Abstract
Platelet activation and aggregation are central to the development of thrombotic complications during acute coronary syndromes (ACS) and following percutaneous coronary interventions (PCIs). Adenosine diphosphate (ADP) and thromboxane (TX) A2 are major secondary agonists released by platelets following activation. 1 These secondary agonists play an important role in the amplification of platelet activation and aggregation and stable thrombus generation at the site of plaque rupture.
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