ABSTRACT
Atherosclerotic coronary artery disease (CAD) is the leading cause of morbidity and mortality in industrialized countries.1 Clinical manifestations of CAD include sudden cardiac death and acute coronary syndromes (ACS) of unstable angina, non-ST-elevation myocardial infarction (MI), and ST-elevation MI. Most acute ischemic events are caused by rupture or superficial erosion of coronary plaques at sites with only mild to moderate luminal stenosis.2 Coronary plaques which are prone to rupture, the so-called vulnerable plaques, tend to have a thin fibrous cap and a large lipid core. Recent data indicate that patients with ACS manifest multiple ruptured/vulnerable plaques in addition to the culprit lesion causing the index ischemic event.3-6 These additional ruptured plaques may be associated with a poor long-term prognosis. The significance of this issue is evidenced by the fact that patients with ACS account for approximately 1.4 million hospitalizations each year in the USA, and more than 2 million admissions worldwide.1
