Abstract

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.

Highlights

  • Multiple biological and mechanical phenomena regulate the process of intracranial aneurysm growth and rupture

  • The inflammatory response to the infiltration of macrophages into the aneurysm internal elastic lamina may initiate a cycle of smooth muscle cell proliferation paired with collagen remodeling that collectively increases the aneurysm wall tension

  • Aneurysm morphology can create hemodynamic patterns that lead to wall remodeling or the formation of blebs [12, 13]

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Summary

Introduction

Multiple biological and mechanical phenomena regulate the process of intracranial aneurysm growth and rupture. The inflammatory response to the infiltration of macrophages into the aneurysm internal elastic lamina may initiate a cycle of smooth muscle cell proliferation paired with collagen remodeling that collectively increases the aneurysm wall tension (wall stress resultant—i.e., wall stress integrated across the thickness). Maladaptation to this wall tension in addition to lipid accumulation may create focal areas in the aneurysm wall that are more susceptible to rupture [4,5,6]. Aneurysm morphology can create hemodynamic patterns that lead to wall remodeling or the formation of blebs [12, 13]

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