Abstract

See related article, pages 227–230. Atrial fibrillation (AF) is not a benign cardiac arrhythmia but instead confers a 5-fold increased risk of stroke compared with age-matched people in sinus rhythm.1 AF patients also have a worse outcome after stroke, with elevated mortality and stroke recurrence rates,2 longer hospital stays,3 and lower discharge rates to their own homes.3 Current estimates suggest that AF afflicts ≈2.2 million Americans,4 whereas in the United Kingdom ≈740 000 individuals are thought to have AF,5 with >46 000 new cases being diagnosed each year.6 Given the increasing prevalence of AF and the associated thromboembolic complications, there are significant numbers of patients who require chronic oral anticoagulation (OAC). Current guidelines7,8 recommend that AF patients at moderate to high risk of stroke should be commenced on chronic anticoagulation with a vitamin K antagonist (VKA). These recommendations are based on data from meta-analyses of 13 randomized controlled trials which have demonstrated significant reductions in stroke9,10 and mortality10 with the use of warfarin. Despite the overwhelming evidence of the benefit of warfarin thromboprophylaxis in patients with AF, such therapy remains significantly underused. OAC care varies considerably from country to country and physicians tend to undertreat more than overtreat.11,12 Physicians’ dilemma of whether to prescribe warfarin is reflected in the recent Euro Heart Survey of AF patients, which revealed that only 67% of patients eligible for VKAs were actually prescribed it,13 although actual ‘real-life’ prescription of OAC may be significantly lower than this. So, why are eligible patients with AF not prescribed OAC? Warfarin itself is plagued by a number of inherent problems, the most important being the narrow therapeutic international normalized ratio (INR) window (target INR 2.5, range 2.0 to 3.0) which must be maintained, given that …

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