I Kronzon1, P A Tunick. 1. New York University Medical Center, New York, USA.
Abstract
PURPOSE: To review recent developments in the diagnosis, clinical epidemiology, pathology, and management of atherosclerosis of the thoracic aorta, especially atherosclerosis of the thoracic aorta as a source of embolization. DATA SOURCES: MEDLINE searches, bibliographies of published papers, and consultation with experts in the field. STUDY SELECTION: English-language publications on atherosclerosis of the thoracic aorta were selected. DATA SYNTHESIS: During the last 6 years, the increasing use of transesophageal echocardiography has shown that atherosclerotic plaque in the thoracic aorta is a source of otherwise unexplained embolic events, including stroke, transient ischemic attack, and peripheral emboli. Retrospective studies have documented a strong independent association between larger lesions (4 mm to 5 mm) and previous embolic disease, and prospective studies have shown that patients with these lesions have a high risk for future events (in one study, the risk for stroke was 12%; in another, the risk for cerebral or peripheral events was 33% in a follow-up period of just 14 months). These lesions also pose a serious risk for embolization caused by manipulation of the aorta during catheterization, intra-aortic balloon-pump placement, and cannulation of the aorta for heart surgery. Pathologic examination has shown atherosclerotic plaque, often with superimposed thrombi that account for the mobile components seen on transesophageal echocardiography. The management of patients who have atherosclerotic lesions in the thoracic aorta has not been determined prospectively. However, anticoagulation may help prevent emboli, as it does for patients who have thrombi in other locations, such as the left atrium and the left ventricle. CONCLUSIONS: Protruding atherosclerotic lesions in the thoracic aorta, often with superimposed mobile thrombi, are an important cause of embolic disease. Transesophageal echocardiography should be considered in the work-up of patients who have unexplained embolic events.
PURPOSE: To review recent developments in the diagnosis, clinical epidemiology, pathology, and management of atherosclerosis of the thoracic aorta, especially atherosclerosis of the thoracic aorta as a source of embolization. DATA SOURCES: MEDLINE searches, bibliographies of published papers, and consultation with experts in the field. STUDY SELECTION: English-language publications on atherosclerosis of the thoracic aorta were selected. DATA SYNTHESIS: During the last 6 years, the increasing use of transesophageal echocardiography has shown that atherosclerotic plaque in the thoracic aorta is a source of otherwise unexplained embolic events, including stroke, transient ischemic attack, and peripheral emboli. Retrospective studies have documented a strong independent association between larger lesions (4 mm to 5 mm) and previous embolic disease, and prospective studies have shown that patients with these lesions have a high risk for future events (in one study, the risk for stroke was 12%; in another, the risk for cerebral or peripheral events was 33% in a follow-up period of just 14 months). These lesions also pose a serious risk for embolization caused by manipulation of the aorta during catheterization, intra-aortic balloon-pump placement, and cannulation of the aorta for heart surgery. Pathologic examination has shown atherosclerotic plaque, often with superimposed thrombi that account for the mobile components seen on transesophageal echocardiography. The management of patients who have atherosclerotic lesions in the thoracic aorta has not been determined prospectively. However, anticoagulation may help prevent emboli, as it does for patients who have thrombi in other locations, such as the left atrium and the left ventricle. CONCLUSIONS: Protruding atherosclerotic lesions in the thoracic aorta, often with superimposed mobile thrombi, are an important cause of embolic disease. Transesophageal echocardiography should be considered in the work-up of patients who have unexplained embolic events.
Authors: K Takahashi; M Ohyanagi; K Ikeoka; M Masai; H Naruse; T Iwasaki; M Fukuchi; T Miyamoto Journal: J Nucl Cardiol Date: 2001 Mar-Apr Impact factor: 5.952
Authors: Dietrich Stoevesandt; Carsten Klempt; Robert Scheubel; Waldemar Herr; Stefan Hettwer; Karl Werdan; Rolf-Edgar Silber; Torsten Kraya; Oliver Thews; Axel Schlitt Journal: J Thromb Thrombolysis Date: 2013-02 Impact factor: 2.300