ABSTRACT
Acute coronary syndromes (ACS) include unstable angina, non-Q-wave myocardial infarction (MI), Q-wave MI, and sudden cardiac death. While these conditions are somewhat arbitrarily differentiated into distinct clinical entities (i.e. the presence or absence of specific cardiac markers distinguish unstable angina from a non-Q-wave MI), in a pathophysiologic sense they are very much the same process. The signal event in the vast majority of ACS (70-80%) is the fissuring or rupture of a coronary plaque. The disruption-prone plaque in the coronary artery is typically a modestly stenotic, lipid-laden plaque with a thin fibrous cap. The plaque disruption sets off a cascade of reactions that culminates in thrombus formation. The thrombus, in turn, compromises to various degrees the lumen of the coronary artery. The culmination of this event depends upon the size and stability of the thrombus, the speed and strength of the body’s inherent thrombolytic action, and the adequacy of collateral flow to the region of myocardium served by the vessel in question. In a minority of patients with an ACS, there is no plaque disruption but only a superficial erosion of a markedly stenotic and fibrotic plaque. Thrombus formation in such cases may be triggered by systemic factors, such as smoking, cocaine, or diabetes, especially in patients whose diabetes is poorly controlled.1
