Platelet inhibition in acute coronary syndrome and PCI: Insights from the past and present
Platelet activation and aggregation have a pivotal role in arterial thrombosis and in the pathogenesis of both acute coronary syndromes (ACS) and in the thrombotic complications that occur in patients undergoing percutaneous coronary intervention (PCI). The last 30 years has seen the progress from early trials of clopidogrel and glycoprotein IIb/IIIa inhibitors, to the application of more potent P2Y12 inhibitors prasugrel and ticagrelor. Early enthusiasm for newer and more potent antiplatelet agents, which could reduce ischaemic events, has led to the understanding of the importance of bleeding and a desire to individualise and optimise treatment. It has increasingly become apparent that the potency and duration of dual antiplatelet therapy (DAPT) has to reflect the balance between ischaemic and bleeding risk. Recently, multiple strategies have been proposed to individualise DAPT intensity and duration, in order to reduce the bleeding and ischaemic risks. Strategies of de-escalation of DAPT intensity, as well as shorter (less than a year) or more prolonged (beyond a year) treatment have been proposed, as well as platelet function test and genotype guidance of P2Y12 inhibitor therapy. Herein, we provide an overview of the progress in the field of antiplatelet therapy for ACS and PCI over the years, showing the current directions of travel. Ongoing studies focusing on personalised antiplatelet treatment will hopefully yield further insight into ways of optimising outcomes for the individual.