A Computational Analysis of Sac Volume Effects on Hemodynamics and Rupture Risk in Cerebral Saccular Aneurysms

Document Type : Research Paper

Authors
1 Department of Mechanical Engineering, Iranian Research Organization for Science and Technology (IROST), Tehran, Iran
2 Department of Electromechanical Engineering, C-MAST-Center for Mechanical and Aerospace Science and Technology, Universidade da Beira Interior, Covilha, Portugal
3 Medical Research Institute/Frontier Science Center for Immunology and Metabolism, Wuhan University, 430072, China
Abstract
This study investigates the influence of aneurysm sac volume on hemodynamic factors associated with rupture risk in patient-specific anterior communicating artery (ACA) aneurysms. Six real patient-specific geometries obtained from the Aneurisk database were analyzed, encompassing a wide range of sac volumes (43–1265 mm3) while maintaining similar parent vessel radii. Blood flow was modeled using transient Navier–Stokes equations with a one-way fluid–structure interaction (FSI) approach, and the Casson non-Newtonian model was employed to represent viscosity variations associated with hematocrit levels. Three cardiac cycles were simulated under physiologically realistic boundary conditions to ensure temporal convergence. Hemodynamic indices including wall shear stress (WSS), oscillatory shear index (OSI), and sac-averaged velocity, and were evaluated across four characteristic cardiac instants. The results indicate that larger aneurysms exhibit higher sac-averaged velocities but lower localized WSS, with peak WSS concentrated at the ostium in smaller aneurysms and at the dome in larger ones. OSI values were highest near curvature-driven recirculation regions, with overall OSI decreasing as sac volume increased, except in complex multi-dome geometries. Variations in hematocrit demonstrated consistent trends of increasing viscosity leading to higher WSS and pressure but reduced intra-saccular velocity. The findings highlight the critical role of sac volume and geometric complexity in modulating intra-aneurysmal flow structures. Larger volumes tend to distribute hemodynamic stresses more uniformly, whereas smaller sacs display localized high WSS that may predispose them to rupture. These results underscore the need for patient-specific modeling to capture morphological and rheological effects that influence aneurysm stability.
Keywords
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