REPLY
Transesophageal Echocardiography in High-Risk Patients with Atrial Fibrillation
Kwan-Leung Chan, MD, and
Jonathan L. Halperin, MD
1 November 1998 | Volume 129 Issue 9 | Page 748
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.
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Author and Article Information
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University of Ottawa Heart Institute; Ottawa, Ontario K1Y 4E9, Canada
Mount Sinai Medical Center; New York, NY 10029
1. Zabalgoitia M, Halperin JL, Pearce LA, Blackshear JL, Asinger RW, Hart RG. Transesophageal echocardiographic correlates of clinical risk of thromboembolism in nonvalvular atrial fibrillation. J Am Coll Cardiol. 1998; 31:1622-6.
2. Amarenco P, Cohen A. Atherosclerotic disease of the aortic arch as a risk factor for recurrent ischemic stroke. N Engl J Med. 1996; 334:1216-21.
3. Tunick PA, Rosenzweig BP, Katz ES, Freedberg RS, Perez JL, Kronzon I. High risk for vascular events in patients with protruding aortic atheromas: a prospective study. J Am Coll Cardiol. 1996; 23:1085-90.
4. Collins LJ, Silverman DI, Douglas PS, Manning WJ. Cardioversion of nonrheumatic atrial fibrillation. Circulation. 1995; 92:160-3.
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