Ventricular remodeling after myocardial infarction. Experimental observations and clinical implications.
Marc A. Pfeffer,Eugene Braunwald +1 more
TLDR
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:
An acute myocardial infarction, particularly one that is large and transmural, can produce alterations in the topography of both the infarcted and noninfarcted regions of the ventricle. This remodeling can importantly affect the function of the ventricle and the prognosis for survival. In the early period, infarct expansion has been recognized by echocardiography as a lengthening of the noncontractile region. The noninfarcted region also undergoes an important lengthening that is consistent with a secondary volume-overload hypertrophy and that can be progressive. 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. The process of ventricular enlargement can be influenced by three interdependent factors, that is, infarct size, infarct healing, and ventricular wall stresses. A most effective way to prevent or minimize the increase in ventricular size after infarction and the consequent adverse effect on prognosis is to limit the initial insult. Acute reperfusion therapy has been consistently shown to result in a reduction in ventricular volume. The reestablishment of blood flow to the infarcted region, even beyond the time frame for myocyte salvage, has beneficial effects in attenuating ventricular enlargement. The process of scarification can be interfered with during the acute infarct period by the administration of glucocorticosteroids and nonsteroidal antiinflammatory agents, which result in thinner infarcts and greater degrees of infarct expansion. Modification of distending or deforming forces can importantly influence ventricular enlargement. Even short-term augmentations in afterload have deleterious long-term effects on ventricular topography. Conversely, judicious use of nitroglycerin seems to be associated with an attenuation of infarct expansion and long-term improvement in clinical outcome. Long-term therapy with an angiotensin converting enzyme inhibitor can favorably alter the loading conditions on the left ventricle and reduce progressive ventricular enlargement as demonstrated in both experimental and clinical studies. With the former therapy, this attenuation of ventricular enlargement was associated with a prolongation in survival. The long-term clinical consequences of long-term angiotensin converting enzyme inhibitor therapy after myocardial infarction is currently being evaluated. Although studies directed at attenuating left ventricular remodeling after infarction are in the early stages, it does seem that this will be an important area in which future research might improve long-term outcome after infarction.read more
Citations
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Effect of captopril on mortality and morbidity in patients with left ventricular dysfunction after myocardial infarction. results of the survival and ventricular enlargement trial
Marc A. Pfeffer,Eugene Braunwald,Lemuel A. Moyé,Lofty L. Basta,Edward J. Brown,Thomas E. Cuddy,Barry R. Davis,Edward M. Geltman,Steven Goldman,Greg C. Flaker,Marc Klein,Gervasio A. Lamas,Milton Packer,Jacques R. Rouleau,Jean L. Rouleau,John D. Rutherford,John H. Wertheimer,C. Morton Hawkins +17 more
TL;DR: In patients with asymptomatic left ventricular dysfunction after myocardial infarction, long-term administration of captopril was associated with an improvement in survival and reduced morbidity and mortality due to major cardiovascular events.
Journal ArticleDOI
Bone marrow cells regenerate infarcted myocardium
Donald Orlic,Jan Kajstura,Stefano Chimenti,Igor Jakoniuk,Stacie M. Anderson,Baosheng Li,James Pickel,Ronald D.G. McKay,Bernardo Nadal-Ginard,David M. Bodine,Annarosa Leri,Piero Anversa +11 more
TL;DR: It is indicated that locally delivered bone marrow cells can generate de novo myocardium, ameliorating the outcome of coronary artery disease.
Journal ArticleDOI
Transplantation of Progenitor Cells and Regeneration Enhancement in Acute Myocardial Infarction (TOPCARE-AMI)
Birgit Assmus,Volker Schächinger,Claudius Teupe,Martina B. Britten,Ralf Lehmann,N. Döbert,Frank Grünwald,Alexandra Aicher,Carmen Urbich,Hans Martin,Dieter Hoelzer,Stefanie Dimmeler,Andreas M. Zeiher +12 more
TL;DR: In patients with AMI, intracoronary infusion of autologous progenitor cells appears to be feasible and safe and may beneficially affect postinfarction remodeling processes.
Journal ArticleDOI
Mobilized bone marrow cells repair the infarcted heart, improving function and survival
Donald Orlic,Jan Kajstura,Stefano Chimenti,Federica Limana,Igor Jakoniuk,Federico Quaini,Bernardo Nadal-Ginard,David M. Bodine,Annarosa Leri,Piero Anversa +9 more
TL;DR: In this article, the authors demonstrate that transplanting primitive bone marrow cells (BMC) into the border zone of acute myocardial infarcts resulted in a significant degree of tissue regeneration 27 days later.
Journal ArticleDOI
Cardiac remodeling—concepts and clinical implications: a consensus paper from an international forum on cardiac remodeling
TL;DR: Left ventricular end-diastolic and end-systolic volume and ejection fraction data provide support for the beneficial effects of therapeutic agents such as angiotensin-converting enzyme (ACE) inhibitors and beta-adrenergic blocking agents on the remodeling process.
References
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Journal ArticleDOI
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Journal ArticleDOI
Myocardial infarct size and ventricular function in rats.
Marc A. Pfeffer,Janice M. Pfeffer,Michael C. Fishbein,P J Fletcher,J Spadaro,Robert A. Kloner,Eugene Braunwald +6 more
TL;DR: In this model of histologically healed myocardial infarction, the impairment of left ventricular function was directly related to the loss of myocardium, and the entire spectrum of postinfarction ventricularfunction was observed, from no detectable impairment to congestive failure.
Journal ArticleDOI
The effect of coronary occlusion on myocardial contraction
Robert Tennant,Carl J. Wiggers +1 more
TL;DR: Desc descriptions of a technique and of a type of optical myograph suitable for such studies and an analysis of the changes in optical myograms which follow clamping of a large coronary vessel are concerned.
Journal ArticleDOI
Effect of captopril on progressive ventricular dilatation after anterior myocardial infarction.
TL;DR: It is indicated that after anterior myocardial infarction, ventricular enlargement is progressive and that captopril may attenuate this process, reduce filling pressures, and improve exercise tolerance.
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