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Ann Thorac Surg 2002;73:291-294
© 2002 The Society of Thoracic Surgeons
a Section of Cardiothoracic Surgery, Yale University School of Medicine, New Haven, Connecticut, USA
b Section of Neurology, Yale University School of Medicine, New Haven, Connecticut, USA
c Department of Pathology, Yale University School of Medicine, New Haven, Connecticut, USA
d Department of Cardiology, Danbury Hospital, Danbury, Connecticut, USA
Accepted for publication May 14, 2001.
* Address reprint requests to Dr Elefteriades, Section of Cardiothoracic Surgery, Yale University School of Medicine, 121 FMB, 333 Cedar St, New Haven, CT 06510, USA
e-mail: john.elefteriades{at}yale.edu
Replacement of the aortic arch for atheroma with cerebral embolization is in its infancy. The appropriateness of such intervention is controversial. Over a 10-month period, a 58-year-old woman suffered multiple debilitating cerebral vascular accidents manifested by motor, sensory, and memory deficits and documented by computed tomographic scanning and magnetic resonance imaging. Carotid and vertebral arteries were free of arteriosclerotic disease. Transesophageal echocardiography demonstrated two large atheromas with friable, pedunculated forms, one in the aortic arch and one in the very proximal descending thoracic aorta. Transcranial ultrasound revealed recurrent cerebral microembolic events. Cerebrovascular events continued, and the atheromas increased in size, despite treatment with Coumadin and aspirin. Under deep hypothermic arrest, the segment of the aortic arch harboring the atheroma was excised and replaced with a Dacron graft. Repeat transcranial ultrasound revealed cessation of embolic signals. All cerebrovascular events ceased. No further anticoagulation therapy was required. The patient has made substantial recovery from the preoperative deficits and continues to do well 1 year after aortic arch replacement. Resection of mobile aortic arch atheromas is likely to become increasingly important in the future as transesophageal echocardiography leads to their more common identification as a cause of cerebral ischemic events.
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