Intimomedial Interface Damage and Adventitial Inflammation Is Increased Beneath Disrupted Atherosclerosis in the Aorta: Implications for Plaque Vulnerability
暂无分享,去创建一个
[1] R. Kamm,et al. Distribution of Circumferential Stress in Ruptured and Stable Atherosclerotic Lesions A Structural Analysis With Histopathological Correlation , 1993, Circulation.
[2] S. Glagov,et al. Transmural Organization of the Arterial Media: The Lamellar Unit Revisited , 1985, Arteriosclerosis.
[3] A. Becker,et al. Leucocyte recruitment in rupture prone regions of lipid-rich plaques: a prominent role for neovascularization? , 1999, Cardiovascular research.
[4] P. Libby. Molecular bases of the acute coronary syndromes. , 1995, Circulation.
[5] T. Paavonen,et al. Association between myocardial infarction and the mast cells in the adventitia of the infarct-related coronary artery. , 1999, Circulation.
[6] R. Virmani,et al. Coronary risk factors and plaque morphology in men with coronary disease who died suddenly. , 1997, The New England journal of medicine.
[7] S E Nissen,et al. Extent and direction of arterial remodeling in stable versus unstable coronary syndromes : an intravascular ultrasound study. , 2000, Circulation.
[8] E L Ritman,et al. Adventitial vasa vasorum in balloon-injured coronary arteries: visualization and quantitation by a microscopic three-dimensional computed tomography technique. , 1998, Journal of the American College of Cardiology.
[9] D. Faxon,et al. Five-year angiographic follow-up of factors associated with progression of coronary artery disease in the Coronary Artery Surgery Study (CASS). CASS Participating Investigators and Staff. , 1993, Journal of the American College of Cardiology.
[10] Renu Virmani,et al. Morphological Predictors of Arterial Remodeling in Coronary Atherosclerosis , 2002, Circulation.
[11] V. Fuster,et al. The pathogenesis of coronary artery disease and the acute coronary syndromes (1). , 1992, The New England journal of medicine.
[12] V. Fuster,et al. The pathogenesis of coronary artery disease and the acute coronary syndromes (2). , 1992, The New England journal of medicine.
[13] M. Nobuyoshi,et al. Significance of adventitial inflammation of the coronary artery in patients with unstable angina: results at autopsy. , 1985, Circulation.
[14] S. Oparil,et al. Direct in vivo evidence demonstrating neointimal migration of adventitial fibroblasts after balloon injury of rat carotid arteries. , 2000, Circulation.
[15] M. Davies. Glagovian remodelling, plaque composition, and stenosis generation , 2000, Heart.
[16] R D Kamm,et al. Vascular mechanics for the cardiologist. , 1994, Journal of the American College of Cardiology.
[17] R. Erbel,et al. Size of emptied plaque cavity following spontaneous rupture is related to coronary dimensions, not to the degree of lumen narrowing. A study with intravascular ultrasound in vivo , 2000, Heart.
[18] B Hillen,et al. Relation of arterial geometry to luminal narrowing and histologic markers for plaque vulnerability: the remodeling paradox. , 1998, Journal of the American College of Cardiology.
[19] R D Kamm,et al. Effects of fibrous cap thickness on peak circumferential stress in model atherosclerotic vessels. , 1992, Circulation research.
[20] G. Pasterkamp,et al. Atherosclerotic arterial remodeling and the localization of macrophages and matrix metalloproteases 1, 2 and 9 in the human coronary artery. , 2000, Atherosclerosis.
[21] T. Noma,et al. Enhanced Expression of Matrix Metalloproteinase-9 in Abdominal Aortic Aneurysms , 2001, World Journal of Surgery.
[22] M J Davies,et al. Stability and instability: two faces of coronary atherosclerosis. The Paul Dudley White Lecture 1995. , 1996, Circulation.
[23] V. Fuster,et al. Angiographic progression of coronary artery disease and the development of myocardial infarction. , 1988, Journal of the American College of Cardiology.
[24] A Zalewski,et al. Adventitial remodeling after coronary arterial injury. , 1996, Circulation.
[25] W. Santamore,et al. Can coronary angiography predict the site of a subsequent myocardial infarction in patients with mild-to-moderate coronary artery disease? , 1988, Circulation.
[26] S. Glagov,et al. A Lamellar Unit of Aortic Medial Structure and Function in Mammals , 1967, Circulation research.
[27] V. Fuster,et al. Coronary plaque disruption. , 1995, Circulation.
[28] C. Zarins,et al. Compensatory enlargement of human atherosclerotic coronary arteries. , 1987, The New England journal of medicine.
[29] S Glagov,et al. Comparison of Abdominal and Thoracic Aortic Medial Structure in Mammals , 1969, Circulation research.
[30] C. Levene,et al. Medial thinning in atheroma. , 1953, The Journal of pathology and bacteriology.
[31] J D Thomas,et al. Toward the quiescent coronary plaque. , 1993, Journal of the American College of Cardiology.
[32] W D Wagner,et al. A definition of advanced types of atherosclerotic lesions and a histological classification of atherosclerosis. A report from the Committee on Vascular Lesions of the Council on Arteriosclerosis, American Heart Association. , 1995, Arteriosclerosis, thrombosis, and vascular biology.
[33] A. Becker,et al. The role of inflammation and infection in coronary artery disease. , 2001, Annual review of medicine.
[34] J. Willerson,et al. Role of inflammation in coronary plaque disruption. , 1994, Circulation.
[35] R. Virmani,et al. Plaque Rupture and Plaque Erosion , 1999, Thrombosis and Haemostasis.
[36] Davies Mj. Glagovian remodelling, plaque composition, and stenosis generation. , 2000 .