Enhanced postischemic dysfunction selective to subendocardium in conscious dogs with LV hypertrophy.

Abstract

The effects of a 15-min coronary arterial occlusion (CAO) and reperfusion (CAR) for 24 h were compared in 11 normal dogs and in 13 conscious dogs with left ventricular (LV) hypertrophy (H) induced by ascending aortic banding, which increased the LV weight-to-body weight ratio by 69%. The dogs were studied 2-4 wk after recovery from instrumentation for measurement of global LV dynamics and regional wall motion. During CAO, heart rate and LV end-diastolic pressure increased similarly in both groups; however, LV systolic pressure decreased (-38 +/- 6 mmHg; P < 0.01) only in LVH. At 1 h of CAR, all measurements of systemic hemodynamics and global LV function returned to baseline levels in normal dogs; however, sustained depression (P < 0.01) in LV systolic pressure (-18 +/- 4 mmHg) and mean velocity of circumferential fiber shortening corrected for heart rate (-0.17 +/- 0.06) were observed in LVH. The recovery in regional myocardial dysfunction was significantly prolonged in the subendocardium (Endo) of LVH, e.g., at 1 h of CAR, Endo wall thickening was depressed more in dogs with LVH compared with normal dogs (-69 +/- 3% vs. -53 +/- 5%; P < 0.01), but not in the subepicardium (Epi). Coronary flow reserve, assessed by intravenous adenosine, was depressed in Endo of LVH compared with normal dogs, but not altered further by CAR. In conclusion, myocardial stunning after a brief period of CAO in dogs with LVH was not enhanced in Epi but was modestly increased in Endo. This regional dysfunction was, however, sufficiently powerful to induce modest impairment of global LV function.