Abstract

Abdominal aortic aneurysm (AAA), defined as a permanent segmental dilatation of the abdominal aorta, is a pathology responsible for significant morbidity and mortality especially among adult population over 60 years of age. Indeed, AAA is one of the fifteen most frequent causes of death among men older than 55 years in Western societies (Lederle et al., 2000). However, despite of its importance, little is known about etiopathogenesis of AAA. The observation by non-invasive imaging methods of an abdominal aorta of 3 cm typically or large in maximal diameter is generally considered to indicate aneurysm formation (Lederle et al., 2000). Diagnosis is typically made by non-invasive imaging modalities such as ultrasound, computerized tomography scan or magnetic resonance imaging with formal aortic angiography utilized in special clinical scenarios. At present, surgical treatment, conventional or endovascular surgery of AAA are very effective to prevent AAA rupture in patients with large AAA, at least 5,5 cm in diameter, with high risk of rupture. However, despite AAA with diameter <5,5 cm (termed as small AAA) have a low risk of rupture there are non well-defined therapeutic strategies for them. Moreover, the group of patients with small AAA should wait expectantly for the aneurysm reaches the minimum size to undergo surgical treatment, living through those days with great anxiety. Many factors may contribute to AAA formation and rupture, there are mechanical and rupture factors among them. Indeed, ultrasound examination showed AAA in 5.8% of World War II amputees, compared with 1% of non-amputees related to asymmetrical flow pattern at the aortic bifurcation. Moreover, evidence of genetic predisposition to the development of AAA has been noteworthy with 19% of AAA patients reporting one or more first-degree relatives with an aneurysm. Therefore, it is important to understand and know the molecular mechanisms involved in AAA expansion and which pharmacological treatments may prevent and delay it.

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