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Indications and appropriate selection of novel oral anticoagulants in patients with atrial fibrillation
  1. Michael Ghannam,
  2. Aman Chugh
  1. Department of Cardiovascular Medicine, University of Michigan, Ann Arbor, Michigan, USA
  1. Correspondence to Michael Ghannam, Department of Cardiovascular Medicine, University of Michigan, Ann Arbor, Michigan,USA; mousajab{at}med.umich.edu

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Learning objectives

  • Understand the major landmark trials of the novel oral anticoagulants and how these agents compare to dose-adjusted warfarin.

  • Learn to identify which patients with atrial fibrillation are candidates for novel oral anticoagulants.

  • Understand how patient specific factors can guide selection between these newer agents.

Introduction

Atrial fibrillation (AF) is the most common cardiac arrhythmia and the incidence and prevalence of this disease are rising.1 2 It is estimated that by the year 2050 there will be over 7.5 million patients with AF in the USA alone.3 This disease carries a significant risk of morbidity and mortality driven in large part by the development of heart failure and thromboembolism.4 Oral anticoagulation therapy is effective in reducing risk of stroke and systemic embolism and is the standard of care for patients undergoing either a rhythm or rate control strategy.

For years warfarin has been the mainstay of stroke prophylaxis. More recently, direct-acting oral anticoagulants (DOACs) have entered the marketplace.5 Their site of action within the coagulation cascade is outlined in figure 1.6 7 These newer agents have rapidly been incorporated into modern practice,8 though there remains a role for warfarin among various subgroups. Selecting an appropriate agent is a complex decision and must take account a patient’s comorbidities, preference for dosing and monitoring, concern over the lack of a specific antidote, and importantly, financial constraints.

Figure 1

Overview of the coagulation system and sites of action of novel oral anticoagulants. The extrinsic pathway is activated by the exposure of tissue factor-expressing cells to blood through vascular injury. The intrinsic pathway is activated by the binding of factor IXa to factor VIIIA on anionic cell surfaces to form the intrinsic tenase complex. Activated platelets provide binding sites for this interaction. These processes then proceed through a common pathway ultimately resulting in activated …

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