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Submitted on June 8, 2005
From the Departments of Neurology and Clinical Neurophysiology (A.H., M.R., A.H.) and Angiology and Cardiology (M.H., A.G.), Albert-Ludwigs-Universität Freiburg, Germany. * To whom correspondence should be addressed. E-mail: harloff{at}nz.ukl.uni-freiburg.de.
Background and Purpose--Transesophageal echocardiography (TEE) is the gold standard in detecting high-risk (ie, aortic thrombi) and potential sources (ie, patent foramen ovale [PFO]) of cerebral embolism. We sought to evaluate the additional information and therapeutic impact provided by TEE in stroke patients and to characterize patients in whom TEE is indispensable. Methods--We included 503 consecutive patients (mean age 62.2 years) with acute brain ischemia. Each patient received TEE and the following routine diagnostics: ultrasound of brain supplying arteries, ECG or Holter-ECG, transthoracic echocardiography, and brain imaging (computed tomography or MRI). Stroke etiology was classified according to the Trial of Org 10172 in Acute Stroke Treatment (TOAST) criteria. High-risk sources in TEE were: aortic thrombi or plaques Results--Stroke etiology was determined by routine diagnostics in 276 of 503 patients (54.9%). Of the remaining 227 patients (undetermined etiology), 212 (93.4%) were candidates for oral anticoagulation (OA). TEE revealed a high-risk source, with indication for OA in 17 of them (8.0%). A potential source leading to OA was found in an additional 48 patients (22.6%). The remaining 147 patients (69.3%) were treated by platelet inhibitors or statins. Conclusions--TEE strongly influenced secondary prevention and led to OA in one third of our patients with stroke of undetermined etiology. TEE is indispensable in all patients being candidates for OA when routine diagnostics cannot clarify stroke etiology.
Revised on November 22, 2005
Accepted on November 27, 2005
Therapeutic Strategies After Examination by Transesophageal Echocardiography in 503 Patients With Ischemic Stroke
Andreas Harloff MD*;
4 mm, thrombi in left atrial cavity/left atrial appendage, spontaneous echo contrast, and left atrial flow velocity <30 cm/s. Potential sources in TEE were PFO, atrial septal aneurysm, and aortic plaques <4 mm.
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