Abstract: AIM:To investigate the effect of qidan tongmai tablet (QDTMT) on cardiac function and myocardial fibrosis in rats after myocardial infarction (MI). METHODS: Sprague Dawley (SD) rats were subjected to MI by ligating the left anterior descending coronary and randomly divided into sham group, MI group, low-dose QDTMT group (MI-QDTMTL, 1.0 g/kg) and high-dose QDTMT group (MI-QDTMTH, 2.0 g/kg). After 24 h of ligation, 15 ml/kg saline for sham and MI groups and 1.0 g/kg or 2.0 g/kg QDTMT for MI-QDTMTL or MI-QDTMTH groups were administered twice daily. Cardiac contractile function of left ventricular end-diastolic pressure (LVEDP) and ejection factor (EF) were measured in vivo. Rats were sacrificed after 4 weeks. Collagen content in the noninfarcted area was detected by Masson’s trichrome stain. Transforming growth factor beta-1 (TGF-β1), collagen type 1 and collagen type 3 mRNA expressions were examined by RT-PCR in the noninfarcted area. The hydroxyproline content of the noninfarcted tissue was measured by hydroxyproline (HYP) ELISA kit for rats. RESULTS: After 4 weeks, rat cardiac function of LVEDD and EF and the heart weight/body weight (HW/BW) index in QDTMTH group and QDTMTL group were significantly better than those in MI group (P<0.01; P<0.05), but poorer than those in the sham group (P<0.01). Myocardial collagen content in noninfarcted area was significantly inhibited in MI-QDTMTL group and MI-QDTMTH group (P<0.01). mRNA expression levels of TGF-β1, Col1 and Col3 in noninfarcted area were significantly inhibited in MI-QDTMTL group and MI-QDTMTH group (P<0.01). Hydroxyproline content of the noninfarcted tissue was significantly inhibited in MI-QDTMTL group and MI-QDTMTH group (P<0.05). CONCLUSION: In post-MI myocardial fibrosis, QDTMT improves cardiac function and reduces myocardial fibrosis by downregulating TGF-β1, Col1and Col3 expressions and decreasing the production of hydroxyproline.