Abdominal aortic aneurysms (AAAs) remain a significant cause of death in the Western world with over 15,000 deaths per year in the US linked to AAA rupture. There is a general belief among the clinical and engineering community that improved methods of risk prediction are needed. The growth and expansion of AAAs over time is thought to be associated with the mechanobiological interactions within the diseased AAA wall. The stresses and strains induced in the wall by the internal blood pressure trigger increased protease activity and turnover of the extracellular matrix (ECM), thus enabling degradation and expansion of the wall. Inflammatory cells also control collagen synthesis and inflammation can reduce the tensile strength of the wall, thus contributing to the likelihood of rupture. Recently, important work by Richards et al. [1] showed that AAAs with specific sites of focal inflammation have threefold higher growth rates than AAAs with non-specific inflammation.

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