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Finite element analysis (FEA) method is a well-established numerical concept that di- vides any geometry into a large number of finite elements, which together can form an equivalent biomechanical model of an ab- dominal aortic aneurysm (AAA).1 The geom- etry of the reconstructed model, the systemic pressure, flow parameters (boundary condi- tions), and the constitutive assumptions de- termine the relationship and interaction between stress (mechanical loading) and strain (deformation) of the structure wall, which comprise the fundamental features of aFEAmodeland,hence,itstheoretical utility.1,2 The influence that the constitutive assumptions (homogenous AAA wall thick- ness and isotropic constitutive properties) and the modeling techniques have on the results of the method, as well as the computationally- demanding equipment needed, remain the Achilles' heel of the concept; yet, the most significant limitations are the lack of clinical validation and correlation of FEA findings with histopathological or biochemical data.3
The A4clinics software (VASCOPS GmbH, Graz, Austria) facilitates the aforementioned process since it allows a clinician to have the reconstructed FEA model (Figure, A) and the color contours with the values of both the peak wall stress (PWS) and the peak wall rupture index (PWRI) in an AAA (Figure, B), as illustrated here, within 20 minutes. The intra- and interobserver variability of the method has been reported to be low.2,4,5
In this issue, Erhart et al.6 attempt to correlate FEA findings of 15 asymptomatic AAAs with histological specimens from areas of low and high PWS and PWRI. Within samples of each patient, the sites of low rupture index were associated with signifi- cantly more smooth muscle cells and elastin fibers than sites of higher PWRI, suggesting an increased local histological integrity in the former. Previous studies have demonstrated a positive correlation between FEA findings and increased uptake of 18F-FDG as a marker of local wall inflammation. Therefore, the impor- tant (and long anticipated!) results from Erhart et al.6 are not only in accord with previous experiments but also provide a direct, straightforward proof of the effects (histological degeneration) that hemodynamic loading exert on the AAA wall structure.7-10
However, AAAs of higher PWRI were not associated with higher tissue degeneration when compared to AAAs of lower PWRI in the study, implying that the attenuation of tensile strength to the point of rupture...