Implantation of drug-eluting stents (DESs) remains central to percutaneous coronary intervention (PCI) for acute coronary syndromes (ACS) and chronic coronary syndromes (CCS). DES platforms, polymers and drugs have evolved significantly to improve deliverability and safety, now being typically thin-strut with a compact layer of biocompatible or bioresorbable polymer, or no polymer at all. Ultra-thin-strut DESs push this concept further, and in some studies perform better than conventional DES, but may recoil in challenging settings such as chronic total occlusion PCI. Stent implantation has also progressed, with greater attention to lesion preparation and poststenting optimisation, increased use of intracoronary imaging helping to recognise and remedy issues. In parallel, antithrombotic therapy for patients undergoing PCI has advanced considerably, with reliable P2Y inhibition now possible with the newest agents. As well as progress in controlling other thrombotic risk factors such as hyperlipidaemia, hypertension and diabetes, these developments have contributed to reducing thrombotic risk. As well as preventing stent thrombosis, antithrombotic therapy can reduce the risk of non-PCI-related thrombotic events, not only in the coronary tree but also in the cerebral and peripheral circulation, however it increases bleeding risk. Twelve months of dual antiplatelet therapy (DAPT) after PCI for ACS (and 6 months after PCI for CCS) remains the default recommended strategy, but given reliable P2Y inhibition, good control of ischaemic risk factors and a minimally thrombogenic stent design and deployment, it is rational that earlier de-escalation to monotherapy, particularly with ticagrelor, is often appropriate, reserving longer-duration DAPT for those with highest ischaemic risk but where bleeding risk is not high. A body of trial evidence now supports this. As well as earlier de-escalation of DAPT, future developments in PCI might include increased use of 'leave nothing behind' strategies and further pharmacological options for optimisation of ischaemic risk factors.

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