Bernard R. Chaitman
Saint Louis University
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Journal of the American College of Cardiology | 2000
Joseph S. Alpert; Elliott M. Antman; Fred S. Apple; Paul W. Armstrong; Jean Pierre Bassand; A. B. De Luna; George A. Beller; Bernard R. Chaitman; Peter Clemmensen; E. Falk; M. C. Fishbein; Marcello Galvani; A Jr Garson; Cindy L. Grines; Christian W. Hamm; U. Hoppe; Allan S. Jaffe; Hugo A. Katus; J. Kjekshus; Werner Klein; Peter Klootwijk; C. Lenfant; D. Levy; R. I. Levy; R. Luepker; Frank I. Marcus; U. Naslund; M. Ohman; Olle Pahlm; Philip A. Poole-Wilson
This document was developed by a consensus conference initiated by Kristian Thygesen, MD, and Joseph S. Alpert, MD, after formal approval by Lars Rydén, MD, President of the European Society of Cardiology (ESC), and Arthur Garson, MD, President of the American College of Cardiology (ACC). All of the participants were selected for their expertise in the field they represented, with approximately one-half of the participants selected from each organization. Participants were instructed to review the scientific evidence in their area of expertise and to attend the consensus conference with prepared remarks. The first draft of the document was prepared during the consensus conference itself. Sources of funding appear in Appendix A. The recommendations made in this document represent the attitudes and opinions of the participants at the time of the conference, and these recommendations were revised subsequently. The conclusions reached will undoubtedly need to be revised as new scientific evidence becomes available. This document has been reviewed by members of the ESC Committee for Scientific and Clinical Initiatives and by members of the Board of the ESC who approved the document on April 15, 2000.*
European Heart Journal | 2012
Kristian Thygesen; Joseph S. Alpert; Allan S. Jaffe; Maarten L. Simoons; Bernard R. Chaitman; Harvey D. White
ACCF : American College of Cardiology Foundation ACS : acute coronary syndrome AHA : American Heart Association CAD : coronary artery disease CABG : coronary artery bypass grafting CKMB : creatine kinase MB isoform cTn : cardiac troponin CT : computed tomography CV : coefficient of variation ECG : electrocardiogram ESC : European Society of Cardiology FDG : fluorodeoxyglucose h : hour(s) HF : heart failure LBBB : left bundle branch block LV : left ventricle LVH : left ventricular hypertrophy MI : myocardial infarction mIBG : meta-iodo-benzylguanidine min : minute(s) MONICA : Multinational MONItoring of trends and determinants in CArdiovascular disease) MPS : myocardial perfusion scintigraphy MRI : magnetic resonance imaging mV : millivolt(s) ng/L : nanogram(s) per litre Non-Q MI : non-Q wave myocardial infarction NSTEMI : non-ST-elevation myocardial infarction PCI : percutaneous coronary intervention PET : positron emission tomography pg/mL : pictogram(s) per millilitre Q wave MI : Q wave myocardial infarction RBBB : right bundle branch block sec : second(s) SPECT : single photon emission computed tomography STEMI : ST elevation myocardial infarction ST–T : ST-segment –T wave URL : upper reference limit WHF : World Heart Federation WHO : World Health Organization Myocardial infarction (MI) can be recognised by clinical features, including electrocardiographic (ECG) findings, elevated values of biochemical markers (biomarkers) of myocardial necrosis, and by imaging, or may be defined by pathology. It is a major cause of death and disability worldwide. MI may be the first manifestation of coronary artery disease (CAD) or it may occur, repeatedly, in patients with established disease. Information on MI rates can provide useful information regarding the burden of CAD within and across populations, especially if standardized data are collected in a manner that …
Circulation | 2002
Raymond J. Gibbons; Gary J. Balady; J. Timothy Bricker; Bernard R. Chaitman; Gerald F. Fletcher; Victor F. Froelicher; Daniel B. Mark; Ben D. McCallister; Aryan N. Mooss; Michael O'Reilly; William L. Winters; Elliott M. Antman; Joseph S. Alpert; David P. Faxon; Valentin Fuster; Gabriel Gregoratos; Loren F. Hiratzka; Alice K. Jacobs; Richard O. Russell; Sidney C. Smith
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 …
Circulation | 2002
Kim A. Eagle; Peter B. Berger; Hugh Calkins; Bernard R. Chaitman; Gordon A. Ewy; Kirsten E. Fleischmann; Lee A. Fleisher; James B. Froehlich; Richard J. Gusberg; Jeffrey A. Leppo; Thomas J. Ryan; Robert C. Schlant; William L. Winters; Raymond J. Gibbons; Elliott M. Antman; Joseph S. Alpert; David P. Faxon; Valentin Fuster; Gabriel Gregoratos; Alice K. Jacobs; Loren F. Hiratzka; Richard O. Russell; Sidney C. Smith
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 …
The New England Journal of Medicine | 2009
