Analysis of Cerebral Aneurysm Wall Tension and Enhancement Using Finite Element Analysis and High-Resolution Vessel Wall Imaging.

Biomechanical computational simulation of intracranial aneurysms has become a promising method for predicting features of instability leading to aneurysm growth and rupture. Hemodynamic analysis of aneurysm behavior has helped investigate the complex relationship between features of aneurysm shape, morphology, flow patterns, and the proliferation or degradation of the aneurysm wall. Finite element analysis paired with high-resolution vessel wall imaging can provide more insight into how exactly aneurysm morphology relates to wall behavior, and whether wall enhancement can describe this phenomenon. In a retrospective analysis of 23 unruptured aneurysms, finite element analysis was conducted using an isotropic, homogenous third order polynomial material model. Aneurysm wall enhancement was quantified on 2D multiplanar views, with 14 aneurysms classified as enhancing (CRstalk≥0.6) and nine classified as non-enhancing. Enhancing aneurysms had a significantly higher 95th percentile wall tension (µ = 0.77 N/cm) compared to non-enhancing aneurysms (µ = 0.42 N/cm, p < 0.001). Wall enhancement remained a significant predictor of wall tension while accounting for the effects of aneurysm size (p = 0.046). In a qualitative comparison, low wall tension areas concentrated around aneurysm blebs. Aneurysms with irregular morphologies may show increased areas of low wall tension. The biological implications of finite element analysis in intracranial aneurysms are still unclear but may provide further insights into the complex process of bleb formation and aneurysm rupture.

Does elevated wall tension cause aortic aneurysm rupture? Investigation using a subject-specific heterogeneous model.

OBJECTIVE: To investigate whether peak wall tension in abdominal aortic aneurysm occurs at the site of rupture to test for a causative relationship. METHODS: Four ruptured and nine unruptured AAA were harvested whole from cadavers, followed by regional measurements of wall thickness, elastic parameters and failure tension. Finite element models were developed with subject-specific load-free AAA morphology and heterogeneous properties interpolated using a geodesic distance weighted approach from the measurements. The wall tension under uniform pressure and tension to failure tension ratio as an index of susceptibility to rupture were computed. As a secondary aim, the peak wall tension using this heterogeneous model approach was compared to the traditional homogeneous model approach in order to evaluate the reliability of the latter. RESULTS: The average peak wall tension in the ruptured group was 43% higher than in the unruptured group without statistical significance even though it was 54% larger in diameter. The site of peak wall tension was in the vicinity of the site of rupture in two ruptured AAA. The peak tension did not breach failure tension at the rupture site in any of the AAA. The traditional population-wide homogeneous model approach overestimated peak wall tension by just 3% compared to the subject-specific heterogeneous model approach. CONCLUSION: We failed to find adequate evidence of a causative relationship between peak wall tension and AAA rupture. The findings are not conclusive owing to study limitations such as ignoring intraluminal thrombus, sparse distribution of specimens procured and small study population.