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Introduction
Atrial fibrillation (AF) is the most common cardiac arrhythmia affecting more than one in 20 Europeans aged over 55. 1 2 AF results in turbulent flow within the atria, predisposing to thrombus formation. Patients live with the constant risk that a fragment of thrombus will dislodge, embolise and occlude a cerebral artery, causing an ischaemic stroke: AF thus markedly increases stroke risk. 3 One might expect that restoring sinus rhythm would obviate the stroke risk posed by AF. Surprisingly, however, a large body of data from the seminal RACE and AFFIRM trials confirm that it does not, likely reflecting ongoing undetected episodes of arrhythmia. 4 5 It is therefore important to deal with the associated risk of stroke directly. This applies to patients with paroxysmal, as well as permanent, AF and also to those with atrial flutter. 6 While the majority of large trials have focused on patients with non-valvular AF, this finding appears to be applicable to the broader AF and flutter populations.
While occlusion devices designed to prevent thrombus from breaking off and entering the circulation have been developed and show a good degree of efficacy, doubts remain as to their safety: at present they are only considered for use in patients at very high risk in whom other approaches are contraindicated. 7 8 For the majority of patients, the mainstays of therapy to reduce stroke risk are antithrombotic medications. The impact of these drugs in reducing stroke risk is well established. 9-15
There are two broad categories of antithrombotic drugs: antiplatelet agents and anticoagulants. Antiplatelet agents interfere with platelet function thereby reducing the likelihood that they will aggregate into a thrombus. Two main types of antiplatelet drugs have been studied for use in AF: aspirin and thienopyridine drugs such as clopidogrel. Of these, aspirin interferes with prostaglandin synthesis while the thienopyridines block binding of ADP to the platelet surface. Anticoagulant drugs, on the other hand, interfere with the clotting cascade, ultimately reducing the rate of fibrin clot formation. Until recently the only commonly used oral anticoagulant was warfarin, which blocks the formation of vitamin K-dependent clotting factors. In recent years, three new oral anticoagulant agents, rivaroxaban, apixaban and dabigatran, which block the final common pathway in clot formation, have come into...