Hemodynamic impact of blood viscosity in intracranial atherosclerotic arteries with varying stenosis severity: A non-newtonian computational fluid dynamics patient specific study

Figures

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  Fig 1. Reconstruction of the patient-derived intracranial arterial geometry from CTA data and generation of simplified stenosis variants (30%, 50%, and 90%) on the same anatomical background. The original bifurcating model exhibits approximately 70% stenosis, and the additional models were created by locally modifying stenosis severity for controlled comparison.

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  Fig 2. Three-dimensional reconstructed intracranial artery geometry showing the inlet, two outlets, and the characteristic cross-sections used for hemodynamic analysis. Three representative sections were defined along the stenotic branch: ES (early-stenotic section), PS (peak stenosis section), and AS (after-stenotic section). The same section definitions were applied consistently across all stenosis and viscosity cases.

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  Fig 3. Mesh dependency analysis for the baseline 70% stenosis model, showing the variation of maximum velocity with mesh density.

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  Fig 4. Mesh dependency analysis for the baseline 70% stenosis model, showing the variation of wall shear stress (WSS) with mesh density. The stabilization of WSS with mesh refinement indicates adequate near-wall resolution.

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  Fig 5. Pressure (A) and velocity (C) distributions in a stenotic intracranial artery. Adapted from Computational Fluid Dynamics Modeling of Symptomatic Intracranial Atherosclerotic Disease to Predict Risk of Stroke Recurrence (Leng et al., PLOS ONE, 2022). Panels (A) and (C) were vertically rearranged to illustrate the pressure-velocity relationship.

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  Fig 6. Velocity distributions at Outlet 1 (a) and Outlet 2 (b) under different stenosis severities (30%, 50%, 70%, and 90%) and blood viscosity conditions (below-normal, normal, and high).

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  Fig 7. Velocity distributions at the early-stenotic section (ES) under different stenosis severities (30%, 50%, 70%, and 90%) and blood viscosity conditions (below-normal, normal, and high).

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  Fig 8. Velocity patterns at peak stenosis (PS) under varying stenosis ratios and viscosity conditions.

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  Fig 9. Blood flow velocity at the after stenosis (AS) site under varying stenosis ratios and viscosity conditions.

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  Fig 10. Velocity variations under below-normal, normal, and high blood viscosity conditions as functions of stenosis severity (30%, 50%, 70%, and 90%). (a) Velocity at Outlet 1, illustrating viscosity-dependent modulation of flow magnitude under moderate stenosis. (b) Velocity at Outlet 2, showing a sharp velocity collapse beyond 70% stenosis, indicating severe downstream flow limitation. (c) Velocity at the early-stenotic section (ES), highlighting the transition from acceleration-dominated to resistance-dominated flow regimes. (d) Velocity at the peak stenotic section (PS), where peak velocities are observed at moderate stenosis and decline markedly under critical narrowing. (e) Velocity at the after-stenotic section (AS), demonstrating pronounced flow deceleration and near-flow arrest at 90% stenosis.

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  Fig 11. Pressure distribution at outlet 1 (a) and outlet 2 (b) under varying stenosis ratios and viscosity conditions.

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  Fig 12. Pressure distribution at the early stenosis (ES) section under varying stenosis ratios and viscosity conditions.