| Structural basis for pathologic left ventricular hypertrophy. | |
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MedLine Citation:
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PMID: 8504584 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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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. |
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Authors:
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K T Weber; C G Brilla |
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Publication Detail:
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Type: Journal Article; Review |
Journal Detail:
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Title: Clinical cardiology Volume: 16 ISSN: 0160-9289 ISO Abbreviation: Clin Cardiol Publication Date: 1993 May |
Date Detail:
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Created Date: 1993-07-08 Completed Date: 1993-07-08 Revised Date: 2005-11-16 |
Medline Journal Info:
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Nlm Unique ID: 7903272 Medline TA: Clin Cardiol Country: UNITED STATES |
Other Details:
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Languages: eng Pagination: II10-4 Citation Subset: IM |
Affiliation:
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Department of Internal Medicine, University of Missouri-Columbia School of Medicine 65212. |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Animals Endomyocardial Fibrosis / pathology, physiopathology Humans Hypertrophy, Left Ventricular / pathology*, physiopathology Myocardium / pathology Renin-Angiotensin System / physiology |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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