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Joseph H. Gorman, III
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Ann Thorac Surg 2002;74:753-760
© 2002 The Society of Thoracic Surgeons

Original article: cardiovascular

An ovine model of postinfarction dilated cardiomyopathy

Sina L. Moainie, MDa, Joseph H. Gorman, III, MD*a, T. Sloane Guy, MDa, Frank W. Bowen, III, MDa, Benjamin M. Jackson, MDa, Theodore Plappert, CVTb, Navneet Narula, MDc, Martin G. St. John-Sutton, MBBSc, Jagat Narula, MD, PhDd, L. Henry Edmunds, Jr, MDa, Robert C. Gorman, MD*a

a Harrison Department of Surgical Research, Philadelphia, Pennsylvania, USA
b Departments of Medicine & Pathology, Philadelphia, Pennsylvania, USA
c University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania, USA
d Center for Molecular Cardiology, MCP/Hahnemann University School of Medicine, Philadelphia, Pennsylvania, USA

Accepted for publication May 28, 2002.

* Address reprint requests to Dr Gorman, Department of Surgery, 6 Silverstein, Hospital of the University of Pennsylvania, Philadelphia, PA 19104, USA
e-mail: rcgorman{at}uphs.upenn.edu

Background. Coronary arterial disease is the major cause of congestive heart failure, but suitable animal models of postinfarction, dilated cardiomyopathy do not exist. This article describes an ovine model that develops after an anterobasal infarction.

Methods. The distribution of ovine myocardium supplied by the first two diagonal branches of the left homonymous artery were determined in 20 slaughterhouse hearts and eight live sheep using methylene blue and tetrazolium injections, respectively. Seven additional animals had the infarction and underwent serial hemodynamic, microsphere and echocardiographic studies more than 8 weeks and histologic studies at the eighth week. Infarcts represented 24.6% ± 4.7% and 23.9% ± 2.2% of the left ventricular mass in slaughterhouse and live hearts, respectively.

Results. During remodeling, left ventricular end-systolic and end-diastolic volumes increased 115% and 73%, respectively, ejection fraction decreased from 41.2% ± 6.7% to 29.1% ± 5.7%, systolic wall thickening remote from the infarct decreased by 68%, sphericity index increased from 0.465 ± 0.088 to 0.524 ± 0.038, and left ventricular end-diastolic pressure increased from 1.7 ± 1.0 to 8.2 ± 3.5 mm Hg. Serial microsphere measurements documented normal blood flow (1.34 mL/g per minute) to all uninfarcted myocardium and 22% of normal to the infarct. Viable myocardium showed mild interstitial fibrosis.

Conclusions. This ovine model meets all criteria for postinfarction, dilated cardiomyopathy and has the advantages of controlling for variations in coronary arterial anatomy, collateral vascularity, and differences in the numbers, location, and severity of atherosclerotic lesions that confound human studies of the pathogenesis of this disease. This simple model contains only infarcted and fully perfused, hypocontractile myocardium produced by a moderate-sized, regional infarction.




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