L. Frye; Phyllis August; Regina M. Hardi; Sheryl F. Kelsey; Trevor J. Orchard; Bernard R. Chaitman
BACKGROUND Optimal treatment for patients with both type 2 diabetes mellitus and stable ischemic heart disease has not been established. METHODS We randomly assigned 2368 patients with both type 2 diabetes and heart disease to undergo either prompt revascularization with intensive medical therapy or intensive medical therapy alone and to undergo either insulin-sensitization or insulin-provision therapy. Primary end points were the rate of death and a composite of death, myocardial infarction, or stroke (major cardiovascular events). Randomization was stratified according to the choice of percutaneous coronary intervention (PCI) or coronary-artery bypass grafting (CABG) as the more appropriate intervention. RESULTS At 5 years, rates of survival did not differ significantly between the revascularization group (88.3%) and the medical-therapy group (87.8%, P=0.97) or between the insulin-sensitization group (88.2%) and the insulin-provision group (87.9%, P=0.89). The rates of freedom from major cardiovascular events also did not differ significantly among the groups: 77.2% in the revascularization group and 75.9% in the medical-treatment group (P=0.70) and 77.7% in the insulin-sensitization group and 75.4% in the insulin-provision group (P=0.13). In the PCI stratum, there was no significant difference in primary end points between the revascularization group and the medical-therapy group. In the CABG stratum, the rate of major cardiovascular events was significantly lower in the revascularization group (22.4%) than in the medical-therapy group (30.5%, P=0.01; P=0.002 for interaction between stratum and study group). Adverse events and serious adverse events were generally similar among the groups, although severe hypoglycemia was more frequent in the insulin-provision group (9.2%) than in the insulin-sensitization group (5.9%, P=0.003). CONCLUSIONS Overall, there was no significant difference in the rates of death and major cardiovascular events between patients undergoing prompt revascularization and those undergoing medical therapy or between strategies of insulin sensitization and insulin provision. (ClinicalTrials.gov number, NCT00006305.)
The New England Journal of Medicine | 2012
Gregory G. Schwartz; Anders G. Olsson; Markus Abt; Christie M. Ballantyne; Philip J. Barter; Jochen Brumm; Bernard R. Chaitman; Ingar Holme; David Kallend; Lawrence A. Leiter; Eran Leitersdorf; Hardi Mundl; Stephen J. Nicholls; Prediman K. Shah; Jean-Claude Tardif; R. Scott Wright
BACKGROUND In observational analyses, higher levels of high-density lipoprotein (HDL) cholesterol have been associated with a lower risk of coronary heart disease events. However, whether raising HDL cholesterol levels therapeutically reduces cardiovascular risk remains uncertain. Inhibition of cholesteryl ester transfer protein (CETP) raises HDL cholesterol levels and might therefore improve cardiovascular outcomes. METHODS We randomly assigned 15,871 patients who had had a recent acute coronary syndrome to receive the CETP inhibitor dalcetrapib, at a dose of 600 mg daily, or placebo, in addition to the best available evidence-based care. The primary efficacy end point was a composite of death from coronary heart disease, nonfatal myocardial infarction, ischemic stroke, unstable angina, or cardiac arrest with resuscitation. RESULTS At the time of randomization, the mean HDL cholesterol level was 42 mg per deciliter (1.1 mmol per liter), and the mean low-density lipoprotein (LDL) cholesterol level was 76 mg per deciliter (2.0 mmol per liter). Over the course of the trial, HDL cholesterol levels increased from baseline by 4 to 11% in the placebo group and by 31 to 40% in the dalcetrapib group. Dalcetrapib had a minimal effect on LDL cholesterol levels. Patients were followed for a median of 31 months. At a prespecified interim analysis that included 1135 primary end-point events (71% of the projected total number), the independent data and safety monitoring board recommended termination of the trial for futility. As compared with placebo, dalcetrapib did not alter the risk of the primary end point (cumulative event rate, 8.0% and 8.3%, respectively; hazard ratio with dalcetrapib, 1.04; 95% confidence interval, 0.93 to 1.16; P=0.52) and did not have a significant effect on any component of the primary end point or total mortality. The median C-reactive protein level was 0.2 mg per liter higher and the mean systolic blood pressure was 0.6 mm Hg higher with dalcetrapib as compared with placebo (P<0.001 for both comparisons). CONCLUSIONS In patients who had had a recent acute coronary syndrome, dalcetrapib increased HDL cholesterol levels but did not reduce the risk of recurrent cardiovascular events. (Funded by F. Hoffmann-La Roche; dal-OUTCOMES ClinicalTrials.gov number, NCT00658515.).
