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Showing papers by "Marc A. Pfeffer published in 1993"


Book ChapterDOI
TL;DR: The extent of ventricular enlargement after infarction is related to the magnitude of the initial damage to the myocardium and, although an increase in cavity size tends to restore stroke volume despite a persistently depressed ejection fraction, ventricular dilation has been associated with a reduction in survival.
Abstract: Acute transmural myocardial infarction initiates a series of changes in left ventricular (LV) volume, regional function and geometry. This process, known as postinfarction LV remodeling, may continue for months or years following the initial ischemic event. To characterize the components of late ventricular remodeling, biplane left ventriculography was performed in 52 patients at 3 weeks and repeated at 1 year after first anterior myocardial infarction. Biplane circumference and contractile and noncontractile segment lengths were measured. Global geometry was evaluated by calculating a sphericity index and regional geometry was assessed by measurement of endocardial curvature. End-diastolic (ED) volume was increased at 3 weeks and enlarged further at one year. This late enlargement was accompanied by an increase in the length of the contractile segment and an increase in sphericity, whereas the length of the noncontractile segment decreased. Curvature analysis revealed that this late increase in sphericity resulted from flattening of regions of presumably high tension negative curvature at the infarct border zone and from less bulging of the infarcted anterior wall. Even in patients selected for late ventricular enlargement (change in ED volume > 20 ml, n = 19), this increase in volume resulted from both lengthening of the contractile segment and an increase in sphericity without a change in the noncontractile segment length. Thus, late ventricular enlargement after anterior myocardial infarction results from an increase in contractile segment length and a change in ventricular geometry and is not a result of progressive infarct expansion.

935 citations


Journal ArticleDOI
TL;DR: The threshold for the admission of patients to a coronary care unit or for the use of invasive diagnostic and therapeutic interventions in the early and late periods after an infarction is higher in Canada than in the United States, which is associated with a higher frequency of activity-limiting angina.
Abstract: Background There are major differences in the organization of the health care systems in Canada and the United States. We hypothesized that these differences may be accompanied by differences in patient care. Methods To test our hypothesis, we compared the treatment patterns for patients with acute myocardial infarction in 19 Canadian and 93 United States hospitals participating in the Survival and Ventricular Enlargement (SAVE) study, which tested the effectiveness of captopril in this population of patients after a myocardial infarction. Results In Canada, 51 percent of the patients admitted to a participating coronary care unit had acute myocardial infarctions, as compared with only 35 percent in the United States (P<0.001). Despite the similar clinical characteristics of the 1573 U.S. patients and 658 Canadian patients participating in the study, coronary arteriography was more commonly performed in the United States than in Canada (in 68 percent vs. 35 percent, P<0.001), as were revascularization pro...

303 citations


Journal ArticleDOI
TL;DR: Although all neurohormones except epinephrine were increased compared with values in age-matched control subjects, plasma norepinephrine values ranged from normal to very high, indicating a wide spectrum of neurohumoral activation.

157 citations


Journal Article
TL;DR: Experimental and early clinical studies have indicated that chronic therapy with an angiotensin converting enzyme inhibitor may attenuate this progressive ventricular enlargement, and the addition of this pharmacological therapy to that of the primary prevention of atherosclerosis and the limitation of infarct size should make a substantial impact on the reduction of the incidence of congestive heart failure.
Abstract: Ischemic heart disease is the major etiology for the development of congestive heart failure. Patients with acute myocardial infarction have a greatly increased risk for mortality and for manifesting symptomatic heart failure. This risk is not a uniform one but is greatly augmented in patients with a more extensive infarction and, consequently, a more depressed global ventricular function. An important concept that was derived from studies in rats with myocardial infarction and has been confirmed in patients is that ventricular enlargement, which has been shown to be a marker for an adverse outcome, can be a progressive process that leads to further deterioration of ventricular performance. Both experimental and early clinical studies have indicated that chronic therapy with an angiotensin converting enzyme inhibitor may attenuate this progressive ventricular enlargement. More definitive clinical trials are currently under way to determine whether this form of therapy, which may diminish the extent of ventricular enlargement over time, will result in an improvement in survival and in the prevention of the development of congestive heart failure. The addition of this pharmacological therapy to that of the primary prevention of atherosclerosis and that of the limitation of infarct size should make a substantial impact on the reduction of the incidence of congestive heart failure.

48 citations


Journal ArticleDOI
TL;DR: Results of this kinetics demonstrate that the agent first perfuses all normal fluid spaces and then slowly diffuses into the occluded zone where it is retained for a prolonged period, in sufficient quantities to be useful as an MRI contrast agent.
Abstract: The potential of a phosphonate-modified-Gd-DTPA for MR image enhancement of myocardial infarction has been demonstrated in imaging experiments on rats. The agent, 1-hydroxy-3-aminopropane-1,1-diphosphonate-modified-Gd-DTPA (Gd-DTPA-HPDP) accumulates in two models of myocardial infarction, (i.e., drug-induced diffusely infarcted whole hearts and in focal acute myocardial infarction from a left coronary artery ligation). The time course of the accumulation of the agent in the focal model of infarction and subsequent washout has also been followed in vitro. Results of this kinetics demonstrate that the agent first perfuses all normal fluid spaces and then slowly diffuses into the occluded zone where it is retained for a prolonged period, in sufficient quantities to be useful as an MRI contrast agent. Wash-out of the agent from normal myocardium is fast and complete with MR signal returning to background in minutes. The specificity of Gd-DTPA-HPDP for soft-tissue calcification and its retention within the infarcts permitted imaging at 1 to 2 h postinjection, (after unbound material has cleared the normal tissues). Infarcted tissue appeared as regions of increased signal intensity in T1-weighted images (> 200% enhancement), and correlated with histopathology. Unmodified Gd-DTPA was not retained under identical conditions. Gd-DTPA-HPDP permits a more accurate infarct delineation than is possible with the unmodified agent.

