseph M. Allen; Steven R. Bailey; Pamela S. Douglas; Robert C. Hendel

The American College of Cardiology Foundation (ACCF), along with key specialty and subspecialty societies, conducted an appropriate use review of common clinical scenarios where cardiac computed tomography (CCT) is frequently considered. The present document is an update to the original CCT/cardiac magnetic resonance (CMR) appropriateness criteria published in 2006, written to reflect changes in test utilization, to incorporate new clinical data, and to clarify CCT use where omissions or lack of clarity existed in the original criteria (1). The indications for this review were drawn from common applications or anticipated uses, as well as from current clinical practice guidelines. Ninety-three clinical scenarios were developed by a writing group and scored by a separate technical panel on a scale of 1 to 9 to designate appropriate use, inappropriate use, or uncertain use. In general, use of CCT angiography for diagnosis and risk assessment in patients with low or intermediate risk or pretest probability for coronary artery disease (CAD) was viewed favorably, whereas testing in high-risk patients, routine repeat testing, and general screening in certain clinical scenarios were viewed less favorably. Use of noncontrast computed tomography (CT) for calcium scoring was rated as appropriate within intermediate- and selected low-risk patients. Appropriate applications of CCT are also within the category of cardiac structural and functional evaluation. It is anticipated that these results will have an impact on physician decision making, performance, and reimbursement policy, and that they will help guide future research.


Circulation | 1993

Guidelines for percutaneous transluminal coronary angioplasty. A report of the American Heart Association/American College of Cardiology Task Force on Assessment of Diagnostic and Therapeutic Cardiovascular Procedures (Committee on Percutaneous Transluminal Coronary Angioplasty).

Thomas J. Ryan; W. B. Bauman; J W Kennedy; D. J. Kereiakes; S. B. King; B. D. McCallister; Sidney C. Smith; D. J. Ullyot

