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(Circulation. 2000;102:1863.)
© 2000 American Heart Association, Inc.

Basic Science Reports

Spontaneously Occurring Arrhythmogenic Right Ventricular Cardiomyopathy in the Domestic Cat

A New Animal Model Similar to the Human Disease

Philip R. Fox, DVM; Barry J. Maron, MD; Cristina Basso, MD, PhD; Si-Kwang Liu, DVM, PhD; Gaetano Thiene, MD

From the Caspary Research Institute of the Animal Medical Center, New York, NY (P.R.F., S.K.L.); Minneapolis Heart Institute Foundation, Minneapolis, Minn (B.J.M.); and Institute of Pathology, University of Padova Medical School, Padova, Italy (C.B., G.T.).

Correspondence to Philip R. Fox, DVM, Caspary Institute, The Animal Medical Center, 510 E 62nd St, New York, NY 10021. E-mail philip.fox{at}amcny.org

Background—Arrhythmogenic right ventricular cardiomyopathy (ARVC) is a primary myocardial disease of incompletely resolved pathogenesis and is a largely unappreciated cause of sudden death in the young.

Methods and Results—Clinical features of 12 domestic cats with ARVC (7 male; 1 to 20 years old, mean 7.3±5.2 years) were right-sided congestive heart failure (n=8), supraventricular tachyarrhythmias (n=5), ventricular tachycardia (n=3), polymorphic ventricular arrhythmias (n=6), and right bundle-branch block (n=5). ARVC was suspected in all 8 cats examined with echocardiography by marked enlargement of the right ventricle (RV) and right atrium and tricuspid regurgitation. Eight died of cardiovascular disease and 4 died of noncardiac conditions. At autopsy, hearts of ARVC cats were characterized grossly by moderate-to-severe RV cavity enlargement and wall thinning (n=12) and apical aneurysm formation (n=6). Histology demonstrated pronounced RV lesions in all 12 ARVC cats, including marked myocardial injury (myocyte death and atrophy) and repair (fibrous and/or fatty replacement). Injury and repair were also evident in the left ventricle (LV) in 10 cats, and 2 had involvement of both atria. Myocarditis was present in 10 of the 12 ARVC cats. Apoptosis was detected in 9 ARVC cats (mean apoptotic index, 28±23% RV, 21±19% LV, and 17±15% ventricular septum) but not in controls.

Conclusions—In the common domestic cat, we identified a clinically relevant cardiomyopathy that closely mimics ARVC in humans. This unique feline model of human disease will be relevant to defining pathogenesis and investigating mechanisms responsible for disease progression in ARVC.

Key Words: arrhythmia • cardiomyopathy • myocarditis • apoptosis • heart diseases

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