An atherosclerotic plaque is a focal thickening of the arterial intima built from a lipid-rich necrotic core, foam cells and inflammatory cells, and a fibrous cap. The necrotic core contains extracellular lipid, cholesterol crystals, and debris from dead macrophages. The fibrous cap is a layer of smooth-muscle cells and collagen that separates the core from the lumen; its thickness and collagen content determine whether the plaque stays intact.
A plaque is called vulnerable when its cap is thin, its lipid core is large, and macrophages and other inflammatory cells are concentrated at the cap's shoulder. These cells release enzymes such as matrix metalloproteinases that degrade collagen, weakening the cap. Two mechanisms can then expose the core to blood: rupture, in which the cap tears and blood contacts the core directly, and erosion, in which the cap remains largely intact but its endothelial surface is denuded or apoptotic, exposing underlying collagen and matrix. Rupture is the more common cause of complete occlusion; erosion is more frequent in younger patients and in women. Once the thrombogenic core or subendothelial matrix is exposed, circulating platelets and coagulation factors can begin to build a thrombus.