Pathophysiology of Coronary Artery Disease

Abstract

Acute coronary syndrome includes unstable angina, acute myocardial infarction, and sudden coronary death. In individuals with sudden coronary death, 50–60% displays acute coronary thrombus at the culprit site, while the remaining cases demonstrate a stable coronary plaques with greater than 75% cross-sectional area luminal narrowing, with or without chronic total occlusion or healed myocardial infarction. Three different causes of coronary thrombus have been shown, i.e., plaque rupture, plaque erosion, and calcified nodule. Plaque rupture (PR) is the most common cause of coronary thrombus, which shows a disrupted fibrous cap and an underlying necrotic core in contact with the flowing blood and a luminal thrombus. The second most common cause of thrombosis is plaque erosion. Plaque erosions show an absence of endothelium with an underlying abundance of smooth muscle cells in a proteoglycan-collagen-rich matrix. The least frequent cause of coronary thrombosis is calcified nodule which occurs in highly calcified arteries. Calcified nodule demonstrates a disrupted fibrous cap due to fragments of calcified spicules typically surrounded by fibrin and an overlying platelet-rich thrombus. Calcified nodules are usually eccentric and usually have an overlying nonocclusive thrombus. The precursor lesion of rupture is a vulnerable plaque which demonstrates all the features of rupture, but there is an intact fibrous cap, and the necrotic core is usually smaller than that observed in ruptures. Erosive plaques mostly show an underlying fibroatheroma or pathologic intimal thickening, while calcified nodules demonstrate a highly calcified plaque in a heavily calcified coronary artery.