Editorials |
From the New England Cardiac Arrhythmia Center (A.A.A.-A., N.A.M.E.), Division of Cardiology, and Institute for Clinical Research and Health Policy Studies (A.A.A.-A.), Department of Medicine, Tufts Medical Center and Tufts University School of Medicine, Boston, Mass.
Correspondence to N.A. Mark Estes III, MD, New England Cardiac Arrhythmia Center, Tufts Medical Center, Professor of Medicine, Tufts University School of Medicine, 750 Washington Street, Boston, MA 02493. E-mail nestes@tuftsmedicalcenter.org
Key Words: anticoagulants hemorrhage stroke thrombosis
An extract of the first 250 words of the full text is provided, because this article has no abstract. |
Atrial fibrillation (AF), the most common sustained arrhythmia in clinical practice, with a prevalence of almost 1 in 10 by the eighth decade of life, is associated with a heavy burden on morbidity, mortality, and healthcare expenditure.1,2 To both patients and physicians, a feared and devastating consequence of AF is a 5-fold increase in the risk of stroke.3,4 To date, the most effective intervention to mitigate the risk of thromboembolic events in patients with AF is adjusted-dose anticoagulation with warfarin.4–6 Evidence-based guidelines and performance measures for optimal management of AF have been developed recently, with particular emphasis on patient selection for anticoagulation.4,7 Multiple studies assessing risks and benefits of anticoagulation with the vitamin-K antagonist warfarin have had consistent clinical implications.3,5,6,8–11 Maintaining patients in the narrow therapeutic range of warfarin, as measured by the international normalized ratio (INR), is critical but represents a major clinical challenge. The benefits of warfarin in prevention of thromboembolic events are accompanied by the risks of bleeding complications, including life-threatening cerebral hemorrhage.8
Article see p 84
Both the risk of the outcome to be prevented (ie, thromboembolic events) and the potential harm from the intervention (ie, bleeding) are related to the intensity of anticoagulation as measured by the INR.4,5,8,11 A "subtherapeutic" INR, typically defined as <2.0 for AF, is associated with an increased risk of thromboembolism, whereas the risk of major bleeding significantly increases with INR values >3.5.4,5,8,11 Given these observations, efforts have been directed at identifying reliable longitudinal measures of monitoring anticoagulation intensity, which could
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