New Insight in Aetiopathogenesis of Aortic Diseases

Background: Knowledge in the aetiopathogeny of aortic disease helps to characterise aortic lesions better and determine the risk of evolution and therapeutic strategies as welt. 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 watt are derived from a variety of cell types in addition to macrophages, including neutrophils on the luminal thrombus, mesenchymal and endothelial cells in the watt. Smooth muscle cells contribute to aortic watt homeostasis against inflammation and proteolysis. The degradation of the watt 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. (C) 2009 European Society for Vascular Surgery. Published by Elsevier Ltd. All rights reserved.