Coronary Artery Disease (CAD) remains globally the leading cause of death and long-term morbidity. Among the many manifestations of CAD, acute coronary syndrome (ACS), ranging from unstable angina to acute myocardial infarction, is the most catastrophic event due to our inability to predict its occurrence. Despite improved treatments of CAD, ACS results in sudden death or permanent disability in a substantial percentage of patients. If we could predict the timing of ACS or better yet prevent its occurrence, we could alter the otherwise unfavorable course of CAD. Several studies have convincingly demonstrated that majority of all ACS develops from previously mild to moderate stenoses. Thus, based on these and autopsy studies, sudden disruption or rupture of the non-obstructive “vulnerable” atherosclerotic lesion is currently considered the cause of ACS. Recent clinical studies have substantiated earlier autopsy observations that plaque vulnerability is a systemic process, involving multiple locations concurrently. Although the exact inciting factors of the vulnerable plaque rupture are unknown, inflammation is accepted to be a pivotal event. The possibility of stabilizing the vulnerable plaques has strongly been supported by the lipid lowering trials, in which dramatic reduction of the acute coronary events was noted despite subtle improvements in luminal diameter. Furthermore, antiplatelet therapies have become an important preventative therapy due to the essential role of platelets in the aftermath of plaque rupture. Finally, various imaging modalities to diagnose the plaque vulnerability could help prevent the acute coronary events in the future.
Keywords: atherosclerosis, coronary artery disease, vulnerable plaque, inflammation, cholesterol, acute coronary syndrome
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