Any room left for new antiplatelet agents in acute coronary syndrome?

Abstract

This editorial refers to ‘Effect of vorapaxar on myocardial infarction in the thrombin receptor antagonist for clinical event reduction in acute coronary syndrome (TRA·CER) trial’[†][1], by S. Leonardi et al. , on page 1723 Over the past two decades, the combination of aspirin and clopidogrel has been the gold standard antiplatelet strategy to prevent recurrent ischaemic events after an acute coronary syndrome (ACS). Several new pharmacological options have been evaluated since then. This includes more potent dual antiplatelet therapy (DAPT) with the new generation of P2Y12 inhibitors, and triple oral antithrombotic therapy (TOAT), a combination of aspirin and clopidogrel with either oral low dose Xa inhibition or oral platelet thrombin receptor blockade. Selecting the most favourable strategy for the post-ACS period warrants a careful evaluation of the risks and benefits for each patient. Although the one size fits all strategy is not ideal, the strategy of selecting drugs and doses according to patient characteristics remains challenging. Indeed, the ischaemic risk decreases over time, and the benefit of a prolonged and stronger antiplatelet treatment is so far unknown, especially in fragile patients who deserve more protection against ischaemic events but are also exposed to more severe bleeding on treatment. A more aggressive P2Y12 receptor blockade has consistently improved clinical outcome of ACS patients as compared with clopidogrel. Shorter and stronger platelet inhibition has also become an option in percutaeous coronary intervention (PCI) with the superiority of cangrelor over clopidogrel in the CHAMPION PHOENIX trial, although even a treatment limited to the time of PCI was associated with more bleeding complications.1 The benefit of stronger P2Y12 inhibition is particularly clear in patients with ST elevation myocardial infarction (STEMI) undergoing … [1]: #fn-2