Background Congestive heart failure (CHF) is a majorrrrrrrrnr cause of morbidity and mortality worldwide and angiotensin convertingenzyme rrrrrrrrninhibitor (ACEI) is the cornerstone in its treatment However, CHF continues torrrrrrrrn progress despite this therapy, perhaps because of production of angiotensin Ⅱ rrrrrrrrn(Ang Ⅱ) by alternative pathways The present study was conducted to examine thrrrrrrrrne combined effects of a chronic ACEI, ramipril, and a chronic Ang Ⅱ type 1 recerrrrrrrrnptor blocker, TCV116, on rat CHF after myocardial infarction (MI) rrrrrrrrnMethods Congestive heart failure was caused by MI in rats, whicrrrrrrrrnh warrrrrrrrns induced by ligating the left anterior descending coronary artery Therrrrrrrrn experiment protocol included shamoperated rats (Sham), MIcontrol rats (MIrrrrrrrrncontrol), MI rats treated with ramipril 3 mg/kg (MIramipril) or TCV116 2 mg/rrrrrrrrnkg (MITCV116) per day, half dosage (MI1/2R&T) or full dosage (MIR&T) combirrrrrrrrnnrrrrrrrrnation of the two At 22 weeks, cardiac hemodynamic parameters such as mean arterrrrrrrrnrial pressure (MAP), left ventricular systolic pressure (LVSP), maximal rate of rrrrrrrrnleft ventricule pressure development and decline (LV dP/dtmax) and left verrrrrrrrnntricular end diastolic pressure (LVEDP), and cardiac morphometric parameters surrrrrrrrnch as heart weight (HW), left ventricular weight (LVW) and left ventricular cavirrrrrrrrnty area (LVCA) were measured, mRNA expressions of cardiac molecule genes such asrrrrrrrrn β myosin heavy chain (βMHC), Btype natriuretic peptide (BNP), transforming rrrrrrrrngrowth factorβ1 (TGFβ1), collagen I and Ⅲ were quantified with reverrrrrrrrrnse trrrrrrrrnranscription polymerase chain reaction (RTPCR) in the surviving septum myocardrrrrrrrrnium, and survival rates were calculated rrrrrrrrnResults There were no significant differences in MI sizes (rrrrrrrrn%) among each MI related experimental groups (33±13, 34±14, 33±13, 35±13 andrrrrrrrrn 33±14 for MIcontrol, MIramipril, MITCV116, MI1/2R&T and MIR&T, resprrrrrrrrnerrrrrrrrnctively, no statistical significance for all) Compared with shamoperatedrrrrrrrrn ratrrrrrrrrns, MI rats without therapy showed significant increases in morphometric parameterrrrrrrrnrs as well as in mRNA expressions of cardiac molecule genes (P<001); whilerrrrrrrrn their hemodynamic parameters were significantly impaired (P<001), and in rrrrrrrrnterms of spontaneous deaths survival rate shortened (P<005) Compared witrrrrrrrrnh MI rats without therapy, MI rats treated with each single drug showed signrrrrrrrrnificrrrrrrrrnant attenuation of mRNA expressions of cardiac molecule genes (P<001); whirrrrrrrrnle their hemodynamic parameters were significantly improved (P<005 or Prrrrrrrrn<001), and in terms of spontaneous deaths survival rate prolonged (P<0rrrrrrrrn05) Both half and full dosage combined treatments exerted more powerful effectrrrrrrrrns on improvement of cardiac phenotypic changes and on attenuation of βMHC, BNP rrrrrrrrnmRNA expressions (P<005 vs monotherapy); while LVEDP was further rrrrrrrrnlowered (rrrrrrrrnP<005 vs monotherapy) However, the total death in MI rats with full dosarrrrrrrrnge combined treatment was more though there were no significant differences whenrrrrrrrrn compared with other treatmentsrrrrrrrrnConclusions The results suggest that treatment with approprirrrrrrrrnate dosage combination of a chronic ACEI and a chronic ARB may further improve crrrrrrrrnardiac remodeling and cardiac function after MI Background Congestive heart failure (CHF) is a majo r r r r r r r nr cause of morbidity and mortality worldwide and angiotensin