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Coronary atherosclerosis is a chronic inflammatory disease of the coronary arteries characterized by the progressive accumulation of atheromatous plaques within the arterial walls [1, 2, 5]. The pathological process typically initiates with endothelial dysfunction and the subendothelial deposition of oxidized low-density lipoproteins (LDL), which trigger an immune response involving macrophage recruitment and foam cell formation [2, 7]. Over time, these deposits harden and narrow the arterial lumen, significantly restricting oxygen-rich blood flow to the heart muscle (myocardium) [1, 4]. In the clinical setting, coronary atherosclerosis manifests as stable or unstable angina and can progress to acute coronary syndrome if a plaque ruptures, causing sudden thrombotic occlusion [2, 4, 12]. Pharmacological management aims to reduce cardiovascular risk and stabilize existing plaques through the use of statins, antiplatelets, and antihypertensive agents [5, 11]. While many drugs treat the symptoms or risk factors of the disease by targeting specific enzymes or receptors, coronary atherosclerosis itself represents a broad disease state rather than a single molecular target [6, 10]. It remains the leading cause of morbidity and mortality worldwide, driving the need for novel therapies targeting vascular inflammation and lipid regulation [6, 10].
Drugs used to manage coronary atherosclerosis act through multiple molecular mechanisms, including the inhibition of HMG-CoA reductase to lower systemic cholesterol, inhibition of cyclooxygenase-1 (COX-1) or P2Y12 receptors to prevent platelet aggregation, and blockade of beta-adrenergic receptors or angiotensin-converting enzyme (ACE) to reduce cardiac workload and manage blood pressure. Additionally, PCSK9 inhibitors enhance the recycling of LDL receptors to further clear cholesterol from the blood.
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