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Coronary artery atherosclerotic plaque is a pathological accumulation of lipids, cholesterol, inflammatory cells, calcium, and extracellular matrix within the wall of the coronary arteries. This process, termed atherosclerosis, causes thickening and stiffening of the vessel wall, leading to progressive narrowing (stenosis) that limits blood supply to the heart muscle. Plaques can be classified as stable—with a firm fibrous cap—or unstable (also called vulnerable), which have a thin cap, are prone to rupture, and can trigger clot formation (thrombosis). Plaque rupture leads to acute coronary syndromes (unstable angina, myocardial infarction). The development and progression of plaque involve complex interactions among lipoprotein metabolism, chronic inflammation, vascular smooth muscle cell proliferation, and blood clotting pathways. The resulting oxygen supply-demand mismatch underlies coronary artery disease, the leading cause of morbidity and mortality worldwide.
Drugs affecting plaque progression or complications reduce LDL cholesterol and inflammation (statins, PCSK9 inhibitors), inhibit platelet aggregation to reduce risk of thrombosis (antiplatelet agents), and lower blood pressure, cardiac workload, and oxygen demand (β-blockers, ACE inhibitors).
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