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Transesophageal Echocardiography in High-Risk Patients with Atrial Fibrillation
The Editors welcome submissions for possible publication in the Letters section. Authors of letters should:
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•Type with double-spacing
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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 Unpublished letters cannot be returned.
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TO THE EDITOR:
The Stroke Prevention in Atrial Fibrillation Investigators Committee on Echocardiography has made an important contribution to our understanding of embolic risk by including the examination of the thoracic aorta in their patients with atrial fibrillation [1]. Aortic atheromas identified by transesophageal echocardiography have been recognized since 1990 as a source of embolism [2]. The Annals study [1] found exactly the same risk for stroke in patients with aortic atheromas (12% in approximately 1 year) as was found in the two previous prospective studies of risk for stroke in these patients [3]. Perhaps the most important finding of the current study is that adjusted-dose warfarin decreased the risk for stroke by 75% in patients with complex aortic plaque. The editorial by Manning and Douglas accompanying the article [4] correctly asks what the mechanism for this action might be. The mobile components of these complex plaques have been found to be thrombi [5], and serial transesophageal studies of the aorta have shown that these thrombi appear and disappear in different locations over time. It is therefore likely that anticoagulation with warfarin prevents thrombus formation (and subsequent embolization) on aortic plaques, just as it does in the left atrium, rather than directly affecting plaque size. Over the long term, plaque size may also be affected by reduction in thrombus formation, although this has not been investigated. It is also interesting to speculate on the mechanism for stroke reduction in the myocardial infarction trials involving the statin drugs. Plaque stabilization in the aorta could also occur with these drugs, as it probably does in the coronary arteries.
Paul A. Tunick, MD
Itzhak Kronzon, MD
New York University Medical Center; New York, NY 10016
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
