ABSTRACT
Plaque rupture and subsequent thrombosis at the site of the plaque rupture is the most common underlying pathophysiological mechanism of acute coronary syndromes (1). The clinical manifestations of acute coronary syndromes are sudden cardiac death, acute myocardial infarction, and unstable angina. Approximately 90% of cases of nonfatal myocardial infarction and many cases of sudden cardiac death are caused by the rupture of a coronary atherosclerotic plaque (2). Plaque rupture may be precipitated by external stresses or ‘triggers’ superimposed on vulnerable coronary plaques (3). It is important to differentiate intrinsic longterm changes of coronary plaques, internal triggering mechanisms, and external triggers (Figure 1). Intrinsic long-term changes consist of progressive lipid accumulation in the atheromatous core and degradation of the fibrous cap by proteolytic processes and inflammation (4, 5). An increased vulnerability of the plaque and a proneness to rupture are the consequences. External triggers probably activate internal triggering mechanisms such as biomechanical and hemodynamic stresses and changes in platelet aggregability and blood viscosity; they may thus determine the actual time of coronary plaque rupture (2). External triggers include physical activity, emotional stress, environmental changes, and other factors. A circadian, weekly, and seasonal variation of coronary events has also been observed.
