The widely accepted hypothesis that mechanobiological transduction plays a central role in pathogenesis of abdominal aortic aneurysm (AAA) is plausible, but so far was never directly proven in vivo for methodical reasons. At present, stresses and strains acting in AAA wall can be assessed by computational finite element analyses (FEA) [1,2,3]. Independently, it has also been reported that glycolytic activity in AAA wall non-invasively assessed by [18F]flourodeoxyglucose positron emission tomography/CT (FDG-PET/CT) is associated with increased proteolytic activity, structure-protein-degradation, AAA progression and consequently AAA wall instability as well as rupture risk [4]. Both methods were studied by our research group in an individual AAA patient [5]. Here, the correlation of computational biomechanics with metabolic activity assessed by FDG-PET/CT is analyzed in a larger patient cohort (n=18) [8].

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