Calcium overload and ischemic myocardial injury.

R eperfusion injury is an issue of concern to every physician treating patients with acute myocardial infarction in the 1990s. For patients without specific contraindictions to therapy presenting for medical care early in the course of myocardial infarction, an attempt at reperfusion of ischemic, but not yet necrotic, myocardium is the current standard of clinical care. Whether a patient is treated with a thrombolytic agent to lyse an intracoronary thrombus or undergoes emergency coronary angioplasty to reperfuse the myocardium, it is the hope, and usually the case, that reversibly ischemic tissue will be reperfused. However, it remains uncertain whether simply restoring blood flow to an area of myocardium lacking adequate blood supply is in fact the optimal strategy for salvage of myocardial tissue. Paradoxically, this seemingly straightforward approach may lead to reperfusion injury and necrosis of tissue that was potentially viable. Almost invariably, a patient with an evolving myocardial infarction who undergoes reperfusion therapy with either a thrombolytic agent or by angioplasty develops evidence for myocardial necrosis as evidenced by release of creatine kinase-MB. While it is convenient to attribute this myocardial necrosis to ischemic