LAUSR

SEE PAGE 371 P 2Y12 receptors on platelet membrane are key modulators of platelet aggregation and thrombosis in acute coronary syndromes (2). Oral P2Y12 receptor inhibitors (clopidogrel, ticagrelor, and prasugrel) combined with aspirin (dual antiplatelet therapy [DAPT]) have revolutionized the antithrombotic management of acute coronary syndromes (3–5). Ticagrelor and prasugrel, the newer members of oral P2Y12 receptor inhibitors, have a stronger and more predictable antiplatelet profile than clopidogrel, resulting in reduced thrombotic outcomes in patients with acute coronary events at the expense of increased bleeding risk (4,5). The duration and potency of DAPT have been an ongoing challenge. Potent P2Y12 receptor inhibition significantly decreases the thrombotic risk related to a culprit lesion, stenting of that lesion, or remote nonculprit lesions in acute coronary syndromes, especially during the first 3 months post–percutaneous coronary intervention (PCI) (6). Hence, the current practice guidelines on the management of acute coronary events recommend the preferential use of potent DAPT with ticagrelor or prasugrel for 12 months after an acute coronary syndrome treated with PCI (7,8). Depending on the individualized thrombotic and bleeding risk, shorter or longer DAPT can be considered. Despite our progress in understanding the pharmacodynamics of P2Y12 receptor inhibitors in acute