Reversibility and pathohistological basis of left ventricular remodeling hibernating myocardium

The phenomenon of left ventricular (LV) remodeling with dilatation, wall th inning, and increased muscle mass has previously been reported in pigs with 7-day myocardial hibernation. This study investigated cellular and extrace llular basis and reversibility of the structural LV remodeling with hiberna ting myocardium. Five groups of pigs were included: Group A: 7-day myocardi al hibernation with a fixed coronary stenosis; Group B: 7-day hibernation w ith subsequent 3-week reperfusion by release of the stenosis; Group C: cont rol group with sham operation; Group D: 24-hour myocar dial hibernation to define structural mechanism of initial wall thinning in the hibernating reg ion without confounding factors of cell loss or hypertrophy, Group E: 4-wee k myocardial hibernation to exclude the possibility of spontaneous regressi on of LV remodeling with hibernation. LAD flow decreased by 38 +/- 12% (p < 0.01) with a significant decrease in systolic wall thickening at 7 days of hibernation with severe coronary stenosis (Group A). End-diastolic wall th ickness decreased by 19% (p < 0.01) accompanied by a decrease in myocyte nu mber across the wall (44% and in myocyte density (24%), a significant incre ase in myocyte width (17%), a mild increase in interstitial tissues in hibe rnating region, and significant increases in LV diastolic volume and in LV mass at 7 days. After reperfusion (Group B), LV volume decreased, LV ejecti on fraction improved, and myocyte hypertrophy regressed with a decreased LV mass index without a significant change in interstitial tissue. LV remodel ing progressed with further increases in LV volume, mass, and interstitial fibrosis in 4-week hibernation. In pigs undergoing 24 hours of myocardial h ibernation (Group D), end-diastolic LV wall thickness decreased si,signific antly in the hibernating region with a proportional decrease in the transmu ral myocyte number but without changes in myocyte width, myocyte density, o r interstitial tissues. Therefore, progressive gross LV remodeling associat ed with hibernating myocardium is accompanied by increasing myocyte hypertr ophy and interstitial fibrosis. In hibernating myocardial region, wall thin ning is proportional to a decreased myocyte number across the LV wall, indi cating slippage of myocytes as a preponderant mechanism for the wall thinni ng. Myocyte hypertrophy develops within 7 days in hibernating myocardium, c ausing an increase in LV mass. These changes are partially reversible after reperfusion. (C) 2000 by Elsevier Science Inc.