OBJECTIVE: To assess the effect of lisinopril and losartan on myocardial remodeling in experimental infarction in rats. METHODS: Male Wistar rats underwent myocardial infarction and were either treated with lisinopril [20 mg/kg/day (LIS, n=13)] or losartan [20 mg/kg/day (LOS, n=11)], or kept without any treatment (NT, n=11) for 3 months. Their results were compared with those of a control group (CONT, n=11) comprising noninfarcted rats. After euthanasia, the left ventricle was isolated and weighed. The following measurements were taken: the sectional area of myocytes (AC), interstitial collagen fraction (CVF), and myocardial hydroxyproline (HOP). The variables were compared by using 1-way ANOVA, with a significance level of P<0.05. RESULTS: Acute myocardial infarction caused left ventricular hypertrophy. The treatments with lisinopril or losartan could prevent hypertrophy, which was quantified by use of left ventricular weight (LOS=1.06±0.12g, LIS=0.97±0.18g, NT=1.26±0.17g, CONT=1.02±0.09g; P<0.05), of left ventricular weight-to-body weight ratio LV/BW (LOS=2.37± 0.21mg/g, LIS=2.41±0.38mg/g, NT=2.82±0.37mg/g, CONT=2.27± 0.15mg/g), and of left ventricular AC measure-ment (LOS=210±39µ², LIS=217±35µ², NT=256±35µ², CONT=158±06 µ²; P<0.05). The CVF was significantly greater in the left ventricle of the infarcted group, and its increase was prevented with treatment (LOS=1.16±0.4%, LIS=1.27±0.5%, NT=1.8± 0.4%, CONT=0.7±0.5%). Myocardial hydroxyproline was greater in the infarcted group (NT=6.91±2.98mg/g vs. CONT=2.81± 1.21mg/g) and did not change with treatment. CONCLUSION: Myocardial remodeling after infarction is characterized by an increase in the remaining ventricular mass and in interstitial collagen. The angiotensin-converting-enzyme blockers and the selective angiotensin II AT1 antagonist prevent hypertrophy of the myocyte and interstitial fibrosis.
myocardial remodeling; experimental acute myocardial infarction; renin-angiotensin-aldosterone system