102. Philippides G, Jacobs AK, Kelsey SF, Yeh W, Detre KM, Ryan TJ, Faxon DP. Changing profiles and late outcome of women undergoing PTCA: a report from the NHLBI PTCA Registry. JAm Coil Cardiol. 1992;19:138A. Abstract. 103. Bell MR, Holmes DR Jr, Berger PB, Garratt KN, Bailey KR, Gersh BJ. The changing in-hospital mortality of women undergoing percutaneous transluminal coronary angioplasty. JAMA. 1993;269:2091-2095. 104. OKeefe JH Jr, Gernon C, McCallister BD, Ligon RW, Hartzler GO. Safety and cost effectiveness of combined coronary angiography and angioplasty. Am Heart J. 1991;122:50-54. 105. OKeefe JH Jr, Reeder GS, Miller GA, Bailey KR, Holmes DR Jr. Safety and efficacy of percutaneous transluminal coronary angioplasty performed at time of diagnostic catheterization compared with that performed at other times. Am J Cardiol. 1989;63:27-29. 106. Schwartz L, Bourassa MG, Lesperance J, Aldridge HE, Kazim F, Salvatori VA, Henderson M, Bonan R, David PR. Aspirin and dipyridamole in the prevention of restenosis after percutaneous transluminal coronary angioplasty. N Engi J Med. 1988;318: 1714-1719. 107. Chesebro JH, Webster MW, Reeder GS, Mock MB, Grill DE, Bailey KR, Steichen S, Fuster V. Coronary angioplasty: antiplatelet therapy reduces acute complications but not restenosis. Circulation. 1989;80(suppl 2):II-64. Abstract. 108. Barnathan ES, Schwartz JS, Taylor L, Laskey WK, Kleaveland JP, Kussmaul WG, Hirshfeld JW Jr. Aspirin and dipyridamole in the prevention of acute coronary thrombosis complicating coronary angioplasty. Circulation. 1987;76:125-134. 109. Myler RK, Stertzer SH, Clark DA, Shaw RE, Fishman-Rosen J, Murphy MC. Coronary angioplasty at the time of initial cardiac catheterization: ad hoc angioplasty possibilities and challenges. Cathet Cardiovasc Diagn. 1986;12:213-214. 110. Califf RM, Fortin DF, Frid DJ, Harlan WR III, Ohman EM, Bengtson JR, Nelson CL, Tcheng JE, Mark DB, Stack RS. Restenosis after coronary angioplasty: an overview. J Am Coll Cardiol. 1991;17:2B-13B. 111. Kadel C, Strecker T, Kaltenbach M, Kober G. Recognition of restenosis: can patients be defined in whom the exercise-ECG result makes angiographic restudy unnecessary? Eur Heart J. 1989;10(suppl G):22-26. 112. Schroeder E, Marchandise B, De Coster P, Brichant C, Mitri K, Pieters D, Kremer R. Detection of restenosis after coronary angioplasty for single-vessel disease: how reliable are exercise electrocardiography and scintigraphy in asymptomatic patients? Eur Heart J. 1989;10(suppl G):18-21. 113. Fioretti PM, Pozzoli MM, Ilmer B, Salustri A, Cornel JH, Reijs AE, Krenning EP, Reiber JH, de Feyter PJ, Roelandt JR. Exercise echocardiography versus thallium-201 SPECT for assessing patients before and after PTCA. Eur Heart J. 1992;13:213-219. 114. Pirelli S, Danzi GB, Alberti A, Massa D, Piccal6 G, Faletra F, Picano E, Campolo L, De Vita C. Comparison of usefulness of high-dose dipyridamole echocardiography and exercise electrocardiography for detection of asymptomatic restenosis after coronary angioplasty. Am J Cardiol. 1991;67:1335-1338. 115. Bengtson JR, Mark DB, Honan MB, Rendall DS, Hinohara T, Stack RS, Hlatky MA, Califf RM, Lee KL, Pryor DB. Detection of restenosis after elective percutaneous transluminal coronary angioplasty using the exercise treadmill test. Am J Cardiol. 1990; 65:28-34. 116. Laarman G, Luijten HE, van Zeyl LG, Beatt KJ, Tijssen JG, Serruys PW, de Feyter J. Assessment of silent restenosis and long-term follow-up after successful angioplasty in single vessel coronary artery disease: the value of quantitative exercise electrocardiography and quantitative coronary angiography. J Am Coll Cardiol. 1990;16:578-585. 117. Kober G, Vallbracht C, Kadel C, Kaltenbach M. Results of repeat angiography up to eight years following percutaneous transluminal angioplasty. Eur Heart J. 1989;10(suppl G):49-53. 118. Holmes DR Jr, Vlietstra RE, Smith HC, Vetrovec GW, Kent KM, Cowley MJ, Faxon DP, Gruentzig AR, Kelsey SF, Detre KM, et al. Restenosis after percutaneous transluminal coronary angioplasty (PTCA): a report from the PTCA Registry of the National Heart, Lung, and Blood Institute.AmJCardiol. 1984;53:77C-81C. 119. Popma JJ, Topol EJ. Factors influencing restenosis after coronary angioplasty. Am J Med. 1990;88:16N-24N. 120. Ellis SG, Muller DW. Arterial injury and the enigma of coronary restenosis. JAm Coll CardioL 1992;19:275-277. 121. Reiber JH, Serruys PW, Kooijman CJ, Wijns W, Slager CJ, Gerbrands JJ, Schuurbiers JC, den Boer A, Hugenholtz PG. Assessment of short-, medium-, and long-term variations in arterial dimensions from computer-assisted quantitation of coronary cineangiograms. Circulation. 1985;71:280-288. 122. Serruys PW, Luijten HE, Beatt KJ, Geuskens R, de Feyter PJ, van den Brand M, Reiber JH, ten Katen HJ, van Es GA, Hugenholtz PG. Incidence of restenosis after successful coronary angioplasty: a time-related phenomenon: a quantitative angiographic study in 342 consecutive patients at 1, 2, 3, and 4 months. Circulation. 