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(Stroke. 2004;35:389.)
© 2004 American Heart Association, Inc.
Advances in Stroke 2003 |
From the Stroke Unit (G.J.H., C.J.M.K.) and Department of Haematology (J.E.), Royal Perth Hospital; and School of Medicine & Pharmacology (G.J.H., J.W.E.), University of Western Australia, Perth, Australia.
Correspondence to Clinical Professor Graeme J. Hankey, Consultant Neurologist and Head of Stroke Unit, Department of Neurology, Royal Perth Hospital, 197 Wellington Street Perth, Australia 6001. E-mail gjhankey@cyllene.uwa.edu.au
Key Words: Advances in Stroke atrial fibrillation stroke prevention warfarin ximelagatran
An extract of the first 250 words of the full text is provided, because this article has no abstract. |
Up to one sixth of all ischemic strokes are attributable to atrial fibrillation (AF).1,2 This proportion is likely to increase in the future as the prevalence of AF increases with the progressive "aging" of the population.
The only 2 treatments that effectively reduce the risk of stroke among individuals with AF are aspirin (relative risk reduction [RRR]: 22%; 95% CI: 2% to 38%) and adjusted-dose oral anticoagulation with the vitamin K antagonist, warfarin (RRR: 62%; 95 CI: 48% to 72%).3,4 Heart rhythm control, by means of cardioversion, although intuitively attractive, has not been shown to be more effective than rate control combined with oral anticoagulation.5,6 Occluding the left atrial appendage using catheter techniques, and surgical excision of the left atrial appendage have not been evaluated in controlled trials and are not widely applicable.7,8
The main limitation of aspirin is that it is only modestly effective in preventing stroke among patients in AF compared with placebo (RRR: 22%) and with oral anticoagulation (warfarin versus aspirin: RRR 45%; 95% CI: 29% to 57%).9
The main limitation of warfarin is that it causes twice as many intracranial and extracranial hemorrhages as aspirin,3,9 particularly in patients with a history of bleeding, the elderly, and those with common polymorphisms for genes encoding the hepatic microsomal enzyme CYP2C910 and the factor IX propeptide.11 The excess bleeding associated with warfarin can be attributed in part to its narrow therapeutic window and numerous interactions with other drugs and foods.12 Other practical limitations to long-term warfarin therapy are its
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