33 citations


Journal ArticleDOI
TL;DR: Key studies that have documented the efficacy of ACE inhibitors in improving clinical outcome for patients with overt congestive heart failure, as well as for those with asymptomatic left ventricular dysfunction are reviewed.

29 citations


Journal Article
01 Dec 1993-Herz
TL;DR: To the list of proved therapies that extend survival following myocardial infarction, the physician can now add ACE inhibition with captopril for patients with left ventricular dysfunction.
Abstract: Myocardial infarction increases the risk of subsequent cardiovascular events (e.g., heart failure or another myocardial infarction) among survivors as compared with the general population. Left ventricular dysfunction is among the major risk factors for such adverse events. Although reductions in cardiovascular risk have been achieved by use of aspirin, beta-blockers (and sometimes revascularization and/or serum lipid-lowering agents), the potential of angiotensin-converting enzyme (ACE) inhibitors to improve the outcome for survivors of myocardial infarction has only recently been examined. The concept that ACE inhibition might be of benefit for these patients originated from animal studies demonstrating that long-term ACE inhibition therapy attenuated left-ventricular enlargement. After clinical confirmation of this initial finding, the Survival and Ventricular Enlargement (SAVE) trial was designed to determine whether long-term ACE inhibition therapy would reduce morbidity and mortality among survivors of myocardial infarction. The SAVE study found the following risk reductions among captopril vs placebo recipients: death (all causes) 19% (95% confidence interval, 3 to 35%; p = 0.019); cardiovascular death 21% (95% confidence interval, 5 to 35%; p = 0.014); myocardial infarction 25% (95% confidence interval, 5 to 40%; p = 0.012). To the list of proved therapies that extend survival following myocardial infarction, the physician can now add ACE inhibition with captopril for patients with left ventricular dysfunction. Survivors of myocardial infarction are at heightened risk for subsequent adverse cardiovascular events.(ABSTRACT TRUNCATED AT 250 WORDS)

18 citations


Patent
09 Apr 1993
TL;DR: In this paper, a method for treating a human survivor of a heart attack and providing further improvement in survival following the heart attack by the early initiation and long-term administration of a renin-angiotensin system inhibitor, preferably an angio-ensin converting enzyme inhibitor.
Abstract: The invention involves a method for treating a human survivor of a heart attack and provides further improvement in survival following the heart attack by the early initiation and long-term administration of a renin-angiotensin system inhibitor, preferably an angiotensin converting enzyme inhibitor. The inhibitor may be used on its own, or in conjuction with other therapeutic compounds such as β blockers and thrombolytic agents. The preferred inhibitor is captopril.

7 citations


Journal Article
TL;DR: Long-term captopril use in patients with asymptomatic left ventricular dysfunction following prior myocardial infarction resulted in survival improvement and decreased morbidity and mortality due to severe cardiovascular events.
Abstract: Left ventricular dilation and dysfunction after myocardial infarction are major predictors of death. In experimental and clinical studies, long-term therapy with captopril, an angiotension-converting enzyme inhibitor, decreased ventricular dilation and rearrangement. This study was undertaken to examine whether captopril may reduce morbidity and mortality in patients with left ventricular dysfunction following myocardial infarction. On days 3 to 16 after myocardial infarction, 2231 patients with -blockers and in those untreated with the above drugs. This suggests that the use of captopril additionally improved the therapeutic outcomes in patients with prior myocardial infection.

3 citations


Patent
09 Apr 1993
TL;DR: In this paper, a method for treating a human survivor of a heart attack and providing further improvement in survival following the heart attack by the early initiation and long-term administration of a renin-angiotensin system inhibitor, preferably an angio-ensin converting enzyme inhibitor.
Abstract: The invention involves a method for treating a human survivor of a heart attack and provides further improvement in survival following the heart attack by the early initiation and long-term administration of a renin-angiotensin system inhibitor, preferably an angiotensin converting enzyme inhibitor. The inhibitor may be used on its own, or in conjuction with other therapeutic compounds such as β blockers and thrombolytic agents. The preferred inhibitor is captopril.

Patent
09 Apr 1993
TL;DR: L'invention se rapporte a un procede permettant de traiter une personne ayant survecu a une crise cardiaque, and d'augmenter davantage ses chances of survie suite a la criseCardiaque par l'amorce precoce.
Abstract: L'invention se rapporte a un procede permettant de traiter une personne ayant survecu a une crise cardiaque, et d'augmenter davantage ses chances de survie suite a la crise cardiaque par l'amorce precoce et l'administration a long terme d'un inhibiteur du systeme renine-angiotensine, de preference un inhibiteur d'enzyme de conversion d'angiotensine. L'inhibiteur peut etre usilite seul ou conjointement avec d'autres composes therapeutiques tels que des β-bloquants et des agents thrombolytiques. L'inhibiteur prefere est le captopril.