Acute coronary syndrome results from atherosclerotic plaque disruption within coronary arteries, triggering a cascade of thrombotic events. Vulnerable plaques (thin fibrous cap, large lipid-rich necrotic core, abundant inflammatory macrophages) are most prone to rupture. Plaque rupture exposes subendothelial collagen and tissue factor to flowing blood. Platelet adhesion occurs via GP Ib-IX-V binding to von Willebrand factor on exposed collagen. Platelet activation follows through multiple agonists: collagen binding to GP VI, thrombin binding to PAR-1 and PAR-4 receptors, ADP binding to P2Y12 receptors, and TXA2 binding to TP receptors. Activated platelets undergo shape change, degranulation (releasing ADP, serotonin, TXA2), and surface expression of GP IIb/IIIa which binds fibrinogen to cross-link adjacent platelets. The coagulation cascade amplifies thrombin generation through the tissue factor-factor VIIa complex (extrinsic pathway) and contact activation (intrinsic pathway), converging at factor Xa which converts prothrombin to thrombin. Thrombin converts fibrinogen to fibrin monomers that polymerize and are cross-linked by factor XIIIa, creating a stable fibrin mesh. The degree of coronary occlusion determines the clinical presentation: non-occlusive thrombus produces unstable angina or NSTEMI, while complete occlusion produces STEMI. Ischemic...