Non-Kolmogorov turbulence in carotid artery stenosis and the impact of carotid stenting on near-wall turbulence

Khalid M Saqr,Sherif Rashad,Teiji Tominaga,Toru Iwama,Kuniyasu Niizuma,Kiyomitsu Kano,Yasuhiko Kaku

doi:10.1063/5.0076271

Khalid M Saqr, Sherif Rashad + Show 5 more

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https://doi.org/10.1063/5.0076271

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Abstract

Endovascular stents have become a standard management procedure for carotid artery stenosis. Recent discoveries related to the complex turbulence dynamics in blood flow necessitate revisiting the pathology of carotid stenosis itself and the impact of stenting on blood hemodynamics. In the present work, and for the first time, the therapeutic hemodynamic changes after carotid artery stenting are explored via high-resolution large eddy simulation of non-Newtonian multiharmonic pulsatile flow in realistic patient-specific geometries. The focus of the present study is the transition to turbulence before and after stent deployment. Transition to turbulence was characterized in space, time, and frequency domains. The multiharmonic flow had generalized a time-dependent Reynolds number of 115 ± 26 at the inlet plane of the computational domain. The inlet boundary condition was defined as a multiharmonic waveform represented by six harmonics that are responsible for transferring at least 94% of the mass flow rate in the common carotid artery. Multiharmonic non-Newtonian pulsatile flow exhibited non-Kolmogorov turbulence characteristics. The stent was found to cause a significant reduction in the velocity oscillations downstream the stenosis throat and restore the inverse kinetic energy cascade. It also stabilized hemorheological fluctuations downstream the stenosis throat. Finally, the stent had a significant effect on the kinetic energy cascade at a distance of 10 µm from the artery wall at the carotid bifurcation and stenosis throat. These findings are important to guide the design and optimization of carotid stents and have significant value in understanding the mechanisms of vascular remodeling and carotid stenosis pathophysiology and symptomatology.

Highlights

Recent discoveries related to the complex turbulence dynamics in blood flow necessitate revisiting the pathology of carotid stenosis itself and the impact of stenting on blood hemodynamics
A number of critical studies10–13 inveighed against the use of Newtonian viscosity assumption that has been promoted in the majority of published Computational Fluid Dynamics (CFD) studies on carotid artery stenosis hemodynamics
Wall Shear Stress (WSS), which is the main hemodynamic parameter investigated in mainstream CFD research,22,23 is strongly dependent on the closure model of the viscous term in the Navier–Stokes equation, and it does not possess intrinsic vector properties

Summary

Introduction

Blood flow regime and dynamics play important roles in the development of numerous vascular diseases, such as atherosclerosis, stenosis, and aneurysm. Endothelial cells (ECs) respond to hemodynamics through numerous pathways that alter the pathophysiology of the arterial wall at many levels. Rapid transient variations in blood hemodynamic pattern, which could be associated with quasi-periodic, transitional, or turbulent flow features, trigger different mechanobiological mechanisms, many of which are yet to be identified and characterized. it is crucial for the progress of vascular medicine to explore and comprehend the physics of such flow regimes as they manifest different layers of complexity in different vascular diseases.Since the emergence of Computational Fluid Dynamics (CFD) in hemodynamics research in the early 1990s, considerable effort has been made to investigate transitional flow (trans-flow) in carotid artery stenosis. Most of the CFD models were based on certain physical assumptions that could be inappropriate to unfold the complexity of the trans-flow problem as it exists. Rapid transient variations in blood hemodynamic pattern, which could be associated with quasi-periodic, transitional, or turbulent flow features, trigger different mechanobiological mechanisms, many of which are yet to be identified and characterized.. Rapid transient variations in blood hemodynamic pattern, which could be associated with quasi-periodic, transitional, or turbulent flow features, trigger different mechanobiological mechanisms, many of which are yet to be identified and characterized.7 It is crucial for the progress of vascular medicine to explore and comprehend the physics of such flow regimes as they manifest different layers of complexity in different vascular diseases. The use of ideal two-dimensional axisymmetric models to investigate the stenotic flow patterns was shown to be inadequate.26 This casts nontrivial uncertainty on the essential elements of the current paradigm of carotid artery stenosis hemodynamics. A number of critical studies inveighed against the use of Newtonian viscosity assumption that has been promoted in the majority of published CFD studies on carotid artery stenosis hemodynamics. In two recent studies, our group have shown in vivo that the Newtonian assumption is inappropriate to represent the Wall Shear Stress (WSS) of the internal carotid artery (ICA). Wall Shear Stress (WSS), which is the main hemodynamic parameter investigated in mainstream CFD research, is strongly dependent on the closure model of the viscous term in the Navier–Stokes equation, and it does not possess intrinsic vector properties. the use of ideal two-dimensional axisymmetric models to investigate the stenotic flow patterns was shown to be inadequate. This casts nontrivial uncertainty on the essential elements of the current paradigm of carotid artery stenosis hemodynamics.

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