Early captopril prevents myocardial infarction-induced hypertrophy but notangiogenesis

Delayed captopril, started after the healing phase of myocardial infarction , improves perfusion by reducing tissue weight without affecting the vascul ar capacity of the heart. Early captopril, during the healing phase, preven ts reactive hypertrophy, but the effects on angiogenesis are unknown. There fore, the effects of early captopril (2 g/l drinking water, from 1 day unti l 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 measur ed during nitroprusside-induced vasodilation, using radioactive microsphere s. Maximal vascular capacity was not changed by captopril. Reactive hypertr ophy in infarcted hearts only reached statistical significance in the left ventricular free wall. Since captopril prevented hypertrophy but did not af fect regional capacity, peak tissue perfusion was improved. Indicating effe cts on metabolism, captopril restored the increased lactate/purine ratio in infarcted hearts. Thus, early captopril treatment prevented post-myocardia l infarction hypertrophy but did not suppress angiogenesis, thus beneficial ly influencing the vascularization/tissue mass ratio, probably reflected by preservation of aerobic metabolism. (C) 1999 Elsevier Science B.V. All rig hts reserved.