Thrombosis is the central process responsible for acute coronary syndromes. Erosion or rupture of atherosclerotic plaque exposes the blood constituents to subendothelial matrix. The coagulation system is activated via contact activation (intrinsic pathway) and tissue factor release from plaque (extrinsic pathway) resulting in thrombin generation and fibrin clot formation. Platelets adhere to the subendothelial matrix and are activated by collagen and thrombin resulting in shape change, thromboxane release, degranulation, and aggregation. Activation of the platelet P2Y12 receptor and recruitment of other platelets amplifies the thrombotic response. Propagation of thrombus formation leads to coronary artery occlusion with resulting distal myocardial ischaemia or infarction, or both.