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The introduction of the non-vitamin K antagonist oral anticoagulants (NOACs) has been a game changer in our management of many thromboembolic conditions. The relative efficacy, safety, and convenience (rapid onset/offset of action, fewer drug and food interactions, and relatively predictable pharmacokinetics) of NOACs compared with oral vitamin K antagonists (VKAs, e.g. warfarin) has accelerated their use globally. Due to appreciable advantages over VKAs, the use of NOACs has been investigated in other medical conditions beyond stroke prevention in atrial fibrillation (AF) and the prevention or treatment of venous thromboembolism (VTE).1  ,  2

Attention of the cardiovascular community has been directed to assess utility of NOACs in secondary prevention of coronary artery disease (CAD) and heart failure, two important conditions with life-limiting potential. Despite use of effective secondary prevention strategies, 5–10% of patients with known CAD have recurrent events annually.3 Aspirin has been the mainstay of treatment for secondary prevention in such patients, with a 19% lowered risk of major adverse cardiovascular event and a 9% lower risk of cardiovascular death than placebo.4 However, long-term treatment with a VKA alone or in a combination with aspirin is found to be superior to aspirin for secondary prevention but has been associated with an increased risk of bleeding.5 In the ATLAS ACS 2-TIMI 51 trial, the addition of low-dose rivaroxaban (a factor Xa inhibitor) to dual antiplatelet therapy in patients with a recent acute coronary syndrome significantly reduced mortality and recurrent ischaemic events including stent thrombosis [in patients undergoing percutaneous coronary intervention (PCI)] for a median of 1.1 years when compared with placebo; however, this was at the cost of an increased risk of major bleeding and intracranial haemorrhage but not the risk of fatal bleeding.6  ,  7

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