1988;77:361-371. 123. Hermans WR, Rensing BJ, Kelder JC, de Feyter PJ, Serruys PW. Postangioplasty restenosis rate between segments of the major coronary arteries. Am J Cardiol. 1992;69:194-200. 124. Muller DW, Ellis SG, Topol EJ. Experimental models of coronary artery restenosis. JAm Coll Cardiol. 1992;19:418-432. 125. Ip JH, Fuster V, Israel D, Badimon L, Badimon J, Chesebro JH. The role of platelets, thrombin and hyperplasia in restenosis after coronary angioplasty. J Am Coil Cardiol. 1991;17(suppl B): 77B-88B. 126. Klein LW, Rosenblum J. Restenosis after successful percutaneous transluminal coronary angioplasty. Prog Cardiovasc Dis. 1990;32:365-382. 127. Halon DA, Merdler A, Shefer A, Flugelman MY, Lewis BS. Identifying patients at high risk for restenosis after percutaneous transluminal coronary angioplasty for unstable angina pectoris. Am J Cardiol. 1989;64:289-293. 128. Arora RR, Konrad K, Badhwar K, Hollman J. Restenosis after transluminal coronary angioplasty: a risk factor analysis. Cathet Cardiovasc Diagn. 1990;19:17-22. 129. Glazier JJ, Varrichione TR, Ryan TJ, Ruocco NA, Jacobs AK, Faxon DP. Outcome in patients with recurrent restenosis after percutaneous transluminal balloon angioplasty. Br Heart J. 1989; 61:485-488. 130. Jones EL, Craver JM, Guyton RA, Bone DK, Hatcher CR Jr, Riechwald N. Importance of complete revascularization in per3006 Circulation Vol 88, No 6 December 1993 formance of the coronary bypass operation. Am J Cardiol. 1983; 51:7-12. 131. Bourassa MG, Holubkov R, Yeh W, Detre KM. Strategy of complete revascularization in patients with multivessel coronary artery disease: a report from the 1985-1986 NHLBI PTCA Registry. Am J Cardiol. 1992;70:174-178. 132. de Feyter PJ. PTCA in patients with stable angina pectoris and multivessel disease: is incomplete revascularization acceptable? Clin Cardiol. 1992;15:317-322. 133. Deligonul U, Vandormael MG, Kern MJ, Zelman R, Galan K, Chaitman BR. Coronary angioplasty: a therapeutic option for symptomatic patients with two and three vessel coronary disease. JAm Coil Cardiol. 1988;11:1173-1179. 134. Reeder GS, Holmes DR Jr, Detre K, Costigan T, Kelsey SF. Degree of revascularization in patients with multivessel coronary disease: a report from the National Heart, Lung, and Blood Institute Percutaneous Transluminal Coronary Angioplasty Registry. Circulation. 1988;77:638-644. 135. Samson M, Meester HJ, de Feyter PJ, Strauss B, Serruys PW. Successful multiple segment coronary angioplasty: effect of completeness of revascularization in single-vessel multilesions and multivessels. Am Heart J. 1990;120:1-12. 136. Thomas ES, Most AS, Williams DO. Coronary angioplasty for patients with multivessel coronary artery disease: follow-up clinical status. Am Heart J. 1988;115:8-13. 137. Faxon DP, Ghalilli K, Jacobs AK, Ruocco NA, Christellis EM, Kellett MA Jr, Varrichione TR, Ryan TJ. The degree of revascularization and outcome after multivessel coronary angioplasty. Am Heart J. 1992;123:854-859. 138. Weintraub WS, King SB III, Jones EL, Craver JM, Douglas JS Jr, Morris DC, Liberman HA, Guyton RA, et al. Completeness of revascularization after coronary angioplasty and coronary surgery: different strategies, different results.JAm Coil CardioL 1993;21:73A. Abstract. 139. Myler RK, Topol EJ, Shaw RE, Stertzer SH, Clark DA, Fishman J, Murphy MC. Multiple vessel coronary angioplasty: classification, results, and patterns of restenosis in 494 consecutive patients. Cathet Cardiovasc Diagn. 1987;13:1-15. 140. Cavallini C, Giommi L, Franceschini E, Risica G, Olivari Z, Marton F, Cuzzato V. Coronary angioplasty in single-vessel complex lesions: shortand long-term outcome and factors predicting acute coronary occlusion. Am Heart J. 1991;122:44-49. 141. Teirstein P, Giorgi L, Johnson W, McConahay D, Rutherford B, Hartzler G. PTCA of the left coronary artery when the right coronary artery is chronically occluded. Am Heart J. 1990;119: 479-483. 142. Eckman MH, Wong JB, Salem DN, Pauker SG. Direct angioplasty for acute myocardial infarction: a review of outcomes in clinical subsets. Ann Intern Med. 1992;117:667-676. 143. Topol EJ, Califf RM, George BS, Kereiakes DJ, Abbottsmith CW, Candela RJ, Lee KL, Pitt B, Stack RS, ONeill WW. A randomized trial of immediate versus delayed elective angioplasty after intravenous tissue plasminogen activator in acute myocardial infarction. N Engl J Med. 1987;317:581-588. 144. Simoons ML, Arnold AE, Betriu A, de Bono DP, Col J, Dougherty FC, von Essen R, Lambertz H, Lubsen J, Meier B, et al. Thrombolysis with tissue plasminogen activator in acute myocardial infarction: no additional benefit from immediate percutaneous coronary angioplasty. Lancet. 1988;1:197-203. 145. Rogers WJ, Baim DS, Gore JM, Brown BG, Roberts R, Williams DO, Chesebro JH, Babb JD, Sheehan FH1, Wackers FJ, et al. Comparison of immediate invasive, delayed invasive, and conservative strategies after tissue-type plasminogen activator: results of the Thr


