Document Detail

Structural basis for pathologic left ventricular hypertrophy.
MedLine Citation:
PMID:  8504584     Owner:  NLM     Status:  MEDLINE    
Left ventricular hypertrophy (LVH) is a major risk factor associated with the emergence of symptomatic congestive heart failure. Cardiac myocyte excitation-contraction coupling has been the biochemical focus in the search for insights into the impaired contractility, relaxation, and stiffness of the hypertrophied myocardium. Although hypertrophied myocytes are the hallmark of LVH, other aspects of myocardial structure may be altered to impair pump function--specifically an abnormal accumulation of connective tissue (interstitial fibrosis). Cardiac fibroblasts, which are nonmyocyte cells of the cardiac interstitium, synthesize and degrade collagen and, therefore, represent an important determinant of pathologic LVH. Significantly, this reactive fibrosis has been found not only in the pressure-overloaded hypertrophied left ventricle but also in the normotensive, nonhypertrophied right ventricle of animals with experimental hypertension. These findings suggest the involvement of a circulating substance that has access to the coronary circulation common to both ventricles. Based on in vivo studies that examined this hypothesis, it can be concluded that chronic elevation of circulating aldosterone, relative to sodium intake, is associated with myocardial fibrosis, which initially adversely alters diastolic function and ultimately systolic ventricular function. The mechanisms by which fibroblast collagen metabolism is invoked in this setting are under investigation. Elucidation of these mechanisms may prepare the way to the prevention as well as the reversal of myocardial fibrosis and, in turn, of pathologic LVH.
K T Weber; C G Brilla
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Publication Detail:
Type:  Journal Article; Review    
Journal Detail:
Title:  Clinical cardiology     Volume:  16     ISSN:  0160-9289     ISO Abbreviation:  Clin Cardiol     Publication Date:  1993 May 
Date Detail:
Created Date:  1993-07-08     Completed Date:  1993-07-08     Revised Date:  2005-11-16    
Medline Journal Info:
Nlm Unique ID:  7903272     Medline TA:  Clin Cardiol     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  II10-4     Citation Subset:  IM    
Department of Internal Medicine, University of Missouri-Columbia School of Medicine 65212.
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MeSH Terms
Endomyocardial Fibrosis / pathology,  physiopathology
Hypertrophy, Left Ventricular / pathology*,  physiopathology
Myocardium / pathology
Renin-Angiotensin System / physiology

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