Acute myocardial infarction

Acute myocardial infarction usually results from coronary thrombosis at the site of a ruptured atherosclerotic plaque. The underlying plaque need not be obstructive. The extent of myocardial infarction is influenced by ischemic preconditioning, induction of coronary collaterals, thrombolysis, reperfusion injury, and coronary reocclusion. Although reperfusion therapy has improved overall outcome in myocardial infarction, there is great variability in the degree of myocardial stunning, injury, infarction, remodeling, and recovery of left ventricular function in individual patients. Some patients with successful early reperfusion therapy have extensive myocardial damage, while others, who present later in the course of myocardial infarction, have less extensive infarction. This paradox is probably a result of deleterious processes predominating in some patients and protective mechanisms in others. The management of patients after myocardial infarction has, therefore, become more difficult in the era of reperfusion therapy. The optimal strategy for assessing patients following initial therapy and the selection of patients for revascularization after myocardial infarction remain controversial. This review focuses on selected recent studies of myocardial infarction concerning coronary anatomy, mechanisms of myocardial injury, case management, risk stratification, and complications. Thrombolytic therapy is reviewed elsewhere.