Abstract
Ascending aortic dilatation (AAD) affects a significant percentage of subjects over 55 years of age and causes a high mortality, and more than 80% of cases of AAD are not associated with a previously detected hereditary syndrome. There is a real need to learn more about its etiopathogenesis in order to help prevent it. The methodology used by us to address the role of norepinephrine in the genesis and progression of AAD was systematic review. The hallmark histological features of aortic disease are cystic spaces filled with mucoid material (CSMM) and the release of matrix metalloproteinases (MMPs). It is interesting to note that there are no histological differences between subjects with syndromic AAD (SAAD), eg, Marfan syndrome, nonsyndromic AAD (NSAAD), and cases of CSMM in the elderly. Moreover, there are no histological differences between AAD and ascending aortic dissection (AD). This paper assesses whether norepinephrine plays a significant role in the genesis of these aortic diseases by modulating MMP expression, elastic fiber fragmentation and the formation of CSMM, and finally participating in the subsequent ascending aortic dilatation, which would have major therapeutic and preventive implications.
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