Computational fluid dynamics investigates hemodynamic changes in cerebral aneurysms due to calcium channel blockers, suggesting clinical benefits.
Cerebral vasospasm following subarachnoid hemorrhage (SAH) can severely compromise cerebral perfusion and elevate the risk of ischemic injury. Calcium channel-blocking (CCB) drugs, such as nimodipine, are widely used to alleviate vasospasm by inducing smooth muscle relaxation and vessel dilation. However, the detailed hemodynamic consequences of such pharmacologically induced vasodilation remain poorly understood. In this study, computational fluid dynamics (CFD) simulations were performed on three patient-specific middle cerebral artery (MCA) aneurysm models to investigate the hemodynamic effects of vessel widening representative of the CCB response. Blood was modeled as a Casson non-Newtonian fluid with hematocrit 0.42 and density 1060 kg/m 3 . Transient, pulsatile flow corresponding to one cardiac cycle (0.89 s) was simulated, and parameters such as velocity, pressure, wall shear stress (WSS), vorticity, oscillatory shear index (OSI), and area-weighted WSS (AWSS) were analyzed for both the original and widened vessel geometries. The widened (CCB-effect) models exhibited lower peak velocity and pressure, along with a 20-30% reduction in WSS and vorticity intensity at the aneurysm neck. The AWSS decreased by 10-26%, while OSI values declined across all cases, indicating reduced shear oscillations and more stable intra-aneurysmal flow. Flow streamlines and iso-surface visualizations revealed attenuated jet impingement and simplified vortex structures following vessel dilation. The findings demonstrate that CCB-induced vasodilation promotes a favorable hemodynamic environment, characterized by reduced shear load, lower pressure gradients, and improved flow stability within cerebral aneurysms. These results provide mechanistic evidence that supports the clinical role of calcium channel blockers not only in preventing vasospasm but also in mitigating hemodynamic stresses that contribute to aneurysm growth and rupture risk.
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Mechai et al. (2026) studied this question.
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