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(Stroke. 2001;32:803.)
© 2001 American Heart Association, Inc.


Comments, Opinions, and Reviews

Atrial Fibrillation and Stroke

Concepts and Controversies

Robert G. Hart, MD Jonathan L. Halperin, MD

From the Department of Medicine (Neurology) (R.G.H.), University of Texas Health Sciences Center (San Antonio); and The Zena and Michael A. Wiener Cardiovascular Institute (J.L.H.), Mt Sinai Medical Center, New York, NY.

Correspondence to Robert G. Hart, MD, Department of Medicine (Neurology), University of Texas Health Science Center, MSC 7883, 7703 Floyd Curl Dr, San Antonio, TX 78229-3900. E-mail hartr@uthscsa.edu


Key Words: anticoagulants • aspirin • atrial fibrillation • cerebral embolism • cerebrovascular disorders • stroke


*    Introduction
 
In 1985, patients with nonvalvular atrial fibrillation (AF) first entered randomized clinical trials that tested antithrombotic therapies for stroke prevention.1 2 3 Since then, >12 000 AF patients have been included in 25 trials that involved >40 randomized treatment comparisons (Table 1Down). During this interval, we reviewed the pathogenesis and prevention of stroke in AF patients in 2 previous editorials in Stroke.4 5 Here, we offer commentary on selected concepts and controversies.


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Table 1. Randomized Trials of Antithrombotic Therapy in Atrial Fibrillation

The prevalence of AF increases with age, affecting {approx}5% of people at age 70 years. Although AF-associated stroke can occur at any age, it is predominantly a problem of the elderly. The median age of AF patients with stroke in population-based studies is {approx}75 years; more than half are women. In people over age 75, AF is the most important single cause of ischemic stroke. This epidemiology is relevant when considering stroke prevention, because the risks of and ability to sustain preventive therapies are special problems for the very elderly.


*    Left Atrial Appendage Thrombi
 
The left atrial appendage is a unique substrate for stroke. It is an elongated cul-de-sac lined with endothelium, a remnant of the embryonic atrium, trabeculated by pectinate muscles (Figure 1Down). The contractility of the appendage is reduced in AF, but the degree varies widely and is an important determinant of stasis and thrombus formation. In AF patients, atrial thrombi almost always originate in the appendage, rather than in the smooth-walled atrium proper, and are not reliably detected with transthoracic echocardiography. . . . [Full Text of this Article]




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