Hemodynamics and wall mechanics of cerebral aneurysms at different internal carotid artery locations: A fluid–structure interaction study
TL;DR
The findings suggest that the combined hemodynamic and structural conditions may contribute to aneurysm wall degradation and progression, particularly at the ICA terminus and PCoMA locations, consistent with the higher instability risk reported clinically, however, these observations require validation in larger cohorts.
Abstract
Growth and rupture of cerebral aneurysms are strongly influenced by local hemodynamics and wall mechanics, which are dependent on aneurysm location and growth status. In this study, fluid–structure interaction is modeled for aneurysms at three internal carotid artery (ICA) locations—cavernous ICA, posterior communicating artery (PCoMA), and ICA terminus, for patient-specific growing and stable cases. Physiological pulsatile flow is prescribed at the inlet and a three-element Windkessel model is applied at the outlets to represent downstream vascular beds. Wall prestress is incorporated to approximate the in-vivo stressed configuration. The results show that the growing aneurysms exhibit larger intra-aneurysmal recirculatory flow regions, lower viscous dissipation ratio, and a greater dome area exposed to low wall shear stress (WSS) when compared with stable aneurysms. Slow-flow regions associated with daughter sacs are observed in growing aneurysms at all locations, accompanied by low WSS and relatively significant oscillatory shear index. Wall displacement and stress distributions are sensitive to flow impingement and local dome geometry, with growing aneurysms at the terminus and PCoMA locations exhibiting larger dome areas subjected to elevated displacement (up to 98% and 90%, respectively) and more concentrated tensile stress within the dome regions. These findings suggest that the combined hemodynamic and structural conditions may contribute to aneurysm wall degradation and progression, particularly at the ICA terminus and PCoMA locations, consistent with the higher instability risk reported clinically. However, these observations require validation in larger cohorts.