AAA are believed to be atherosclerotic in origin. Several factors have been suggested including genetic alterations in biochemical structure of the aortic wall as well as infectious and immune factors. One feature of AAA is the breakdown of the extracellular matrix of the aortic wall. The primary deficiency has been found to be elastin. This may be due to deficiencies in formation or increased breakdown by proteases such as elastin. Marfan's syndrome patients, prone to AAA, have a defect in the fibrillin gene and have a deficiency in functional fibrillin. Fibrillin is a glyco-protein that acts as the scaffolding for elastin.

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