Document Detail

Left ventricular dilatation and failure post-myocardial infarction: pathophysiology and possible pharmacologic interventions.
MedLine Citation:
PMID:  2149059     Owner:  NLM     Status:  MEDLINE    
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.
B G Firth; P M Dunnmon
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Publication Detail:
Type:  Journal Article; Review    
Journal Detail:
Title:  Cardiovascular drugs and therapy / sponsored by the International Society of Cardiovascular Pharmacotherapy     Volume:  4     ISSN:  0920-3206     ISO Abbreviation:  Cardiovasc Drugs Ther     Publication Date:  1990 Oct 
Date Detail:
Created Date:  1991-03-14     Completed Date:  1991-03-14     Revised Date:  2007-11-15    
Medline Journal Info:
Nlm Unique ID:  8712220     Medline TA:  Cardiovasc Drugs Ther     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  1363-74     Citation Subset:  IM    
Cardiology Division, University of Texas Southwestern Medical Center, Dallas 75235-9047.
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MeSH Terms
Cardiomegaly / etiology,  physiopathology*,  prevention & control*
Dilatation, Pathologic / physiopathology,  prevention & control
Disease Models, Animal
Heart Failure / etiology,  physiopathology*,  prevention & control*
Myocardial Infarction / complications*
Ventricular Function, Left / drug effects*,  physiology*

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine

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