Abstract
Abdominal aortic aneurysm (AAA) rupture is an important cause of death in older adults. In clinical practice, the most established predictor of AAA rupture is maximum AAA diameter. Aortic diameter is commonly used to assess AAA severity in mouse models studies. AAA rupture occurs when the stress (force per unit area) on the aneurysm wall exceeds wall strength. Previous research suggests that aortic wall structure and strength, biomechanical forces on the aorta and cellular and proteolytic composition of the AAA wall influence the risk of AAA rupture. Mouse models offer an opportunity to study the association of these factors with AAA rupture in a way not currently possible in patients. Such studies could provide data to support the use of novel surrogate markers of AAA rupture in patients. In this review, the currently available mouse models of AAA and their relevance to the study of AAA rupture are discussed. The review highlights the limitations of mouse models and suggests novel approaches that could be incorporated in future experimental AAA studies to generate clinically relevant results.
Highlights
Abdominal aortic aneurysm (AAA) is a chronic degenerative disease that results in the focal expansion of all layers of the abdominal aortic wall
A systematic review and meta-analysis which collated published data from 9 independent studies, found that Peak wall stress (PWS) was significantly higher in patients with a symptomatic or ruptured AAA compared to patients with an intact AAA (n = 144 and 204, respectively; p < 0.001) [26]
This study provides the first proof-of-concept data for PET-computer tomography (CT) as a potential imaging assessment for AAA risk-stratification
Summary
Abdominal aortic aneurysm (AAA) is a chronic degenerative disease that results in the focal expansion of all layers of the abdominal aortic wall. AAA is usually diagnosed when an asymptomatic person undergoes incidental imaging or ultrasound screening, which identifies a focal abdominal aortic dilatation with a diameter ≥30 mm [1,2,3]. Even though the exact mechanisms of AAA rupture are unknown, several pathological processes, including infiltration of inflammatory cells including T regulatory cells [8], proteolytic degradation of the extracellular matrix (ECM), and neovascularization have been implicated in the process. These biological processes are believed to cause elastin degradation and alter collagen composition that compromises the strength and elasticity of the aorta [9,10]. It is still unclear to what extent the different biological processes individually contribute to the mechanical changes and eventual rupture of the aortic wall
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