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J Am Coll Cardiol, 2000; 35:545-554 © 2000 by the American College of Cardiology Foundation |
a Department of Medicine, New York University School of Medicine, New York, New York, USA
Manuscript received June 8, 1999; revised manuscript received October 14, 1999, accepted November 18, 1999.
Reprint requests and correspondence: Dr. Itzhak Kronzon, Department of Medicine, New York University School of Medicine, 560 First Avenue, New York, New York 10016
Atherosclerotic lesions of the thoracic aorta have recently been recognized as an important cause of stroke and peripheral embolization, which may result in severe neurologic damage as well as multiorgan failure and death. Their prevalence is
27% in patients with previous embolic events. Transesophageal echocardiography is the modality of choice for the diagnosis of these atheromas, although computed tomography, magnetic resonance imaging and intraoperative epiaortic ultrasound are complementary. Two clinical syndromes account for the embolic phenomena, atheroemboli and, more commonly, thromboemboli. In addition to such superimposed thrombi, plaque thickness (especially
4 mm) also correlates with embolic risk. This risk is high, with 12% of patients having a recurrent stroke within approximately one year, and up to 33% of patients having a stroke or peripheral embolus. In addition, aortic atheromas (as seen with intraoperative transesophageal echocardiography and intraoperative epiaortic ultrasound) are an important cause of stroke during heart surgery requiring cardiopulmonary bypass. Such strokes occur during
12% of cardiac operations employing cardiopulmonary bypass when aortic arch atheromas are seen with transesophageal echocardiography (six times the general intraoperative stroke rate). Although anticoagulant strategies have been reported with encouraging results in nonrandomized studies, prospective, randomized data must be developed before an effective and safe treatment strategy can be determined. This review details the current state of knowledge in this area, including the clinical and pathologic evidence that thoracic aortic atherosclerosis is an important embolic source, data which guide current therapy and future directions for clinical investigation.
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