Atherosclerotic cardiovascular disease (ASCVD) encompasses coronary artery disease, cerebrovascular disease, and peripheral arterial disease — all driven by the progressive accumulation of lipid-laden plaques within arterial walls. The pathogenesis begins with endothelial injury from hypertension, smoking, hyperglycemia, or turbulent flow, which increases endothelial permeability and allows LDL cholesterol to infiltrate the subendothelial space. Oxidized LDL triggers monocyte recruitment and macrophage transformation into lipid-laden foam cells, forming fatty streaks. Over decades, smooth muscle cell proliferation and extracellular matrix deposition create fibrous plaques with necrotic lipid cores. Vulnerable plaques (thin fibrous cap, large lipid core, extensive inflammatory infiltrate) are prone to rupture, exposing the thrombogenic core to circulating blood and triggering acute thrombosis — manifesting as MI, ischemic stroke, or acute limb ischemia. The Pooled Cohort Equations (PCE) estimate 10-year ASCVD risk using age, sex, race, total cholesterol, HDL, systolic BP, BP treatment status, diabetes, and smoking status to guide primary prevention statin therapy decisions per ACC/AHA guidelines.