An atherosclerotic plaque is a deposit of fatty material, cholesterol, inflammatory cells, calcium, and fibrous tissue that builds up within the inner lining (intima) of an artery wall. Plaque formation is the hallmark of atherosclerosis, the underlying process in coronary artery disease and peripheral artery disease.
Plaque develops over many years through a process triggered by injury or dysfunction of the arterial lining (endothelium), often caused by hypertension, smoking, high cholesterol, and diabetes. LDL cholesterol particles enter the vessel wall and are oxidised, triggering an inflammatory response. Immune cells migrate into the wall and engulf the LDL, becoming foam cells. These accumulate along with smooth muscle cells to form a fatty core, which becomes covered by a fibrous cap.
Plaques vary in their stability. Stable plaques have a thick, fibrous cap and are more calcified; they narrow the artery and cause symptoms like angina on exertion but are less likely to rupture acutely. Vulnerable (unstable) plaques have a thin fibrous cap overlying a large lipid-rich core and are prone to sudden rupture. When a plaque ruptures, the blood-clotting system activates rapidly at the site, forming a thrombus (clot) that can completely block the artery, causing an acute heart attack and potentially cardiac arrest.
Statin therapy reduces cardiovascular events by stabilising plaques and lowering LDL cholesterol, not merely by reducing the degree of arterial narrowing. Coronary angiography can visualise plaque burden, and intravascular imaging (such as IVUS or OCT) can characterise plaque composition in detail.
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