title: Left ventricular remodeling in myocardial hibernation.
abstract: BACKGROUND
  Left ventricular (LV) remodeling as a consequence of extensive myocardial infarction has been well established in animal and human studies. This study was designed to determine whether regional LV dysfunction with myocardial hibernation without transmural or extensive infarction could initiate the remodeling process.
  
  
  RESULTS
  A severe left anterior descending coronary artery stenosis was created to reduce resting flow by approximately 40% (from 0.99+/-0.10 to 0.56+/-0.11 mL x min(-1) x g[-1]) and was maintained for 7 days in 13 pigs. The reduction of regional coronary flow initially produced acute myocardial ischemia, as evidenced by reduced regional wall thickening, from 37+/-3% at baseline to 9+/-7%, regional lactate production and a decrease in regional coronary venous pH. All pigs had significant regional LV dysfunction and reduced LV ejection fraction (41+/-11%). The LV end-diastolic volume increased from 59+/-9 mL at baseline to 74+/-13 mL immediately after placement of the stenosis and to 78+/-17 mL 7 days later with hibernating myocardium. The LV mass did not change immediately (60+/-8 g baseline versus 59+/-11 g immediately after creation of the stenosis) but increased modestly yet significantly to 67+/-15 g after 7 days of myocardial hibernation subtending the severe LAD stenosis. The reductions of coronary flow and wall thickening were unchanged at 7 days, whereas myocardial lactate production recovered. By 4 weeks after restoration of LAD flow, regional function had recovered in all 7 pigs with follow-up. Of the 13 pigs, 6 were free from any evidence of myocardial infarction, and 4 had patchy necrosis involving less than 6% of the area at risk.
  
  
  CONCLUSIONS
  LV remodeling, which is commonly associated with extensive myocardial infarction, can be initiated by regional dysfunctional hibernating myocardium resulting from a severe coronary stenosis. Myocardial necrosis is not a prerequisite for LV remodeling in response to regional dysfunction.
authors.affiliation: Division of Cardiology, Hartford Hospital, the University of Connecticut School of Medicine, 06102, USA.
authors.forename: C
authors.initials: C
authors.lastname: Chen
authors.forename: L
authors.initials: L
authors.lastname: Ma
authors.forename: W
authors.initials: W
authors.lastname: Dyckman
authors.forename: F
authors.initials: F
authors.lastname: Santos
authors.forename: T
authors.initials: T
authors.lastname: Lai
authors.forename: L D
authors.initials: LD
authors.lastname: Gillam
authors.forename: D D
authors.initials: DD
authors.lastname: Waters
mesh_terms: D000818:Animals; D003326:Coronary Circulation; D017379:Hypertrophy, Left Ventricular / Q000209:etiology; D009200:Myocardial Contraction; D017682:Myocardial Stunning / Q000150:complications / Q000503:physiopathology*; D009206:Myocardium / Q000473:pathology; D013552:Swine; D016277:Ventricular Function, Left