Coronary artery atherosclerosis is the principal cause of coronary artery disease (CAD) and is the single largest killer of both men and women in the United States.
Approximately 14 million Americans have CAD. Each year, 1.5 million individuals develop acute myocardial infarction (AMI), the most deadly presentation of CAD, and more than 500,000 of these individuals die. Survivors of myocardial infarction (MI) continue to have a poor prognosis, and their risk of mortality and morbidity is 1.5-15 times greater than that of the rest of the population. This fact remains true despite a 30% reduction in mortality from CAD over the past 3 decades. Many factors have led to a decrease in mortality and morbidity from AMI, including the introduction of coronary care units, coronary artery bypass grafting, thrombolytic therapy, percutaneous coronary intervention (eg, percutaneous transluminal coronary angioplasty [PTCA]), and a renewed emphasis on lifestyle modification.
A major recent advance has been a refined understanding of the nature of atherosclerotic plaque and the phenomenon of plaque rupture, which is the predominant cause of acute coronary syndrome (ACS) and AMI. Cardiologists now know that, in many cases (perhaps more than half), the plaque that ruptures and results in the clinical syndromes of ACS and AMI is less than 50% occlusive. These so-called vulnerable plaques, as compared with stable plaques, consist of a large lipid core, inflammatory cells, and thin fibrous caps that are subjected to greater biomechanical stress, thus leading to rupture that perpetuates thrombosis and ACS.
The treatment of such ruptured plaques has also taken a leap forward with the widespread use of newer antiplatelet and antithrombotic agents. Nonetheless, the greatest impact on the CAD epidemic can only be achieved through therapies tailored to prevent the rupture of these vulnerable plaques. Such plaques are likely more prevalent than occlusive plaques. Currently, it is not possible to clinically identify most so-called vulnerable plaques, and no data support the local treatment of such plaques. On the other hand, strong evidence from many randomized trials over the past decade supports the efficacy of statin-class drugs for lipid lowering and ACE inhibitors for improving endothelial function, both of which likely lead to plaque stabilization.
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