Circulation | 2008
Leslee J. Shaw; Daniel S. Berman; David J. Maron; G.B. John Mancini; Sean W. Hayes; Pamela Hartigan; William S. Weintraub; Robert A. O’Rourke; Marcin Dada; John A. Spertus; Bernard R. Chaitman; John D. Friedman; Piotr J. Slomka; Gary V. Heller; Guido Germano; Gilbert Gosselin; Peter B. Berger; William J. Kostuk; Ronald G. Schwartz; Merill L Knudtson; Emir Veledar; Eric R. Bates; Benjamin D. McCallister; Koon K. Teo; William E. Boden
Background— Extent and severity of myocardial ischemia are determinants of risk for patients with coronary artery disease, and ischemia reduction is an important therapeutic goal. The Clinical Outcomes Utilizing Revascularization and Aggressive Drug Evaluation (COURAGE) nuclear substudy compared the effectiveness of percutaneous coronary intervention (PCI) for ischemia reduction added to optimal medical therapy (OMT) with the use of myocardial perfusion single photon emission computed tomography (MPS). Methods and Results— Of the 2287 COURAGE patients, 314 were enrolled in this substudy of serial rest/stress MPS performed before treatment and 6 to 18 months (mean=374±50 days) after randomization using paired exercise (n=84) or vasodilator stress (n=230). A blinded core laboratory analyzed quantitative MPS measures of percent ischemic myocardium. Moderate to severe ischemia encumbered ≥10% myocardium. The primary end point was ≥5% reduction in ischemic myocardium at follow-up. Treatment groups had similar baseline characteristics. At follow-up, the reduction in ischemic myocardium was greater with PCI+OMT (−2.7%; 95% confidence interval, −1.7%, −3.8%) than with OMT (−0.5%; 95% confidence interval, −1.6%, 0.6%; P<0.0001). More PCI+OMT patients exhibited significant ischemia reduction (33% versus 19%; P=0.0004), especially patients with moderate to severe pretreatment ischemia (78% versus 52%; P=0.007). Patients with ischemia reduction had lower unadjusted risk for death or myocardial infarction (P=0.037 [risk-adjusted P=0.26]), particularly if baseline ischemia was moderate to severe (P=0.001 [risk-adjusted P=0.08]). Death or myocardial infarction rates ranged from 0% to 39% for patients with no residual ischemia to ≥10% residual ischemia on follow-up MPS (P=0.002 [risk-adjusted P=0.09]). Conclusions— In COURAGE patients who underwent serial MPS, adding PCI to OMT resulted in greater reduction in ischemia compared with OMT alone. Our findings suggest a treatment target of ≥5% ischemia reduction with OMT with or without coronary revascularization.
