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In an era of incremental gains in preventative cardiology, the ongoing pursuit of reduction in ischaemic events has led to advances in the antiplatelet armamentarium that is available for use after percutaneous coronary intervention (PCI). The protection offered by antithrombotic may be enhanced by extending their duration of use, or through the application of more potent drugs—longer, stronger or both. The corollary, of course, is the potential for increased bleeding, which may carry significant associated morbidity and mortality. What combination and duration of aspirin, clopidogrel, ticagrelor or prasugrel is optimal in a given patient? This is a nuanced question that is pertinent in both acute and chronic coronary syndromes. Current guidelines broadly recommend the use of dual antiplatelet therapy (DAPT) for at least 12 months in patients undergoing PCI for an acute coronary syndrome (ACS) and at least 6 months in chronic coronary syndrome, with the proviso that shorter duration DAPT may be considered in patients at high risk of bleeding.1 2 Within these boundaries, clinicians must gauge the ischaemic and bleeding risk of an individual patient in order to optimise their DAPT regime.
The advent of potent P2Y12 inhibitors and iterative improvements in drug-eluting stents (DES), the latest of which have thinner struts, improved drug delivery and are associated with lower rates of stent thrombosis and restenosis, have raised the possibility of a shorter duration of DAPT after PCI, with the goal of minimising bleeding while offering non-inferior protection from ischaemic events. Multiple randomised trials have studied various combinations of drugs and DAPT duration, including short-term DAPT followed by aspirin monotherapy and short-term DAPT followed by P2Y12 inhibitor monotherapy.3–5 Although somewhat heterogenous, collectively, these data suggest that short-term DAPT may be considered as a safe option in selected individuals. The authors of the current paper conducted one …
Contributors TS drafted the manuscript. TS and RB edited the final version.
Funding This work was supported by the Medical Research Council (MR/T029153/1) and the British Heart Foundation (PG/19/40/34422).
Competing interests None declared.
Patient and public involvement Patients and/or the public were not involved in the design, or conduct, or reporting, or dissemination plans of this research.
Provenance and peer review Commissioned; externally peer reviewed.
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