Left ventricular dilatation and failure post-myocardial infarction : pathophysiology and possible pharmacologic interventions

An important antecedent to the development of late congestive heart failure is left ventricular dilatation and remodeling following myocardial infarction, which occurs in 30-40% of acute anterior transmural infarcts. Dilatation and remodeling commence within the first 24 hours following myocardial i...

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Bibliographic Details
Published in:Cardiovascular drugs and therapy 1990-10, Vol.4 (5), p.1363-1374
Main Authors: FIRTH, B. G, DUNNMON, P. M
Format: Article
Language:English
Subjects:
Animals
Antianginal agents. Coronary vasodilator agents
Biological and medical sciences
Cardiomegaly - etiology
Cardiomegaly - physiopathology
Cardiomegaly - prevention & control
Cardiovascular system
Dilatation, Pathologic - physiopathology
Dilatation, Pathologic - prevention & control
Disease Models, Animal
Heart Failure - etiology
Heart Failure - physiopathology
Heart Failure - prevention & control
Humans
Medical sciences
Myocardial Infarction - complications
Pharmacology. Drug treatments
Ventricular Function, Left - drug effects
Ventricular Function, Left - physiology
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Summary:An important antecedent to the development of late congestive heart failure is left ventricular dilatation and remodeling following myocardial infarction, which occurs in 30-40% of acute anterior transmural infarcts. Dilatation and remodeling commence within the first 24 hours following myocardial infarction and may be steadily progressive over months to years. Both the infarcted and uninfarcted regions of the myocardium are equally involved in the process. The remodeling process comprises left ventricular wall thinning (mainly due to cell slippage), chamber dilatation, and compensatory hypertrophy of the uninfarcted segment of the myocardium. The hypertrophy may initially be physiologic but may ultimately become a pathologic process, and thereby contribute to pump dysfunction. The possible reasons why the ventricular hypertrophy may ultimately be dysfunctional include alterations in local architecture and their sequelae alone or in concert with local changes in the beta-adrenergic, alpha-adrenergic, or renin angiotensin systems. At the present time, there are encouraging data to suggest that nitroglycerin, or the angiotensin converting enzyme inhibitor captopril, may ameliorate this process.
ISSN:0920-3206
1573-7241
DOI:10.1007/BF02018264