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Ann Thorac Surg 2004;78:2110-2111
© 2004 The Society of Thoracic Surgeons
Division of Cardiothoracic Surgery, Medical University of South Carolina, Strom Thurmond Research Bldg, 770 MUSC Complex, Rm 625, 114 Doughty St, Charleston, SC 29425, USA
| The first 20% of the full text of this article appears below. |
Thoracic aortic aneurysms (TAAs) and dissections represent significant clinical challenges to the cardiothoracic surgeon and are associated with a high incidence of perioperative morbidity. Thus, identifying the cellular and molecular mechanisms that drive the formation and progression of these processes holds great clinical relevance. To date, most of our knowledge of the pathobiology has not been a product of direct study, but rather an extension of studies regarding abdominal aortic aneurysms. Hence, the study undertaken by Koullias and colleagues in this issue of The Annals is significant in that studies were performed in aortic tissue samples collected from patients with TAAs and dissections.
A generalized feature of aneurysm development is that significant remodeling of the vascular wall occurs and is characterized by degeneration of the aortic medial layer and degradation of extracellular matrix (ECM). Important ECM proteins that provide support and distensibility to the aortic wall include elastin, collagens and glycoproteins. A family of proteolytic enzymes
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