Objectives The purpose ofthis study was to investigate the effects of long-termramipril on ventricular remodeling, cardiac functionand survival in rat congestive heart failure after my-ocardial infarction. Methods Myocardial infarction(MI) was caused by ligation of the left anterior de-scending coronary artery in rats. 7 days after thesurgery, the surviving rats were randomly assigned tothe following treatment protocols: 1) MI ras with notherapy, 2) MI rats treated with ramipril 3 mg/kg perday, 3) Sham-operated control rats, and 4) Sham-op-erated rats treated with ramipril 3 mg/kg per day. At22 weeks, cardiac hemodynamic parameters such asMAP, LVSP, ±dP/dtmax and LVEDP were measured,and cardiac morphometric parameters such as HW,LVW and LVCA were measured, mRNA of cardiacmolecule genes, such as βMHC, BNP, collagen Ⅰ andⅢ, and TGF-β_1, were quantified, and survival rateswere calculated. Results Compared with sham-operated rats, MI rats without therapy showed significantincreases in cardiac morpholog Objectives The purpose of this study was to investigate the effects of long-termramipril on ventricular remodeling, cardiac function and survival in rat congestive heart failure after my-ocardial infarction. Methods Myocardial infarction (MI) was caused by ligation of the left anterior de-scending coronary artery in rats. 7 days after the surgeries, the surviving rats were randomly assigned tothe following treatment protocols: 1) MI ras with notherapy, 2) MI rats treated with ramipril 3 mg / kg perday, 3) Sham-operated control rats, and 4 At22 weeks, cardiac hemodynamic parameters such as MAPP, LVSP, ± dP / dtmax and LVEDP were measured, and cardiac morphometric parameters such as HW, LVW and LVCA were measured , mRNA of cardiacmolecule genes, such as βMHC, BNP, collagen Ⅰ and Ⅲ, and TGF-β_1, were quantified, and survival rates were calculated. Results Compared with sham-operated rats, MI rats without therapy showed significant in- creases in cardiac morpholog