Murry and colleagues in 1986 described a paradoxical phenomenon that exposure of the heart to repeated brief ischemic episodes delayed the severity of myocardial infarction of a following prolonged myocardial ischemia and termed it myocardial ischemic preconditioning (IP). From then on, IP had been extensively studied in various kinds of experimental models as well as in humans. Besides delaying myocardial infarction, IP has been proved to be a potent endogenous factor in preserving high energy phosphates, suppressing arrhythmias and improving postischemic functional recovery. Delaying myocardial ultrastructure damage, reducing lactate, reducing the utilization of myocardial glycogen and protecting coronary endothelium after IP has also been found. Different experimental models and conditions resembling cardiac surgery have also been investigated. The mechanism of IP is not yet clear, however. The conclusions derived from animal studies could not totally stand for the situation in open heart surgery. IP was found effective in preserving high energy phosphate, improving heart performance and decreasing cardiac troponin T release during open heart surgery. Controversial exists because in same reports there were no effects of IP. The difference in IP protocol, myocardial protective method and study object might be the reason of the controversial results. Several clinical factors may affect IP effects during clinical practice. The purpose of the present study was to review the recent literature on IP, especially the IP mechanism, IP phenomenon in cardiac surgery and the possible influential factors, to summarize whether IP might prefer additional protection of current protective strategy in cardiac surgery.