Patients who undergo coronary artery stenting require dual antiplatelet therapy (DAPT) in order to reduce their risk of stent thrombosis. Long-term oral anticoagulation (OAC) is indicated for the primary and secondary prevention of thrombotic events in patients with atrial fibrillation (AF), mechanical heart valves, intra-cardiac thrombus, venous thromboembolic disease and some hypercoagulable states. Those patients who undergo percutaneous coronary intervention (PCI) and who have an indication for long-term OAC present a clinical dilemma in relation to their antithrombotic therapy – should they be treated with DAPT and OAC (‘triple therapy’), a regimen which is effective at the prevention of thrombotic events but which is associated with an increased risk of bleeding;1–4 should OAC be deferred in order to reduce the risk of bleeding but at the increased risk of systemic arterial or venous thrombotic events;5 or should the duration of DAPT be curtailed in order to reduce the risk of bleeding but with the potential increased risk of stent thrombosis? The advent of non-vitamin K antagonist oral anticoagulants (NOACs) and the increasing use of prasugrel and ticagrelor in patients who undergo PCI following an acute coronary syndrome (ACS) has further complicated clinical decision-making. This article aims to provide a summary of the evidence regarding antithrombotic therapy following PCI for patients who have an indication for OAC with a focus on recent randomised trials, which have influenced clinical practice in this area.
Antiplatelet Therapy to Prevent Coronary Artery Stent Thrombosis
Stent thrombosis is an infrequent but serious complication following PCI. Stent thrombosis within one month of PCI occurs with a frequency of 0.2–0.8 %, while stent thrombosis more than one month after PCI occurs at an approximate rate of 0.1–0.4 % per year.6 Stent thrombosis is associated with a mortality rate of up to 45 %.7 Platelet activation consequent to atheromatous plaque disruption during coronary angioplasty and stent deployment is one of the main mechanisms underlying stent thrombosis. Delayed stent strut epithelialisation and reactions to polymer are important mechanisms in cases of late drug-eluting stent (DES) thrombosis. Dual antiplatelet therapy is central to the prevention of stent thrombosis. Historical randomised trials showed a lower rate of stent thrombosis and of bleeding complications in patients who were treated with aspirin and ticlopidine than in patients who received aspirin and OAC.8–11 Ticlopidine use was associated with the common occurrence of side effects and blood dyscrasias, so aspirin and clopidogrel emerged as the standard post-PCI prophylaxis against stent thrombosis once trial data suggested equivalent efficacy for these two DAPT regimens.12 DAPT is required for four weeks after the deployment of a bare metal stent (BMS). Concerns regarding the incidence of late stent thrombosis in patients who were treated using first generation DES have largely dissipated with modifications in stent design and polymer technology.13 Nevertheless, it is usual for DAPT to be taken for at least 6–12 months after second or third generation DES use. Premature discontinuation of DAPT is the most consistent predictor of stent thrombosis.7