Circulation | 1995

Public Access Defibrillation A Statement for Healthcare Professionals From the American Heart Association Task Force on Automatic External Defibrillation

Myron L. Weisfeldt; Richard E. Kerber; R. P. McGoldrick; Arthur J. Moss; Graham Nichol; Joseph P. Ornato; David G. Palmer; Barbara Riegel; Sidney C. Smith

In October 1993 the American Heart Association appointed the Task Force on Automatic External Defibrillation. The task force was charged with conducting a conference on automatic external defibrillation, evaluating research needed for broader community use of automatic external defibrillators, and overseeing evaluation of the feasibility and desirability of their use by healthcare professionals and the lay public. nnIn December 1994 a conference on public access defibrillation was held in Washington, DC. More than 300 persons attended, representing science, industry, the healthcare professions, law, and the federal government. During the meeting the participants reached a consensus on the general proposition of greater public access to defibrillation and the need for broad-based clinical …


Circulation | 1996

Risk-Reduction Therapy: The Challenge to Change Presented at the 68th Scientific Sessions of the American Heart Association November 13, 1995 Anaheim, California

Sidney C. Smith

One of my great pleasures as President of the American Heart Association is addressing this distinguished group as we begin our 68th Scientific Sessions.nnThis year we return to Anaheim. For decades our children have come here to marvel at the wonders of Disneyland. From Frontierland to Tomorrowland, they have been inspired to understand the past and think about the future, and with that, to ponder the changes that challenge their lives.nnToday, we in medicine certainly face great challenge and change. Molecular biology has expanded our knowledge and the frontiers of cardiovascular science. At the same time, our healthcare system faces revolutionary change. Clinicians worry about providing optimal care for their patients, and researchers wonder about continued funding for their projects. During the next 4 days, as we share our scientific discoveries and renew friendships, many conversations will turn to these changes and challenges occurring in medicine.nnThis morning I want to talk about challenge and change: the challenge to bring results of research to the bedside, and the need to change our treatment strategies to emphasize risk-reduction therapy for patients with cardiovascular disease. I’d like to begin by reviewing the American Heart Association and the strategies that have made it successful.nnThe American Heart Association has a history of translating research findings into effective clinical therapies and public education programs. Founded in 1924, the American Heart Association sprang from recommendations of five clinical cardiologists: Drs Lewis Conner, James B. Herrick, Joseph Sailer, Paul Dudley White, and Hugh McCullough.1 Seventy years ago, in May 1925, the American Heart Association held its first Scientific Sessions in Atlantic City. That meeting’s program2 shows a remarkable similarity to the cardiovascular issues that confront us today. The first four papers dealt with primary prevention, secondary prevention, economic pressures, and concern about …


Circulation | 1996

Report of the Expert Panel on Awareness and Behavior Change to the Board of Directors, American Heart Association

Richard A. Carleton; Terry L. Bazzarre; John Drake; Andrea Dunn; Edwin B. Fisher; Scott M. Grundy; Laura L. Hayman; Martha N. Hill; Edward Maibach; James Prochaska; Tom Schmid; Sidney C. Smith; Mervyn W. Susser; John W. Worden

