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Volume 37, Issue 5, Pages 531-537 (May 2009)


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New Insight in Aetiopathogenesis of Aortic Diseases

E. AllaireabCorresponding Author Informationemail address, F. Schneiderab, F. Saucyac, J. Daia, F. Cochennecab, S. Michineaua, M. Zidia, J.-P. Becqueminab, M. Kirschad, M. Gervaisa

Received 4 February 2009; accepted 4 February 2009. published online 18 March 2009.

Abstract 

Background

Knowledge in the aetiopathogeny of aortic disease helps to characterise aortic lesions better and determine the risk of evolution and therapeutic strategies as well. This article focusses on aneurysms and dissections, and excludes causes related to infection, systemic inflammatory diseases and trauma.

Methods and results

The biomedical literature of the past 10 years has been reviewed here. Aortic diseases are heterogeneous along the aorta as far as their genetic determinants, contribution of smooth muscle cells, inflammation and thrombus formation are concerned. Degradation of extracellular matrix by proteases causing aortic disease is a ‘terminal’ event, modulated by genetic background, haemodynamic strain, cellular events and thrombus formation. New genetic determinants of aortic disease have been identified. Proteases degrading the aortic wall are derived from a variety of cell types in addition to macrophages, including neutrophils on the luminal thrombus, mesenchymal and endothelial cells in the wall. Smooth muscle cells contribute to aortic wall homeostasis against inflammation and proteolysis. The degradation of the wall is followed by, or paralleled with, a failure of aortic reconstruction.

Conclusions

Aortic diseases are diverse, and involve a multiplicity of biological systems in the vascular wall and at the interface with blood. Future research needs to unravel distinct cellular and molecular mechanisms causing the clinical events, in particular, dissection, expansion of already formed aneurysms and rupture.

a Surgical Research Center, Paris 12 University, CNRS EAC 7054, 8 rue du Général Sarrail, 94010 Créteil Cedex, France

b Department of Vascular Surgery, Henri Mondor Hospital, Assistance Publique–Hôpitaux de Paris, 51 Avenue du Maréchal de, Lattre de Tassigny, 94010 Créteil, France

c Department of Vascular and Thoracic Surgery, Centre Hospitalier Universitaire Vaudois, Rue du Bugnon 46, 1011 Lausanne-CHUV, Switzerland

d Department of Cardiac and Thoracic Surgery, Hôpital Henri Mondor, 51 Avenue du Maréchal de Lattre de Tassigny, Créteil, France

Corresponding Author InformationCorresponding author at: Eric Allaire, Department of Vascular Surgery, Henri Mondor Hospital, 51 avenue du Maréchal de, Lattre de Tassigny, 94010 Créteil, France. Tel.: +33 1 49 81 44 20; fax: +33 1 49 81 24 35.

PII: S1078-5884(09)00062-8

doi:10.1016/j.ejvs.2009.02.002


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