Document Detail


The pathophysiologic profile of congestive heart failure.
MedLine Citation:
PMID:  3154647     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Congestive heart failure (CHF) evolves either from an excessive workload or in response to loss of myocardium, both of which cause cardiac hypertrophy, increased cardiac pressure, and loss of functional reserve. Nearly 60% of patients in heart failure present with ischemic cardiomyopathy, which in its chronic form exhibits biventricular dilatation, elevated left ventricular mass, and extensive large-vessel atherosclerosis. The hypertrophy is proportional to the loss of myocardium, although animal studies suggest this varies with the infarct size. However, recent studies indicate that early afterload reduction may relieve the hypertrophic stimulus and prevent degeneration. Some 30% to 40% of patients in heart failure present with an idiopathic dilated cardiomyopathy, with a patchy but diffuse loss of tissue on microscopy, reactive hypertrophy in the surviving cells, and interstitial fibrosis and replacement scarring. The ultrastructural changes still await clarification. The role of pharmacologic intervention still remains unclear. However, any reduction in mortality will necessitate the identification of those cellular changes that inevitably lead to secondary degeneration of the remaining viable myocardium.
Authors:
R H Haber; T LeJemtel; E H Sonnenblick
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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:  2 Suppl 1     ISSN:  0920-3206     ISO Abbreviation:  Cardiovasc Drugs Ther     Publication Date:  1988 Nov 
Date Detail:
Created Date:  1991-04-25     Completed Date:  1991-04-25     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:  397-400     Citation Subset:  IM    
Affiliation:
Albert Einstein College of Medicine, Bronx, New York 10461.
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MeSH Terms
Descriptor/Qualifier:
Cardiomyopathy, Dilated / physiopathology
Coronary Disease / complications
Heart Failure / etiology,  physiopathology*
Humans

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


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