The Pathology of Myocardial Infarction

Coronary artery thrombosis, due either fissuring or erosion of atherosclerotic plaque, is the usual cause of acute myocardial infarction (1) and results in a progressive increase of the infarct size with a wavefront transmural extension from the endocardium towards the epicardium (2,3). Although thrombolysis and reperfusion can occur spontaneously, thrombotic coronary artery occlusion usually persists in the majority of patients suffering an acute myocardial infarction. Thus, timely coronary artery recanalization and myocardial reperfusion, either by thrombolytic therapy or primary angioplasty and/or stenting, represents the most effective way of restoring the balance between myocardial oxygen supply and demand. However, although beneficial in terms of myocardial salvage, the process of reperfusion may elicit itself pathologic consequences and the term “reperfusion injury” has been introduced (4-7). The morphologic features typical of reperfused myocardial infarction will be here analyzed, ie contraction-band necrosis and the no-reflow phenomenon as well as the metamorphosis of acute myocardial infarction after coronary artery recanalization (Table 1).