Hemostasis Management of Patients Undergoing Emergency Cardiac Surgery After Ticagrelor Loading

Pharmacologic Inhibition of platelet P2Y₁₂ receptors has become the mainstay of therapy in the management of acute coronary syndrome (ACS). Ticagrelor (Brilinta; AstraZeneca, Wilmington, DE) is a non-thienopyridine P2Y₁₂ receptor antagonist that exerts a reversible but potent inhibition of platelet aggregation triggered by adenosine diphosphate (ADP). Upon exposure to extravascular collagen, platelets release ADP stored in dense granules, triggering secondary aggregation and localized platelet recruitment.¹ Ticagrelor and its major active metabolite, AR-C124910XX, potently inhibit platelet P2Y₁₂ receptor activation, but ticagrelor appears to exert additional antiplatelet and anti-inflammatory effects by elevating adenosine levels via equilibrative nucleoside transporter 1 receptor blockade. The mortality benefit observed with ticagrelor over thienopyridines (clopidogrel and prasugrel) has been attributed to the non-P2Y₁₂ actions of ticagrelor.