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Coronary artery stenosis refers to the **narrowing of the coronary arteries**, usually caused by the buildup of atherosclerotic plaque comprised of cholesterol, fatty substances, and calcium within the artery walls[1][3][4][7]. This narrowing restricts blood flow to heart muscle tissue, leading to symptoms such as chest pain (angina), shortness of breath, and, if severe or acute, myocardial infarction (heart attack)[3][4][5]. Diagnosis is typically established by imaging (angiography, CT angiography), coronary calcium scoring, or functional testing. Treatment includes risk factor modification (lifestyle, lipid and blood pressure control), pharmacotherapy (antiplatelets, statins, beta blockers, nitrates), and, in advanced cases, revascularization such as percutaneous coronary intervention (angioplasty with stenting) or coronary artery bypass grafting[7][1]. The root pathological process is atherosclerosis; therefore, "coronary artery stenosis" is a **condition** rather than a protein, receptor, or direct molecular target.
Antiplatelet agents inhibit platelet aggregation and reduce risk of thrombosis; Statins lower cholesterol and reduce atherosclerotic progression; Beta blockers reduce cardiac workload and oxygen demand; Nitrates cause vasodilation and improve blood flow.
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