Effects of fosinopril, irbesartan and combined treatment on ventricular remodeling after myocardial infarction

Objective The purpose of this study was to compare the effects of fosinopril, irbesartan, and their combination on ventricular remodeling after myocardial infarction (MI) Methods MI was induced by ligating the left anterior descending coronary artery in the rats Twenty four hours after coronary ligation, rats were randomly divided into four groups and treated for 2 weeks (1) MI+placebo; (2) MI+fosinopril; (3) MI+irbesartan; (4)MI+fosinopril+irbesartan; (5) sham ligation: We examined: (1)mean blood pressure, left ventricular end diastolic pressure(LVEDP); (2)heart weight(HW)/body weight (BW) ratio; (3) interstitial collagen and nonmyocyte cellular proliferation within the noninfarct zone Results Placebo treated infarcted rats developed significant increase in LVEDP( P 0 05), HW/BW( P 0 01), collagen content ( P 0 01), and nonmyocyte cellular proliferation ( P 0 01) compared with sham ligation control In fosinopril and irbesartan treated rats HW/BW, nonmyocyte cellular proliferation and mean blood pressure decreased compared with those in placebo treated rats Combination therapy attenuated significantly the changes of these parameters (all P 0 01 vs placebo) Fosinopril, irbesartan, and combination therapy limited the increase in LVEDP( P 0 05 vs placebo) Fosinopril or irbesartan alone, and combination therapy prevented collagen desposition ( P 0 01 vs placebo). Fosinopril or irbesartan alone did not completely inhibit collagen desposition. ( P 0 05 vs Sham control), combination therapy normalized collagen content (p=NS vs sham control)within the noninfarct zone The differance of every parameter among fosinopril, irbesartan, and combination therapy did not reach statistical significance Conclusion The present study demonstrated that both fosinopril and irbesartan could equally limit myocardial hypertrophy, attenuate the development of myocardial interstitial fibrosis, and prevent nonmyocyte cellular proliferation in the noninfarcted LV, which were not more significant in combination therapy of two weeks