Brief Reviews |
From the Heart Lung Institute (G.P., D.P.V.d.K.), Laboratory of Experimental Cardiology, Utrecht University Hospital, Utrecht, The Netherlands; Department of Medicine (Z.S.G.), Division of Cardiology, Emory University and Wallace H. Coulter School of Biomedical Engineering, Georgia Institute of Technology/Emory University, Atlanta, Ga.
Correspondence to G. Pasterkamp, UMCU, Heart Lung Institute, Experimental Cardiology Laboratory, Room G02-523, Heidelberglaan 100, 3584CX Utrecht, The Netherlands. Web site: www.vascularbiology.org. E-mail g.pasterkamp{at}hli.azu.nl
Series Editor:: Robert W. Thompson
ATVB In Focus Abdominal Aortic Aneurysms: Pathophysiological Mechanisms and Clinical Implications
Previous Brief Reviews in this Series:
Powell JT, Brady AR. Detection, management, and prospects for the medical treatment of small abdominal aortic aneurysms. 2004;24:241245.
Daugherty A, Cassis LA. Mouse models of abdominal aortic aneurysms. 2004;24:429434.
The artery is a dynamic organ capable of changing its geometry in response to atherosclerotic plaque formation. Expansion of the vessel diameter retards luminal narrowing and is considered a compensatory response. However, the expansive remodeling response is a "wolf in sheeps clothes," because expansion is associated with the presence of inflammatory cells, proteolysis, and a thrombotic plaque phenotype. The prevalence and clinical presentation of expansively remodeled lesions may differ among vascular beds. However, it is evident that all types of atherosclerotic arterial expansive lesions share the presence of inflammatory cells and subsequent protease activities. The potential role of inflammation and protease activity in the development of the different remodeling modes is discussed.
Key Words: remodeling atherosclerosis toll-like receptor inflammation compensatory enlargement
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