Topic overview

Start with the big picture

Atherosclerotic plaques form in medium and large arteries and contain a lipid-rich necrotic core beneath a fibrous cap. Endothelial injury or dysfunction promotes LDL entry and oxidation, monocyte recruitment, and macrophage formation of foam cells; their accumulation creates the earliest visible lesion, the fatty streak. Smooth-muscle cells and extracellular matrix contribute to plaque maturation. Over time, plaques may enlarge or become unstable. A thick cap and smaller lipid core characterize a more stable plaque associated with chronic ischemia, whereas a thin cap and larger lipid pool increase vulnerability to rupture. Rupture or erosion can trigger thrombosis and acute occlusion; progressive narrowing and other plaque-related changes can also lead to ischemia, emboli, aneurysm, or dissection. The lesson places these outcomes alongside common sites, risk factors, and prevention.