The Board of Directors of the American Heart Association charged the Expert Panel on Awareness and Behavior Change to:nnnnnnPanel members reviewed background material on the structure and function of the AHA, then met in Dallas on October 17, 1995. Extensive discussions and the subsequent deliberations clarified the purpose of the decisions to be made by the Board of Directors. The panel spent a substantial amount of time and effort evaluating alternatives and assessing the strengths and risks or limitations of each. These alternatives are presented in Tables 1 through 5⇓⇓⇓⇓⇓. This report presents the recommendations of the Expert Panel to the Board of Directors.nnView this table:nn Table 1. nAwareness and Knowledge as Elements of Heart-Health PromotionnnnnView this table:nn Table 2. nCardiovascular Disease Risk Factor–Related Behavioral Change as an Element of Heart-Health PromotionnnnnView this table:nn Table 3. nInfluencing the Physical and Social Environments and the Healthcare System Through Advocacy and Policy Changes as Elements of Heart-Health PromotionnnnnView this table:nn Table 4. nMedia, Other Information Paths, and Social Marketing as a Means of …


American Journal of Emergency Medicine | 1996

Public access to defibrillation

Myron L. Weisfeldt; Richard E. Kerber; R.Pat McGoldrick; Arthur J. Moss; Graham Nichol; Joseph P. Ornato; David G. Palmer; Barbara Riegel; Sidney C. Smith

During the past 20 years, morbidity and mortality rates for nearly all types of cardiovascular disease have declined. Progress in these areas is in stark contrast to that for sudden cardiac death, which continues unabated at a rate of approximately 1,000 times per day in the United States, with little decline in incidence or improved outcome. Clearly, the problem of sudden cardiac death is best approached through prevention, but horizons in that area seem no more promising and in some respects less promising and substantially more costly than 2 decades ago. The means necessary for the successful resuscitation of a patient in cardiac arrest were known by the early 1960s. Externally performed cardiopulmonary resuscitation (CPR) could maintain an oxygen plateau and delay permanent brain damage long enough to allow external defibrillation using direct current (DC). The possibility of long-term survival was increasingly recognized, as early anecdotal experiences accumulated into published series. 1-3 Given the hindsight of 3 decades, the obstacles to be overcome before significant progress could be made in out-of-hospital resuscitation were formidable. First, cardiac arrest was perceived as an event that typically occurred in the hospital. In-hospital cardiac arrests are now recognized to represent only a small proportion of sudden deaths based in the community. Second, the CPR technique was known to only a limited number of hospital-based physicians. CPR is no longer restricted to hospitals or physicians; it is routinely taught to the lay public. Third, only line-powered, bulky, and awkward defibrillators were available. The first out-ofhospital defibrillation device weighed 110 lb. Contemporary external defibrillators are available that weigh less than 10 lb.


Journal of the American College of Cardiology | 1995

Preventing heart attack and death in patients with coronary disease

Sidney C. Smith; Steven N. Blair; Michael H. Criqui; Gerald F. Fletcher; Valentin Fuster; Bernard J. Gersh; Antonio M. Gotto; K.Lance Gould; Philip Greenland; Scott M. Grundy; Martha N. Hill; Mark A. Hlatky; Nancy Houston-Miller; Ronald M. Krauss; John C. LaRosa; Ira S. Ockene; Suzanne Oparil; Thomas A. Pearson; Elliot Rapaport; Rodman D. Starke


Journal of the American College of Cardiology | 1995

AHA consensus panel statement. Preventing heart attack and death in patients with coronary disease. The Secondary Prevention Panel.

Sidney C. Smith; Steven N. Blair; Michael H. Criqui; Gerald F. Fletcher; Valentin Fuster; Bernard J. Gersh; Antonio M. Gotto; K. L. Gould; Philip Greenland; Scott M. Grundy

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Elliott M. Antman

Brigham and Women's Hospital

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Loren F. Hiratzka

American Heart Association

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Joseph P. Ornato

National Institutes of Health

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Raymond J. Gibbons

American College of Cardiology

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Barbara Riegel

University of Pennsylvania

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Valentin Fuster

Icahn School of Medicine at Mount Sinai

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