Biomechanical study of intracranial arterial stenosis based on fractional fluid–structure interaction

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Intracranial arterial stenosis alters local hemodynamics and arterial-wall mechanics; however, the extent to which changes in stenosis geometry and bifurcation configuration alter the coupled fluid-induced wall displacement and stress response remains insufficiently quantified. In this study, a two-way fluid–structure interaction framework incorporating a fractional Maxwell model is developed to characterize the viscoelastic response of the arterial wall. The effects of plaque length, stenosis severity, and bifurcation angle on flow patterns, wall shear stress (WSS), time-averaged wall shear stress (TAWSS), oscillatory shear stress index, displacement, and von Mises stress are investigated. Increasing plaque length enhances the spatial heterogeneity of TAWSS, producing coexisting high-shear regions near the stenosis and extended low-shear regions downstream. Increasing stenosis severity promotes jet acceleration, flow separation, vortical structures, and oscillatory shear, whereas bifurcation angle has a comparatively limited influence within the investigated range. More importantly, the fluid and solid responses exhibit a distinct spatial mismatch in the representative (plaque length of 5 mm, a bifurcation angle of 45°, and stenosis rate of 70%): the highest regional WSS occurs in middle cerebral artery M1 segment, while the largest wall displacement and von Mises stress are concentrated in the stenotic segment. These results suggest that elevated WSS does not necessarily coincide spatially with the greatest wall displacement or von Mises stress, because the structural response depends on the combined effects of fluid traction, local geometry, boundary constraints, and the assumed viscoelastic constitutive behavior. In addition, increasing α or decreasing β increases the stenotic-wall displacement and alters its temporal persistence, confirming the contribution of fractional viscoelasticity to the predicted structural response.