Republished Education in Heart: New P2Y12 inhibitors

The management and prevention of arterial thrombosis has been transformed by the recognition of the role of platelets in this process and the development of effective antiplatelet drugs. The limited role of thromboxane A2 in platelet activation explains why aspirin therapy, which effectively inhibits release of thromboxane A2 by platelets, is insufficient in high risk conditions such as acute coronary syndromes (ACS) or percutaneous coronary intervention (PCI). The platelet P2Y12 receptor, one of two adenosine diphosphate (ADP) receptors on platelets, plays a central and unique role in platelet activation through amplifying the effects of numerous platelet agonists (figure 1).1 Platelet activation leads not only to aggregation but also to the release of pro-thrombotic and pro-inflammatory granule contents as well as the formation of thrombin. Strong amplification of all these platelet responses by P2Y12 explains why this receptor plays such an important part in thrombosis and haemostasis and is a successful target for antiplatelet drugs.