Dual antiplatelet therapy (DAPT) is indicated in patients who need to undergo percutaneous coronary intervention (PCI) procedures.1 Compared with oral anticoagulation (OAC) and aspirin, DAPT has been shown to reduce the risk of thrombotic events and the rate of bleeding events.2 Chronic OAC is required in up to 10 % of the patients undergoing PCI, and is usually indicated for AF and mechanical heart valves.3 However, when combining OAC with DAPT, which is also known as triple therapy (TT), the risk of bleeding increases two- to threefold.4–7 In contrast, the thromboembolism risk increases when OAC is not prescribed in the antithrombotic regimen, while the risk of stent thrombosis, leading to MI, increases when DAPT is not prescribed as part of the TT.8–11 To further complicate this antithrombotic regimen, newer and stronger P2Y12 inhibitors such as prasugrel and ticagrelor are currently recommended as standard treatment in patients with acute coronary syndromes (ACS). It remains unclear whether prasugrel or ticagrelor should be included as part of antiplatelet therapy in these patients with ACS who are on chronic OAC and need to undergo PCI. Another issue to address is that several non-vitamin K oral anticoagulants (NOACs) such as dabigatran, rivaroxaban, apixiban and edoxaban have been shown to be at least equal or superior to vitamin K antagonists (VKAs) in reducing the risk of stroke in patients with AF.12–15 Hence, the anticoagulated patient undergoing PCI faces a treatment dilemma. At present, evidence from randomised controlled trials (RCTs) regarding the optimal antithrombotic regimen is minimal. This article will describe a case report and discuss the optimal anticoagulant and antiplatelet treatment with an overview of the literature.
Case report
An 81-year-old man was admitted to the St Antonius Hospital, Nieuwegein, The Netherlands, with typical chest pain during the night. He experienced no pain at hospitalisation despite his ECG showing ST-segment depression. He had a medical history of hypertension, diabetes mellitus and paroxysmal non-valvular AF. He was diagnosed with non-ST segment elevation MI (NSTEMI), as his ECG showed ST depression and his troponin-T test result was positive. He had been treated with an angiotensin-converting enzyme inhibitor, oral antidiabetics and an NOAC for 2 years. Prior to this treatment, he had been treated with VKA; however, his international normalised ratio (INR) levels remained unstable, which led to the switch to NOAC.
A loading dose of aspirin 300 mg, then 80 mg/day, and a loading dose of clopidogrel 600 mg, then 75 mg/day were started and a coronary angiography was planned. Neither prasugrel nor ticagrelor were given due to their association with increased risk of bleeding in combination with an OAC. The lower-dose NOAC tested for AF was administered. Angiography was performed via the radial approach and low-dose unfractionated heparin (60 IE/kg) was added to prevent catheter thrombosis. A second-generation drug-eluting stent (DES) was implanted when it became clear that this diabetic patient suffered from a long lesion in the left anterior descending artery. No glycoprotein IIb/ IIIa inhibitor was added to the antithrombotic regimen, as the risk of bleeding was deemed high. On the second day after PCI, the patient was discharged with the combination of low-dose aspirin, clopidogrel, lower-dose NOAC and a proton pomp inhibitor (PPI). Unfortunately, he was readmitted to the hospital 5 weeks later presenting with shock due to a major bleeding in the gastrointestinal tract. At this time, all antithrombotic agents were temporarily discontinued; red blood cell and platelet transfusions, prothrombin complex concentrate and intravenous PPI were given. A gastric visible vessel was sclerosed, and after 2 days the patient returned to a stable condition. Due to a high risk of stent thrombosis and an acceptable risk of rebleeding, clopidogrel and the lower-dose NOAC were restarted. Aspirin was omitted from the regimen and clopidogrel was discontinued 3 months later.