title: An ovine model of postinfarction dilated cardiomyopathy.
abstract: 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.
authors.affiliation: Harrison Department of Surgical Research, University of Pennsylvania School of Medicine, Philadelphia, USA.
authors.forename: Sina L
authors.initials: SL
authors.lastname: Moainie
authors.forename: Joseph H
authors.initials: JH
authors.lastname: Gorman
authors.forename: T Sloane
authors.initials: TS
authors.lastname: Guy
authors.forename: Frank W
authors.initials: FW
authors.lastname: Bowen
authors.forename: Benjamin M
authors.initials: BM
authors.lastname: Jackson
authors.forename: Theodore
authors.initials: T
authors.lastname: Plappert
authors.forename: Navneet
authors.initials: N
authors.lastname: Narula
authors.forename: Martin G
authors.initials: MG
authors.lastname: St John-Sutton
authors.forename: Jagat
authors.initials: J
authors.lastname: Narula
authors.forename: L Henry
authors.initials: LH
authors.lastname: Edmunds
authors.forename: Robert C
authors.initials: RC
authors.lastname: Gorman
mesh_terms: D000818:Animals; D002306:Cardiac Volume / Q000502:physiology; D002311:Cardiomyopathy, Dilated / Q000473:pathology / Q000503:physiopathology*; D003326:Coronary Circulation / Q000502:physiology; D004195:Disease Models, Animal; D004452:Echocardiography; D006439:Hemodynamics / Q000502:physiology*; D009200:Myocardial Contraction / Q000502:physiology; D009203:Myocardial Infarction / Q000473:pathology / Q000503:physiopathology*; D009206:Myocardium / Q000473:pathology; D012756:Sheep; D013318:Stroke Volume / Q000502:physiology; D020257:Ventricular Remodeling / Q000502:physiology*