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Transesophageal Echocardiography in High-Risk Patients with Atrial Fibrillation
- Kwan-Leung Chan, MD; and
- Jonathan L. Halperin, MD
- University of Ottawa Heart Institute; Ottawa, Ontario K1Y 4E9, Canada Mount Sinai Medical Center; New York, NY 10029
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IN RESPONSE:
We appreciate the cogent comments of Drs. Tunick and Kronzon. Thoracic aortic plaque is associated with a high risk for stroke, both in patients with [1] and without [2, 3] atrial fibrillation. The magnitude of risk has been measured only within broad confidence limits, however, and seems to persist despite antithrombotic therapy with a low-intensity combination of warfarin and aspirin in patients with coexisting atrial fibrillation. The reduction in stroke among patients treated with higher-intensity anticoagulation with adjusted-dose warfarin may have been due to disappearance of thrombus in the left atrial appendage. This phenomenon, previously described in selected patients with atrial fibrillation [4], is consistent with the lower prevalence of appendage thrombus in patients receiving anticoagulation than in those given the combination therapy. Changes in thrombotic activity on the surface of atherosclerotic lesions in the aorta or in the cerebral vessels could have contributed to the difference in clinical outcome, but data on treatment efficacy in other clinical settings have not been accumulated in controlled trials. However, detection of aortic plaque in patients with atrial fibrillation correlates with reduced flow velocity, dense spontaneous echocardiographic contrast, and thrombus formation in the left atrial appendage, and in our study there were too few events in patients who had complex aortic plaque without associated left atrial abnormalities to define the efficacy of warfarin.
Much remains unanswered about the interaction between atherosclerotic disease of the thoracic aorta and left atrial abnormalities in patients with atrial fibrillation. As Tunick and Kronzon rightly point out, inhibition of thrombosis is but one avenue for prevention of thromboembolism in patients with atherosclerosis, and other treatments aimed at regression of vascular disease should also be considered in the design of future trials.
Kwan-Leung Chan, MD
University of Ottawa Heart Institute; Ottawa, Ontario K1Y 4E9, Canada
Jonathan L. Halperin, MD
Mount Sinai Medical Center; New York, NY 10029
The Editors welcome submissions for possible publication in the Letters section. Authors of letters should:
•Include no more than 300 words of text, three authors, and five references
•Type with double-spacing
•Send three copies of the letter, an authors' form signed by all authors, and a cover letter describing any conflicts of interest related to the contents of the letter.
Letters commenting on an Annals article will be considered if they are received within 6 weeks of the time the article was published. Only some of the letters received can be published. Published letters are edited and may be shortened; tables and figures are included only selectively. Authors will be notified that the letter has been received. If the letter is selected for publication, the author will be notified about 3 weeks before the publication date. Unpublished letters cannot be returned.
Annals welcomes electronically submitted letters.
- Copyright ©2004 by the American College of Physicians
