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(Circulation. 2002;105:2580.)
© 2002 American Heart Association, Inc.

Patent Foramen Ovale and Recurrent Stroke

Another Paradoxical Twist

Jonathan L. Halperin, MD; Valentin Fuster, MD, PhD

From the Mount Sinai Medical Center, New York, New York.

Correspondence to Valentin Fuster, MD, PhD, Mount Sinai Medical Center, 1 Gustave L. Levy Place, Box 1030, New York, NY 10029-6574. E-mail valentin.fuster@msnyuhealth.org

Key Words: Editorials • stroke • anticoagulants • embolism • shunt

Clinical management of patients with acute stroke and the approach used for secondary prevention depends upon clarification of pathogenesis. Although most strokes are a consequence of cerebrovascular disease, 15% to 20% of ischemic (nonhemorrhagic) strokes have been attributed to cardiogenic embolism.¹ In practice, determination of the stroke mechanism is fraught with uncertainty, particularly when the possibility of thromboembolism emanating from atherosclerotic lesions in the aorta or cervical arteries is considered. When cardiogenic embolism is suspected, cardiac ultrasound is the principal method used to identify the potential source. The finding of left atrial enlargement has been shown to bear a significant relationship to the risk of stroke in a multivariate analysis of population-based data from the Framingham Heart Study². The most frequent confounding variable is atrial fibrillation, occurring in >2 million patients in North America and in over half of all patients with cardiogenic embolism. Criteria for selection of patients with acute ischemic stroke for transesophageal echocardiography (TEE) to search for a potential cardiac source of embolism are controversial, particularly because cardiogenic embolism is often an uncertain diagnosis that is inferred merely on the basis of the finding of potential cardiac source. Even after extensive investigation, 40% of ischemic stroke patients have no clearly identifiable pathogenesis (cryptogenic stroke).³ In one study, 62% of patients younger than 60 years of age without an obvious source of cerebral infarction and 23% of those with arterial lesions had potential sources of cardiogenic embolism identified by TEE (P=0.0007 for the difference).⁴

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