Background Cardiac troponin-I (cTnl) is one of the three regulatory subunits of the cardiac troponin which has the high sensibility and specificity of responding to myocardial injury. Studies have demonstrated that cTnl is released into the blood stream within hours following acute myocardial reperfusion injury. The clinical utility of cTnl for the assessment of myocardial damage is that it is more specific than creatine kinase MB (CKMB). This study investigated cTnl as a sensitive marker of myocardial reperfusion injury and its clinical value on beating heart surgery with right sub-axiliary incision. Methods From December 2002 threugh December 2004,100 patients with atrial septal defect (ASD), ventricular septal defect (VSD), atrial septal defect and ventricular septal defect (ASD+VSD), and tetralogy of Fallot were randomly divided into two groups: the treatment group (n=50) was operated on with a beating heart under extracorporeal circulation (ECC), and the control group (n=50) on an conventional arresting heart under ECC. The two groups both used a right sub-axillary incision. Blood samples from a central venous catheter (CVC) were collected before, at the end of aortic clamping, immediately after discontinue cardiopulmonary bypass (CPB), 3, 6, 24, and 48 hours after operation. The Abbott Axsym system with hol-automation fluorescent immunity analyzer was used for the quantitative determination of cTnl. cTnl was detected to investigate the effect of myocardial ischemia reperfusion injury and the clinical value of beating heart surgery with right sub-axillary incision. Results There were no significant differences between the two groups before operation. At the end of aortic clamping and thereafter, cTnl significantly increased in both groups, and reached the peak point at 6 hours after operation. At all the tested points, cTnl was significantly higher in the control group than the beating heart group (P