Circulation | 1992
Gerald F. Fletcher; Steven N. Blair; James A. Blumenthal; Carl J. Caspersen; Bernard R. Chaitman; Stephen Epstein; Harold B. Falls; Erika Sivarajan Froelicher; Victor F. Froelicher; Ileana L. Piña
Physical inactivity is recognized as a risk factor for coronary artery disease. Regular aerobic physical activity increases exercise capacity and plays a role in both primary and secondary prevention of cardiovascular disease.1 2 3 4 5 The known benefits of regular aerobic exercise and current recommendations for implementation of exercise programs are described in this revised report.6 Exercise training increases cardiovascular functional capacity and decreases myocardial oxygen demand at any level of physical activity in apparently healthy persons as well as in most subjects with cardiovascular disease. Regular physical activity is required to maintain these training effects. The potential risk of physical activity can be reduced by medical evaluation, risk stratification, supervision, and education.4 Exercise can help control blood lipid abnormalities, diabetes, and obesity. In addition, aerobic exercise adds an independent blood pressure–lowering effect in certain hypertensive groups with a decrease of 8 to 10 mm Hg in both systolic and diastolic blood pressure measurements.7 8 9 10 There is a direct relation between physical inactivity and cardiovascular mortality, and physical inactivity is an independent risk factor for the development of coronary artery disease.11 12 13 14 There is a dose-response relation between the amount of exercise performed from approximately 700 to 2000 kcal of energy expenditure per week and all-cause mortality and cardiovascular disease mortality in middle-aged and elderly populations.14 15 The greatest potential for reduced mortality is in the sedentary who become moderately active.15 Most beneficial effects of physical activity on cardiovascular disease mortality can be attained through moderate-intensity activity (40% to 60% of maximal oxygen uptake, depending on age).14 15 16 The activity can be accrued through formal training programs or leisure-time physical activities. Although most of the supporting data are based on studies in men, more recent findings …
Circulation | 2003
Ileana L. Piña; Carl S. Apstein; Gary J. Balady; Romualdo Belardinelli; Bernard R. Chaitman; Brian D. Duscha; Barbara J. Fletcher; Jerome L. Fleg; Jonathan N. Myers; Martin J. Sullivan
Heart failure (HF) may be defined as the inability of the heart to meet the demands of the tissues, which results in symptoms of fatigue or dyspnea on exertion progressing to dyspnea at rest. The inability to perform exercise without discomfort may be one of the first symptoms experienced by patients with HF and is often the principal reason for seeking medical care. Therefore, exercise intolerance is inextricably linked to the diagnosis of HF. It might be expected that a tight relationship would exist between indices of resting ventricular function and exercise capacity. Data indicate, however, that indices of resting ventricular function (such as ejection fraction [EF]) are only weakly correlated to exercise tolerance.1 Exercise intolerance is defined as the reduced ability to perform activities that involve dynamic movement of large skeletal muscles because of symptoms of dyspnea or fatigue. Many investigators have sought mechanisms to explain the source of exercise intolerance. The aims of this position statement are to review (1) factors that affect exercise tolerance, with specific emphasis on chronic HF due to systolic dysfunction; (2) data that support the role of exercise training in chronic systolic HF, including the risks and benefits; (3) data on exercise training in patients with HF due to diastolic dysfunction; and finally (4) the subgroups of patients with HF for which data are lacking, and (5) the subgroups of patients who should not be included in exercise training programs. We anticipate this report will stimulate appropriate use of exercise training in patients with HF when indicated and encourage further studies in those areas in which data are lacking. ### Cardiovascular The capacity for performing aerobic exercise depends on the ability of the heart to augment its output to the exercising muscles and the ability of these muscles to utilize oxygen from the delivered …
The New England Journal of Medicine | 1979
Donald A. Weiner; Thomas J. Ryan; Carolyn H. McCabe; J. Ward Kennedy; Michael Schloss; Felix E. Tristani; Bernard R. Chaitman; Lloyd D. Fisher
Abstract To determine to what extent the diagnostic accuracy of stress testing is influenced by the prevalence of coronary-artery disease, we correlated the description of chest pain, the result of stress testing and the results of coronary arteriography in 1465 men and 580 women from a multicentered clinical trial. The pre-test risk (prevalence of coronary-artery disease) varied from 7 to 87 per cent, depending on sex and classification of chest pain. A positive stress test increased the pre-test risk by only 6 to 20 per cent, whereas a negative test decreased the risk by only 2 to 28 per cent. Although the percentage of false-positive results differed between men and women (12±1 per cent versus 53±3 per cent P < 0.001), this difference was not seen in a subgroup matched for prevalence of coronary-artery disease. We conclude that the ability of stress testing to predict coronary-artery disease is limited in a heterogeneous population in which the prevalence of disease can be estimated through classificat...