Fluid-structure interaction analysis of stenosed carotid arteries: Evaluating hemodynamics, plaque vulnerability, and endothelial stimulation potential

Document Type

Article

Publication Title

Results in Engineering

Abstract

Atherosclerosis is a serious cardiovascular disease because of its asymptomatic behavior at its initial stage. This study investigates the hemodynamics in an idealized stenosed carotid artery using Fluid – Structure Interaction (FSI) approach to enumerate the interaction of arterial wall and blood flow. This study evaluated the hemodynamic parameters such as velocity, wall shear stress (WSS), oscillatory shear index, relative residence time (RRT), endothelial stimulation potential (ESP), vorticity and helicity. A non – Newtonian Carreau – Yasuda model was used to mimic the non – Newtonian behavior and a linear isotropic material was used for arterial wall. An idealized plaque was added in the arterial wall at the sinus region that induced approximately 20 % stenosis. The results reveal signification variations in the hemodynamic patterns near the stenosis, with increased velocity, high OSI, and reduced WSS at critical locations. Elevated OSI at the sinus suggest turbulent flow patterns and disruption of endothelial layers that potentially accelerate atherosclerosis progression. The study also highlights the plaque induced flow disturbances that include recirculation zones and altered helicity contours that impair particle retention and plaque growth. The relative residence time metric (RRT) emphasize prolonged blood residence at the sinus, contributing to accumulation of lipids and progression of plaque. The study underscores the importance of FSI in capturing realistic behavior as compared to rigid wall assumption. The study gives important information about how atherosclerosis develops and how vulnerable plaque is. Future research that incorporates patient-specific geometries and hyperelastic artery properties could improve these findings and increase predictive models for ischemic stroke and related cardiovascular disorders.

DOI

10.1016/j.rineng.2025.105943

Publication Date

9-1-2025

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