Background
Thrombus formation in the coronary tree is the principal cause of acute coronary syndromes (ACS).1 Following plaque rupture or erosion, platelets adhere to exposed ligands (collagen, von Willebrand factor [vWF]) under high-flow conditions and this leads to platelet activation. Following platelet adhesion and activation, multiple agonists are secreted, including thromboxane A2 (TXA2) and adenosine diphosphate (ADP). TXA2 further activates platelets and ADP amplifies and sustains platelets’ activation, particularly through platelet P2Y12 receptors.2 In view of the pivotal role of platelets in arterial thrombosis, blocking TXA2 pro