convertingenzyme r r r r r r r r ninhibitor (ACEI) is the cornerstone in its treatment However, CHF continues to this therapy, perhaps because of production angiotensin Ⅱ r r r r r r r r n (Ang Ⅱ) by alternative pathways The present study was conducted to examine th r r r r r r r r ne combined effects of a chronic ACEI, ramipril, and a chronic Ang II type 1 rece / r r r r r r r nptor blocker, TCV116, on rat CHF after myocardial infarction MI)  r r r r r r r nMethods Congestive heart failure was caused by MI in rats, whic r r r r r r r nh wa r r r r r r r r ns induced by ligating the left anterior descending coronary artery  The r r r r r r r n experiment protocol included shamoperated rats (Sham), MIcontrol rats (MI r r r r r r ncontrol), MI rats treated with ramipril 3 mg / kg ramipril) or TCV116 2 mg / r r r r r r nkg (MI  TCV116) per day, combi r r r r r r r nn r r r r r r r r nation ’s nation of the two  At 22 weeks, cardiac hemodynamic parameters such as mean arte r r r r r r r n nrial pressure (MAP), left ventricular systolic pressure (LVSP), maximal rate of r r r r r r r nleft ventricule pressure development and decline (LV dP / dtmax) and left ve r r r r r r r nntricular end diastolic pressure (LVEDP) parameters su r r r r r r r nch as heart weight (HW), left ventricular weight (LVW) and left ventricular cavi r r r r r r r nty area (LVCA) were measured, mRNA expressions of cardiac molecule genes such as r r r r r r r n β myosin heavy chain peptide (BNP), transforming r r r r r r r r ngrowth factor β1 (TGF  β1), collagen I and Ⅲ were quantified with rever r r r r r r r r nse t r r r r r r r r n nranscription polymera se chain reaction (RT-PCR) in the surviving septum myocard r r r r r r r r nium, and survival rates were calculated r r r r r r r nResults There were no significant differences in MI sizes ( r r r r r r r n%) among each MI related experimental groups (33 ± 13, 34 ± 14, 33 ± 13, 35 ± 13 and r r 33 ± 14 for MI  control, MI  PAMIPril, MI  TCV116, MI  1 / 2R & T and MI  R & T, resp r r r r r r r r ne r r r r r r r nctively, no statistical significance for all)  Compared with shamoperated r r r r r r r r n rat r r r r r r r ns MI rats without therapy showed significant increases in morphometric paramete r r r r r r r r n nrs as well as in mRNA expressions of cardiac molecule genes (P <001); while r r r r r r r n their hemodynamic parameters were significantly impaired (P <001), and in r r r r r r r nterms of spontaneous deaths survival rate shortened (P <005) wit r r r r r r r nh MI rats without therapy, MI rats treated with each single drug showed sign r r r r r r r r nific r r r r r r r nant attenuation of mRNA expressions of cardiac molecule genes (P <001); whi r r r r r r r r nle their hemodynamic parameters were significantly improved (P <005 or P r r r r r r r n <001 ), and in terms of spontaneous deaths survival rate prolonged (P <0 r r r r r r r n05)  Both half and full dosage combined treatments exerted more powerful effect r r r r r r r r on improvement of cardiac phenotypic changes and on attenuation of β MHC, BNP r r r r r r r P <005 vs monotherapy); while LVEDP was further r r r r r r r r nlowered ( r r r r r r r nP <005 vs monotherapy) However, the total death in MI rats with full dosa r r r r r r nge combined treatment was more though there were no significant differences when r r r r r r r r n compared with other treatments  r r r r r r r nConclusions The results suggest that treatment with appropri r r r r r r r n nate dosage combination of a chronic ACEI and a chronic ARB may further improve c r r r r r r r nardiac remodeling and cardiac function after MI 