Asymptomatic Abdominal Aortic Aneurysms Show Histological Signs of Progression: A Quantitative Histochemical Analysis

Abstract

Objective: Abdominal aortic aneurysm (AAA) is a serious disease due to its covert nature, relatively high prevalence and fatal prognosis in the case of rupture. To obtain new insights into AAA pathogenesis, we examined the relationships between histopathology, multiplex in vitro immunoassay data, diameter and symptomatology. Methods: In a prospective, non-randomised study, we evaluated samples from 6 normal infrarenal aortae and 65 AAA patients (65 walls, 55 thrombi). The AAA patients were either asymptomatic (n = 44), symptomatic (n = 7) or with ruptured AAA (n = 14). The AAA diameter was classified as small (<5 cm, n = 18), medium (5–7 cm, n = 26) and large (>7 cm, n = 21). We quantified the histopathology of the AAA wall and the adjacent thrombus. We assessed the expression of proteins in the same samples. Results: Asymptomatic AAAs had walls with more abundant inflammatory infiltrates, lower amounts of PAI-1, a higher number of tPA-positive elements, a tendency towards decreased collagen content, whereas the adjacent thrombi had a greater concentration of VCAM-1 and MMP-2 when compared with symptomatic AAAs. Compared with the aneurysmatic aorta, the normal aorta contained less collagen and more elastin, actin, desmin and PAI-1-positive elements; in addition, it was more vascular. Medium-sized AAAs were the most actin and vimentin rich, and large AAAs were the most vascular. Conclusion: Our results show that asymptomatic AAA walls often have more potentially deleterious histopathological alterations than symptomatic AAA walls. This result indicates that a progression from an asymptomatic AAA to rupture can be expected and screening patients who are at risk of rupture could be beneficial.

MicroRNAs as possible biomarkers for screening of aortic aneurysms: a systematic review and validation study

“…One of these genes is SERPINE1, which encodes for plasminogen activator inhibitor-1 (PAI-1). The expression of PAI-1 was reported to be lower in abdominal aneurysmal tissue compared to control samples (Eberlov a et al 2013).…”

“…Numerous proteins were identified to be differentially expressed in aneurysmal aortic tissue when compared with normal aorta, affecting different mechanisms. This included the expression of proteins of vascular smooth muscle cell, actin, elastin and desmin as well as extracellular matrix and fibrolysis mechanisms (Borges et al 2010, Eberlov a et al 2013.…”

“…In addition, there are aortic aneurysms with thrombus covering the aortic wall. Studies have shown that in these situations the aortic wall presents inflammation, fibrinolysis, and extracellular matrix degradation (Treska et al 2002, Kazi et al 2003, Houard et al 2007, Eberlov a et al 2013.…”

Segmental and age differences in the elastin network, collagen, and smooth muscle phenotype in the tunica media of the porcine aorta

“…VSMCs can modulate their phenotype from contractile (more actin and desmin) to synthesis (less actin and desmin, more vimentin, and higher proliferative activity) (Miyazaki et al, 2002;Owens et al, 2004;Boccardi et al, 2007). Actin, desmin, and vimentin can be detected in both porcine and human aortic samples using the same antibodies, their immunopositivity is robust and therefore easily to be quantified Houdek et al, 2013;Eberlova et al, 2013). The Advanced models of the aortic wall are currently able to link the macroscopic mechanical behavior of the whole arteries with the cytoskeletal filaments of individual VSMCs (Unterberger et al, 2013).…”

Evolving anisotropy and degree of elastolytic insult in abdominal aortic aneurysms: Potential clinical relevance?

“…AAAs are characterized histologically by loss of functional elastin and smooth muscle and altered turnover of collagen (Eberlová et al, 2013; He and Roach, 1994). These changes not only lead to geometric dilatation, but also a “stiffening” of the aortic wall that can be appreciated as a leftward shift of a standard stress-stretch curve (i.e., a loss of extensibility).…”