Objective To explore the effectiveness of induced pluripotent stem cell derived cardiomyocytes for myocardial repair in rat models of myocardial infarction， and clarify the mechanism for improving cardiac function.Methods Induced pluripotent stem cells were cultured in vitro and differentiated into cardiomyocytes. SD rats with myocardial infarction model were randomly divided into myocardial infarction group and cell transplantation group， and normal SD rats were used as control group， with 10 rats in each group. After modeling， the myocardial infarction group and the cell transplantation group were injected 30 μL normal saline and differentiated myocardial cells at 3 sites near the boundary of myocardial infarction， respectively. The control group underwent thoracotomy without coronary artery ligation. Cardiac function was measured by color echocardiography and invasive hemodynamics at days 7， 14， and 28. On day 28， the tissue senescence index was detected by RT-PCR， the infarct area was evaluated by Masson staining and the capillary density was detected by immunohistochemistry.Results At 28 days， compared with myocardial infarction group， left ventricular ejection fraction (LVEF)， left ventricular end diastolic diameter (LVEDD)， Left ventricular end systolic diameter (LVESD)， left ventricular end diastolic pressure (LVEDP) and maximum，both the positive and negative left chamber pressure change rate (±dP/dt) were significantly improved (P＜0.05). The infarct area of the cell transplantation group was significantly smaller than that of the myocardial infarction group， and capillary angiogenesis was significantly higher than that of the myocardial infarction group (P＜0.05). The mRNA expression of matrix metalloproteinase-3 (MMP-3)， endothelial cell-type plasminogen activator inhibitor (PAI-1) and interleukin-6 (IL-6) in the myocardial infarction group was significantly increased (P<0.05).Conclusion Transplantation of cardiomyocytes differentiated from induced pluripotent stem cells can improve the cardiac function of rat models of myocardial infarction through paracrine action.