Early captopril prevents myocardial infarction-induced hypertrophy but not angiogenesis

Delayed captopril, started after the healing phase of myocardial infarction, improves perfusion by reducing tissue weight without affecting the vascular capacity of the heart. Early captopril, during the healing phase, prevents reactive hypertrophy, but the effects on angiogenesis are unknown. Therefore, the effects of early captopril (2 g/l drinking water, from 1 day until 3 weeks after myocardial infarction) on regional coronary flow related to tissue mass, were studied in isolated perfused hearts from rats, subjected to coronary artery ligation. Regional maximal vascular capacity was measured during nitroprusside-induced vasodilation, using radioactive microspheres. Maximal vascular capacity was not changed by captopril. Reactive hypertrophy in infarcted hearts only reached statistical significance in the left ventricular free wall. Since captopril prevented hypertrophy but did not affect regional capacity, peak tissue perfusion was improved. Indicating effects on metabolism, captopril restored the increased lactate/purine ratio in infarcted hearts. Thus, early captopril treatment prevented post-myocardial infarction hypertrophy but did not suppress angiogenesis, thus beneficially influencing the vascularization/tissue mass ratio, probably reflected by preservation of aerobic metabolism. Copyright (C) 1999 Elsevier Science B.V.

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