Fluid-structure Interaction Analysis of Intracranial Atherosclerosis Disease (ICAD): Moderate and Severe Stenosis Cases

Q: What is the clinical evidence from this study?

Population: Intracranial Atherosclerosis Disease (ICAD) (n=1). Intervention: Severe intracranial arterial stenosis (70% blockage) vs. Moderate intracranial arterial stenosis (50% blockage). Primary outcome: Vessel hemodynamic parameters (velocity, pressure, wall shear stress) and structural responses (deformation, equivalent stress, elastic strain).

Q: What does this research mean for the field?

Severe intracranial atherosclerosis disease stenosis (70%) markedly increases hemodynamic loading—elevating maximum velocity by 70.5% and wall shear stress by 20.9%—and raises arterial structural deformation and stress by approximately 17–18% compared to moderate stenosis (50%). Novelty: ClaimNovelty.NOVEL_FINDING. Consensus alignment: ConsensusAlignment.NEUTRAL.

M. N. I. Muhamad Nazri; Adi Azriff Basri; M. Tamagawa; K. Sagara; A. H. K. Yusof Khan; E. R. M. Tohit; M. F. Al-Khafiz Kamis; M. T. H. Sultan

doi:10.47176/jafm.20.1.4738

November 12, 2026Journal of Applied Fluid MechanicsOpen Access

Fluid-structure Interaction Analysis of Intracranial Atherosclerosis Disease (ICAD): Moderate and Severe Stenosis Cases

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Key result

Severe vs moderate ICAD increases peak velocity ~71% and worsens wall shear stress in FSI models.

n=1

Why the study?

This study was conducted to investigate the effects of intracranial atherosclerosis disease (ICAD) severity on vessel hemodynamics and structural response across the cardiac cycle.

Key Points

To evaluate how intracranial atherosclerosis disease severity affects vessel hemodynamics and arterial wall structural mechanics using fluid-structure interaction simulations.
Constructed patient-specific models of the Circle of Willis from computed tomography scans, focusing on moderate (50%) and severe (70%) stenosis in the left posterior communicating artery.
Conducted one-way fluid-structure interaction simulations in ANSYS 25 across the cardiac cycle to quantify velocity, pressure drop, wall shear stress, total deformation, equivalent stress, and elastic strain.
Performed a pulsatile physical flow experiment using pressure transducers across four outlets to validate computational pressure predictions.
Compared with 50% stenosis, the 70% stenosis model showed a 70.5% increase in maximum velocity, 6.74% higher pressure, and 20.9% higher wall shear stress.
Pressure drops during peak systole reached 6.6% for 70% stenosis compared to 1.1% for 50% stenosis.
Structural wall loading increased near the stenosis, with deformation, equivalent stress, and elastic strain rising by approximately 18%, 17%, and 18.1%, while experimental validation demonstrated a 6.54% mean difference in periodic pressure.

Structured PICO

P

Population

Computational fluid-structure interaction model of a single patient's Circle of Willis with left posterior communicating artery stenosis simulated across three cardiac cycles (3 seconds).

E

Exposure

One-way Fluid-Structure Interaction (FSI) simulation of severe intracranial atherosclerosis (70% lumen diameter stenosis by WASID method) over 3 cardiac cycles (3 seconds).

C

Comparator

One-way Fluid-Structure Interaction (FSI) simulation of moderate intracranial atherosclerosis (50% lumen diameter stenosis by WASID method) over 3 cardiac cycles (3 seconds).

O

Outcome

Hemodynamic parameters (maximum velocity, pressure drop, wall shear stress, flow streamlines) and structural vessel wall responses (total deformation, equivalent stress, equivalent elastic strain) throughout the cardiac cycle (early systole, peak systole, early diastole, late diastole).surrogate

Limitations

Simplified stenosis characteristics without variations in stenosis length, eccentricity, lumen centerline geometry, or plaque morphology
Boundary conditions used general blood flow properties from literature rather than patient-specific measurements
Linearly elastic vessel wall material assumption with uniform 0.3 mm thickness rather than hyperelastic properties
Plaque-specific material properties were not considered
One-way FSI coupling approach used instead of two-way coupling
Experimental validation only assessed outlet pressure and did not directly validate local flow quantities such as wall shear stress and velocity distribution
Simplified stenosis characteristics ignoring variations in stenosis length, eccentricity, lumen centerline geometry, and plaque morphology
General literature-based blood flow boundary conditions rather than patient-specific hemodynamic data
Linearly elastic vessel wall assumption with uniform 0.3 mm thickness rather than hyperelastic material modeling, and lack of plaque-specific material properties
One-way FSI coupling rather than two-way coupling
Experimental validation evaluated only outlet pressures and did not directly validate local velocity distributions or wall shear stress

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Implication

Computational fluid-structure interaction modeling demonstrates that progression from moderate (50%) to severe (70%) intracranial arterial stenosis markedly amplifies local flow velocity, wall shear stress, pressure drop, and mechanical wall strain near the stenotic throat.

Abstract

This study investigated the effects of Intracranial Atherosclerosis Disease (ICAD) severity on vessel hemodynamics and structural response using one-way Fluid–Structure Interaction (FSI) simulations performed in ANSYS 25, comparing moderate (50% stenosis) and severe (70% stenosis) cases. A validation experiment was also conducted to support the simulation results. Key parameters including velocity profile, pressure drop, wall shear stress, flow vectors, total deformation, equivalent stress, and equivalent elastic strain were analyzed throughout the cardiac cycle. The results showed that increasing ICAD severity significantly altered both hemodynamic and structural behavior. Compared to 50% stenosis, the 70% stenosis model exhibited a 70.5% increase in maximum velocity, 6.74% higher pressure, and 20.9% higher wall shear stress. During peak systole, pressure drops were 6.6% for 70% stenosis and 1.1% for 50% stenosis. Structural responses also increased, with deformation, equivalent stress, and elastic strain rising by approximately 18%, 17%, and 18.1%, respectively, concentrated near the stenotic region.

Discussion

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Cite This Study

Nazri et al. (2026) studied Intracranial Atherosclerosis Disease (ICAD) (n=1). Severe intracranial arterial stenosis (70% blockage) vs. Moderate intracranial arterial stenosis (50% blockage) was evaluated on Vessel hemodynamic parameters (velocity, pressure, wall shear stress) and structural responses (deformation, equivalent stress, elastic strain). Severe ICAD stenosis increased maximum velocity by 70.5%, wall shear stress by 20.9%, and arterial wall deformation by 18% compared to moderate stenosis in FSI simulations.

synapsesocial.com/papers/6af73ac79badce7b6084da26 https://doi.org/10.47176/jafm.20.1.4738

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Fluid-structure Interaction Analysis of Intracranial Atherosclerosis Disease (ICAD): Moderate and Severe Stenosis Cases

Key Points

Structured PICO

Limitations

Ask about this paper

Implication

Abstract

Discussion

Cite This Study

Fluid-structure Interaction Analysis of Intracranial Atherosclerosis Disease (ICAD): Moderate and Severe Stenosis Cases

Key Points

Structured PICO

Limitations

Ask about this paper

Implication

Abstract

Discussion

Cite This Study

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