Fibrosis, Myocyte Degeneration and Heart Failure in Chronic Experimental Aortic Regurgitation

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Abstract

Myocardial fibrosis and myocyte degeneration have been reported in patients with chronic aortic regurgitation (AR), and may be related to the pathophysiology of congestive heart failure (CHF) in this disease. To define the relationship between myocardial histopathologic variations and CHF in chronic AR, we performed gross and microscopic evaluations of postmortem tissue from a rabbit model of chronic AR manifesting left ventricular (LV) responses to AR similar to those in humans. Moderate-to-severe chronic AR (echocardiographic regurgitant fraction = 52 ± 13%) was induced by closed-chest aortic valve perforation in 11 New Zealand White rabbits; 5 control rabbits were sham operated. Six of the 11 AR rabbits died 1.5 ± 0.8 years (range 0.6–2.8 years) after AR induction; all 6 had gross and histologic anatomic evidence of CHF at necropsy. The remaining 5 AR rabbits survived until sacrifice at 2.9 ± 0.1 years of AR; none had pathologic evidence of CHF. Cardiac hypertrophy and the extent of LV fibrosis and myocyte necrosis all were greatest among the 6 AR CHF rabbits. No inflammatory response was apparent in any animal. Moderate-to-severe chronic experimental AR frequently results in CHF which is strongly associated with myocardial fibrosis and necrosis, without evidence of inflammation. These histopathologic variations may be pathophysiologically related to CHF development.

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Author and article information

Journal

Journal ID (publisher-id): CRD

Journal ID (nlm-ta): Cardiology

Journal ID (doi): 10.1159/issn.0008-6312

Title: Cardiology

Publisher: S. Karger AG

ISSN (Print): 0008-6312

ISSN (Electronic): 1421-9751

Publication date Subscription-year: 1998

Publication date (Print): October 1998

Publication date (Electronic): 28 October 1998

Volume: 90

Issue: 2

Pages: 101-109

Affiliations

^b Division of Cardiovascular Pathophysiology, Cornell University Medical College, New York Hospital- Cornell Medical Center, and ^a Caspary Institute for Veterinary Research, New York, N.Y., USA

Article

Publisher ID: 6827 Other ID: Cardiology 1998;90:101–109

DOI: 10.1159/000006827

PubMed ID: 9778546

SO-VID: 9d1a22f5-53d5-4821-93a0-625a111b2f9d

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