Early and chronic captopril or Losartan therapy reduces infarct size and avoids congestive heart failure after myocardial infarction in rats

Background ensin converting enzyme (ACE) inhibitors and angiotensin II AT1-receptor antagonists prolong survival in experimental postischemic heart failure (CHF) in rats. The aim of this study was to investigate whether potential beneficial effects of early and long-term therapy with low doses of captopril or losartan occur in hemodynamics and heart morphometry, as well as in infarct size during establishment of CHF after myocardial infarction. s istar rats were subjected to myocardial infarction by left coronary ligation. Subsequently, 24 h after surgery captopril (2.5 mg/kg/day/28 days) or losartan (3 mg/kg/day/28 days) was administered by mini-osmotic pump release. Hemodynamics, infarct size, and heart morphometry were measured in sham, untreated, and treated operated rats. s metric and hemodynamic parameters were modified after myocardial infarction indicating hypertrophy of the heart and CHF establishment; however, either captopril or losartan partially avoided hypertrophy. Captopril reverted hemodynamics to sham values, while losartan induced further decrease in systolic blood pressure. Both drugs were able to drastically reduce infarct size produced by myocardial infarction. sions how that early and chronic therapy with low doses of captopril or losartan prevent CHF establishment, probably by limiting extension of infarcted area after coronary occlusion, and suggest AT1 receptor pathway involvement in this pathology.