In Silico Fluid-Structure Interaction Reveals Wall Strain as a Potential Trigger for Aneurysm Initiation in a Rat Model

Both hemodynamics and vessel stretching have been reported to be implicated in the initiation of intracranial aneurysms. However, most computational fluid dynamics (CFD) studies assume a rigid vessel wall, while only a few considered wall deformation. In this study, we performed weakly coupled one-way fluid-structure interaction (FSI) analysis to evaluate both hemodynamics and vessel wall deformation in silico, aiming to investigate the mechanical factors contributing to aneurysm initiation.

A rat aneurysm model was created via bilateral common carotid artery anastomosis, as previously reported by Shimizu et al., and serial magnetic resonance angiography was performed. Five cases in which aneurysms developed near the vascular bifurcations were selected. CFD analysis was conducted using images acquired immediately before aneurysm initiation. Measured blood flow velocity and blood pressure were applied as inlet and outlet boundary conditions, respectively. For the FSI analysis, a two-layer model representing the vascular wall and surrounding tissues was added outside the lumen; its thickness was estimated by ultrasound and excised-vessel measurements. Material properties such as Young’s modulus were calibrated to match in vivo deformation observed on ultrasound imaging. Principal strain at each prospective aneurysm site was calculated as an index of wall stretch. For one representative case, vascular tissues were harvested for histopathological analyses.

In all cases, FSI analysis revealed a high-pressure region on the vessel wall near the apex of the bifurcation, where branching flow produced elevated wall shear stress divergence. Principal strain was observed in the same region, with a mean value of 12.3% ± 2.99% at the aneurysm sites. Previous in vitro studies have reported that stretching fibroblasts can elicit inflammatory responses. The strain magnitude obtained in this study aligns with the threshold of wall stretch reported to induce such inflammation. Furthermore, histology of the representative case revealed cellular damage and macrophage infiltration at the aneurysm initiation site. Therefore, integrating principal strain quantified through FSI with conventional hemodynamic indices offers the possibility of prospectively identifying sites of aneurysm initiation.