Aortic atherosclerotic disease and stroke.
نویسندگان
چکیده
In the 1940s, most strokes were attributed to cerebral vasospasm, a mechanism that is not given a great deal of credence today. It was not until the early 1950s that Harvard neurologist C. Miller Fisher1 stressed the importance of carotid artery atherosclerosis as a major cause of cerebral infarction. Later that decade, the importance of atrial fibrillation as a cause of cerebral embolism began to be stressed,2 and the presence of a left atrial thrombus was first seen on angiocardiography in 1965.3 Despite the established importance of these 2 causes of stroke, carotid disease and atrial fibrillation, nearly half of strokes were listed as “of undetermined cause” in a large stroke registry as recently as 1989.4 In this series, 40% of 1273 cerebral infarctions in the Stroke Databank of the National Institute of Neurological and Communicative Disorders and Stroke (NINCDS) were thought to be cryptogenic (from the Latin crypticus, meaning secret or mysterious). The clinical syndrome in those patients, as well as the angiographic and computed tomographic (CT) findings, could be reclassified as embolic; however, because no source of embolus could be identified, the authors kept these strokes in the undetermined cause category. In 1990, a third leading cause of embolic stroke was identified on transesophageal echocardiography (TEE), namely severe atherosclerotic plaques in the aortic arch.5 The 3 patients described in that initial report were a 68-year-old woman with dysarthria and an embolus to the foot, a 77-year-old woman with a cerebellar infarction after cardiac catheterization, and a 70-year-old man with staggering, diplopia, and a visual field cut. All 3 had severe plaque in the aortic arch on TEE. In addition, freely mobile projections were seen superimposed on the plaques, making it seem likely that these findings were the reason for the patients’ embolic events. That atherosclerosis of the aorta and arterial emboli are related is not a new concept. In fact, since 1862, pathologists have suggested that “eroded atherosclerotic plaque” may result in embolic arterial occlusions.5–7 However, it required sophisticated imaging technology such as TEE (Figure 1) (and later CT and magnetic resonance imaging [MRI]) to view these lesions in vivo. The subject of the risk of aortic arch plaque as seen on TEE has been reviewed several times in the last 15 years.8–10 More recently, the ability to image aortic plaque and its contents has improved significantly through the use of different imaging modalities, and our understanding of the associated clinical syndromes has increased. Although most investigators feel that aortic atherosclerosis is a leading cause of embolic disease, doubts have been raised.11 All of these issues are discussed in this review.
منابع مشابه
Evaluation the effect of Boron on histopathological changes of atherosclerotic plaque in aortic arch and lipid profiles in New Zealand hyperlipidemic male rabbits
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ورودعنوان ژورنال:
- Circulation
دوره 114 1 شماره
صفحات -
تاریخ انتشار 2006