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(Stroke. 2001;32:1931.)
© 2001 American Heart Association, Inc.

Letters to the Editor

Letters to the Editor

Atrial Fibrillation and Stroke: More Concepts and Controversies

Dwayne Conway, MRCP Gregory Y.H. Lip, MD, FRCP

University Department of Medicine, City Hospital, Birmingham, England, UK

Stroke welcomes Letters to the Editor and will publish them, if suitable, as space permits. They should not exceed 1000 words (excluding references) and may be subject to editing or abridgment. Please submit letters in duplicate, typed double-spaced. Include a fax number for the correspondling author and a completed copyright transfer agreement form (published in the January and July issues).

To the Editor:

We wish to congratulate Hart and Halperin¹ on their excellent overview of the current "concepts and controversies" surrounding atrial fibrillation (AF) and stroke.

In discussing the formation of thrombus within the left atrial appendage (LAA), they focus a large part of their discussion on the issue of blood stasis in the LAA that occurs in AF, suggesting this mechanism of thrombogenesis to perhaps be of greatest importance, although conceding that "many questions remain about the formation and embolism of left atrial thrombi and, consequently, about the pathogenesis of AF-associated stroke".¹ They also comment that "endothelial lesions in the appendage have not been found, and systemic prothrombotic diastheses that contribute to thrombus formation have been suggested but not convincingly identified."¹ We would suggest, however, that there is a growing body of evidence suggesting that endothelial (or endocardial, within the LAA) changes and hemorrheological (or prothrombotic) abnormalities may indeed play a role in the formation of intra-atrial thrombus and subsequent stroke and thromboembolism in AF, thus fulfilling the 3 components of Virchow’s "triad" of thrombogenesis.

Evidence of endothelial abnormalities among patients with AF is suggested by numerous studies documenting elevated plasma levels of circulating surrogate markers of endothelial damage/dysfunction, most notably von Willebrand factor (vWf). The latter has been demonstrated to independently predict the presence of LAA thrombus on transesophageal echocardiography (TEE).² In addition, direct evidence of atrial endocardial abnormalities has been reported. From necropsy studies, endocardial fibroelastosis in the LAA³ and (among cases of fatal thromboembolic stroke) areas of left atrial . . . [Full Text of this Article]

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