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European Heart Journal 1995 16(Supplement N):12-18; doi:10.1093/eurheartj/16.suppl_N.12
Copyright © 1995 by the European Society of Cardiology.
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© 1995 The European Society of Cardiology

Structural remodelling of the heart by fibrous tissue: Role of circulating hormones and locally produced peptides

K. T. Weber, Y. Sun and S. E. Campbell

Division of Cardiology, Department of Internal Medicine, University of Missouri Health Sciences Center Columbia, Missouri, U.S.A.

Correspondence: Karl T. Weber, MD, Division of Cardiology, Room MA432 Medical Science Building. Univeraity of Missouri Health Sciences Center, Columbia, MO 65212, U.S.A.

Symptomatic heart failure is accompanied by diastolic ventricular dysfunction due largely to an extensive reactive and reparative fibrosis. Experimental evidence suggests a clear association between myocardial fibrosis and chronic inappropriate elevations in circulating angiotensin II (Ang II) and/or aldosterone. Although not entirely elucidated, injury follows Ang lI-associated release of adrenal medullary catecholamines and aldosterone-induced myocardial potassium depletion. Increasing evidence indicates locally produced cardiac Ang II plays an important role in tissue repair that may underlie myocardial remodelling, the fibrous tissue accumulation both at and remote to the site of myocardial infarction (MI). Angiotensin converting enzyme (ACE) binding density markedly increases at these fibrous tissue sites after experimental MI, indicating an involvement in wound healing regardless of the cause and location of fibrosis; cells expressing Ang II receptors are primarily myofibroblasts. Therapy with A CE inhibitors and aldosterone receptor antagonist have each been shown to attenuate development of fibrosis.

Key Words: Myocardial remodelling • angiotensin • aldosterone • reparative fibrosis • reactive fibrosis • angiotensin converting enzyme • ACE inhibition • chronic RAAS activation


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