Rupture of an atherosclerotic plaque is the usual initiating event in an acute coronary syndrome (ACS). Persistent thrombotic occlusion at the site of plaque rupture results in acute myocardial infarction (MI). (See "The role of the vulnerable plaque in acute coronary syndromes".) The role of platelets in thrombus formation during ACS is discussed in detail elsewhere. (See "Congenital and acquired disorders of platelet function", section on 'Normal platelet function' and "The role of platelets in coronary heart disease".)
This topic will review the evidence that antiplatelet therapy is beneficial in patients with an acute ST-elevation MI (STEMI), and will provide recommendations for its use. Information regarding antiplatelet agents in non-ST elevation ACS (unstable angina or non-ST elevation MI) and the role of anticoagulant therapy in STEMI are discussed separately. (See "Antiplatelet agents in acute non-ST elevation acute coronary syndromes" and "Anticoagulant therapy in acute ST elevation myocardial infarction".)
CLASSIFICATION OF ANTIPLATELET AGENTS
Antiplatelet agents can interfere with a number of platelet functions, including aggregation, release of granule contents, and platelet-mediated vascular constriction. They can be classified according to their mechanism of action (figure 1):
●Aspirin and related compounds (nonsteroidal antiinflammatory drugs and sulfinpyrazone) block the enzyme cyclooxygenase (prostaglandin G/H synthase) that mediates the first step in the biosynthesis of prostaglandins and thromboxanes (including TXA2) from arachidonic acid (picture 1). Thromboxane A2 is a potent stimulator of platelet aggregation. (See "Overview of hemostasis", section on 'Platelet aggregation'.)
●The platelet P2Y12 receptor blockers clopidogrel, ticlopidine, ticagrelor, prasugrel, and cangrelor block the binding of adenosine diphosphate to a specific platelet receptor P2Y12, thereby inhibiting activation of the glycoprotein (GP) IIb/IIIa complex and platelet aggregation .