In this model, there is an initial influx of inflammatory cells which degrade the aortic ECM and subsequently leads to aneurysm formation over seven to 14 days. In addition, a rodent model in which the infrarenal aorta is perfused with porcine pancreatic elastase, leading to infrarenal aortic aneurysms has been developed ( 13). In contrast, treating explanted arteries with elastase resulted in varying degrees of arterial dilation ( 12). demonstrated that treating explanted arteries in vitro, from various species, with collagenase resulted in artery rupture. However, the concentration of collagen in AAAs may be decreased, unchanged, or increased, compared with normal aortic tissue ( 7, 10, 11).ĭobrin et al. It is clear that aortic elastin concentration is markedly reduced with a loss of elastic lamellae in AAAs ( 7, 8, 9). The mechanical and molecular mechanisms behind this observation are unknown.Īlthough the pathogenesis of AAAs is not entirely understood, a few distinguishing characteristics of AAAs include: significant inflammation complex atherosclerosis and changes in the levels, production, and degradation of extracellular matrix (ECM) proteins. In contrast, women have a higher risk of rupture and increased morbidity following elective AAA repair ( 6). Uncontrollable risk factors include age (risk increases with increasing age) and gender ( 2, 3), with males developing AAAs four times more often than females ( 4, 5). and the 14 th leading cause of overall death in the US ( 1). Abdominal aortic aneurysms (AAAs) are the 10 th leading cause of death of men in the U.S.
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