Dual antiplatelet therapy with aspirin and a P2Y12 receptor inhibitor represents the cornerstone therapy for patients with acute coronary syndromes or undergoing percutaneous interventions, leading to a reduction of subsequent ischemic events. Variable response to clopidogrel has received close attention, and pharmacokinetic, pharmacodynamic, and pharmacogenomic factors have been identified as culprits. This led to the introduction of newer, potentially safer, and more effective antiplatelet agents (prasugrel and ticagrelor). Additionally, several point-of-care assays of platelet function have been developed in recent years to rapidly screen individuals on antiplatelet therapy. While the routine use of platelet function testing is uncertain and not currently recommended, it may be useful in instances when the degree of platelet inhibition may be uncertain such as high-risk patients undergoing percutaneous coronary intervention or when there may be a suspected pharmacodynamic interaction with other drugs. The current paper focuses on the P2Y12 receptor inhibitors and their pharmacogenetics and indications in patients with acute coronary syndromes or receiving percutaneous coronary interventions as well as the applicability of platelet function testing in this clinical context. 1. Introduction The clinical presentation of patients with coronary atherosclerosis is either as stable angina or as an acute coronary syndrome (ACS). The ACSs represent the more acute clinical manifestations of coronary artery disease (CAD) and include unstable angina (UA), non-ST elevation myocardial infarction (NSTEMI), and ST elevation myocardial infarction (STEMI). Despite maximal therapy, 5%–10% of patients with ACS will suffer a recurrent cardiac event or death within the first month after the initial presentation. While patients with stable angina have only narrowing of their coronary arteries, those with ACS have atheromatous plaque rupture and acute thrombus formation. Therefore, it is well recognized that platelet activation and aggregation play a central role in the physiopathology of ACS. In addition to aspirin and anticoagulants, antiplatelet agents represent an important therapeutic step for this patient population, with newer and more potent agents becoming available on the market [1, 2]. During an acute coronary event, vascular wall injury exposes collagen that leads to adhesion of inactive platelets, which subsequently become activated. Platelet activation results in degranulation and secretion of adenosine diphosphate (ADP), thromboxane A2 (TXA2), and
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