Duration of dual antiplatelet therapy after coronary artery stenting: where is the sweet spot between ischaemia and bleeding?

Permanent1 or transient2 intraluminal scaffolding of coronary arteries achieved by currently available stents effectively lowers the rate of acute vessel occlusion, persistent dissection, and restenosis.3 The latter complication is further reduced by local anti-proliferative drug delivery4 (drug eluting stent, DES), albeit delaying vascular healing with complete re-endothelialization. Blood exposed to foreign bodies may clot, which in case of coronary stent struts increases the risk of vascular occlusion (i.e. stent thrombosis, ST), myocardial infarction, and death. As ST is associated with high mortality, it is a feared complication of percutaneous coronary intervention (PCI). Anti-thrombotic therapy effectively reduces blood clotting and is mandatory during and after PCI. Platelet activation and aggregation on the stent surface is the main mechanism leading to ST. Pharmacological inactivation of the enzyme cyclooxygenase by its acetylation by acetylsalicylic acid (Aspirin®) and concomitant blockade of the P2Y12 receptor on the platelet surface by reversible or irreversible receptor antagonists (e.g. clopidogrel, ticagrelor, or prasugrel) effectively reduces platelet aggregation. A combination of these drug classes (i.e. dual antiplatelet therapy, DAPT) has become a cornerstone of post-PCI management5–7 and effectively reduces the risk of ST. After the roll-out of the first-generation DES (CYPHER® and TAXUS™), an increased incidence of late and very late ST was observed in comparison with bare metal stents.8,9 At the same time, there was no evidence available from randomized controlled trials (RTCs) defining the optimal duration of DAPT after DES implantation. Therefore, an arbitrary recommendation for 12 months DAPT after DES implantation was issued by guideline committees.10 In the meantime evidence has accumulated suggesting that in stable coronary …