EPIDEMIOLOGY. Acute myocardial infarction (MI) is the leading cause of death in North America and Europe. Each year, an estimated 650,000 Americans will sustain a new MI, and another 300,000 will have a recurrent MI.
Coronary artery disease is the leading cause of death in the United States and has been for the past 90 years.
However, the incidence of and mortality associated with acute MI have declined dramatically over the last 30 years with the advent of the coronary care unit, fibrinolytic therapy, catheter-based reperfusion, and lipid-modifying therapy.
The aging of the population in advanced economies and the global increased incidence of diabetes and obesity will, however, increase the burden of atherosclerotic coronary artery disease in the future.
II. PATHOPHYSIOLOGY. In most patients, coronary plaque rupture is the initiating event of acute MI.
Rupture of the thin fibrous cap of a coronary atheroma exposes the underlying subendothelial matrix to formed elements of circulating blood, leading to activation of platelets, thrombin generation, and thrombus formation.
Erosion of a coronary plaque without rupture can also lead to thrombus formation and is estimated to cause up to 25% of MIs. Acute coronary syndrome (ACS) is a dynamic process that involves cyclical transitioning among complete vessel occlusion, partial vessel occlusion, and reperfusion.
Occlusive thrombus in the absence of significant collateral vessels most often results in acute ST-segment elevation myocardial infarction (STEMI).
The pathophysiology of STEMI and non-STEMI (NSTEMI) is similar, and this explains the substantial overlap in ACSs with regard to ultimate outcome, extent of necrosis, and mortality rates.
The recognition of ST-segment elevation is particularly important because it generally mandates the need for emergent reperfusion therapy.
