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Stroke. 2003;34:e143-e145
Published online before print August 21, 2003, doi: 10.1161/01.STR.0000089496.16101.2E
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(Stroke. 2003;34:e143-a.)
© 2003 American Heart Association, Inc.


Letters to the Editor

Hyperhomocysteinemia and Left Atrial Thrombus in a Stroke Patient With Sinus Rhythm

Letizia Maria Cupini, MD Roberto De Simone, MD

Clinica Neurologica, Ospedale S. Eugenio, Rome, Italy


An extract of the first 250 words of the full text is provided, because this article has no abstract.
 

To the Editor:

We read with great interest the recent article by Ay et al1 concerning the relationship between high plasma homocysteine levels and risk for left atrial thrombus formation in patients with stroke caused by nonvalvular atrial fibrillation. Their finding supports the thrombogenic role of high homocysteine in conditions associated with blood stasis. We recently observed a cardioembolic ischemic stroke from a left atrial thrombus formation in a man with sinus rhythm and a previous history of coronary heart disease. Laboratory analysis revealed an hyperhomocysteinemia.

A 56-year-old man was admitted to our department presenting with an acute visual disturbance and a mild speech disorder. He was a previous smoker with a 5-year history of hypertension, currently treated with an ACE inhibitor. At age 51 he had had an anteroseptal myocardial infarction. Since that time he was under treatment with aspirin. Neurologic examination revealed right upper quadrantanopsia and anomic aphasia. A CT brain scan showed a hypodense, ischemic lesion in the left temporo-occipital region. Brain MRI confirmed the temporo-occipital ischemic lesion and disclosed an additional small ischemic lesion in the subcortical right hemisphere. EKG confirmed the signs of a previous anteroseptal myocardial infarction. Duplex ultrasonography of carotid and vertebral arteries did not show stenosis although it revealed an increased carotid artery intima-media thickness. MRI angiography was normal. Transthoracic echocardiography revealed a mild left ventricular dysfunction (systolic ejection fraction of 50%) with apical akinesia and lateral wall and septal ipokinesia. Transesophageal echocardiography showed a slight left atrium enlargement and disclosed the . . . [Full Text of this Article]

Hakan Ay, MD E. Murat Arsava, MD

Department of Neurology, Hacettepe University Hospitals, Ankara, Turkey