Effects of early reperfusion on creatine kinase release in patients with acute myocardial infarction: Implications for reperfusion injury

摘要

Conversion of reversibly injured cells to irreversibly injured cells during reperfusion is called lethal reperfusion injury [1 ]. The occurrence of lethal reperfusion injury is evident from the protective effects of post-conditioning procedures [2] in patients with acute myocardial infarction (MI). Given that lethal reperfusion injury occurs in humans, early reperfusion should cause a larger number of early cell deaths due to lethal reperfusion injury. This is likely to be the case because severely injured, yet viable myocardial cells are present at the end of an ischemic event, and these cells are most susceptible to lethal reperfusion injury. Conversely, fewer viable cells exist in the myocardium subjected to more longstanding ischemia. In the former case, cell death, represented by enzyme release, would be expected to be greater during the reperfusion period, reflecting a larger contribution of lethal reperfusion injury to total cell death. This hypothesis was tested by examining the relationship between time to reperfusion and time to peak creatine kinase (CK) release in patients with acute MI.