Continuum Scale Non Newtonian Particle Transport Model for Hæmorheology

Schenkel, Torsten; Halliday, Ian

doi:10.3390/math9172100

Cited by 5 publications

(3 citation statements)

References 35 publications

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“…Nevertheless, it would be of value to simulate blood as a particulate and we have developed a single framework methodology for this [ 35 ], but the computational requirements preclude its routine use to analyse stent haemodynamics on whole vessel scales. This suggests one should assess non-Newtonian effects using a modified constitutive law with (for a fuller description) a coupled solution of species convection-diffusion, to account for the transport of haematocrit [ 36 ]. Though very computationally expensive, this is achievable in principle, even in the presence of complex stent geometry.…”

Section: Discussionmentioning

confidence: 99%

Integrating particle tracking with computational fluid dynamics to assess haemodynamic perturbation by coronary artery stents

et al. 2022

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Aims Coronary artery stents have profound effects on arterial function by altering fluid flow mass transport and wall shear stress. We developed a new integrated methodology to analyse the effects of stents on mass transport and shear stress to inform the design of haemodynamically-favourable stents. Methods and results Stents were deployed in model vessels followed by tracking of fluorescent particles under flow. Parallel analyses involved high-resolution micro-computed tomography scanning followed by computational fluid dynamics simulations to assess wall shear stress distribution. Several stent designs were analysed to assess whether the workflow was robust for diverse strut geometries. Stents had striking effects on fluid flow streamlines, flow separation or funnelling, and the accumulation of particles at areas of complex geometry that were tightly coupled to stent shape. CFD analysis revealed that stents had a major influence on wall shear stress magnitude, direction and distribution and this was highly sensitive to geometry. Conclusions Integration of particle tracking with CFD allows assessment of fluid flow and shear stress in stented arteries in unprecedented detail. Deleterious flow perturbations, such as accumulation of particles at struts and non-physiological shear stress, were highly sensitive to individual stent geometry. Novel designs for stents should be tested for mass transport and shear stress which are important effectors of vascular health and repair.

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Section: Discussionmentioning

confidence: 99%

Integrating particle tracking with computational fluid dynamics to assess haemodynamic perturbation by coronary artery stents

et al. 2022

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“…The vessel geometry was modelled as rigid. Blood was modelled as a non-Newtonian Quemada fluid 27 with an average haematocrit of 45 percent. The maximum Reynolds number based on the inlet diameter is around 500, therefore, the flow was modelled as laminar.…”

Section: Methodsmentioning

confidence: 99%

EPAS1 Attenuates Atherosclerosis Initiation at Disturbed Flow Sites through Endothelial Fatty Acid Uptake

Pirri,

Tian,

Tardajos-Ayllon

et al. 2023

Preprint

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BackgroundAtherosclerotic plaques form unevenly due to disturbed blood flow, causing localized endothelial cell (EC) dysfunction. Obesity exacerbates this process, but the underlying molecular mechanisms are unclear. The transcription factor EPAS1 (HIF2A) has regulatory roles in endothelium, but its involvement in atherosclerosis remains unexplored. This study investigates the potential interplay between EPAS1, obesity, and atherosclerosis.MethodsResponses to shear stress were analysed using cultured porcine aortic EC exposed to flowin vitrocoupled with metabolic and molecular analyses, and by en face immunostaining of murine aortic EC exposed to disturbed flowin vivo. Obesity and dyslipidemia were induced in mice via exposure to high-fat diet or through Leptin gene deletion. The role of Epas1 in atherosclerosis was evaluated by inducible endothelial Epas1 deletion, followed by hypercholesterolemia induction (AAV-PCSK9; high-fat diet).ResultsEn facestaining revealed EPAS1 enrichment at sites of disturbed blood flow that are prone to atherosclerosis initiation. Obese mice exhibited substantial reduction in endothelial EPAS1 expression, correlating with hyperlipidaemia. Sulforaphane, a compound with known atheroprotective effects, restored EPAS1 expression and concurrently reduced plasma triglyceride levels in obese mice. Consistently, triglyceride derivatives (free fatty acids) suppressed EPAS1 in cultured EC by upregulating the negative regulator PHD3. Clinical observations revealed that reduced plasma EPAS1 correlated with increased endothelial PHD3 in obese individuals. Functionally, endothelial EPAS1 deletion increased lesion formation in hypercholesterolemic mice, indicating an atheroprotective function. Mechanistic insights revealed that EPAS1 protects arteries by maintaining endothelial proliferation by positively regulating CD36 and LIPG expression to increase fatty acid beta-oxidation.ConclusionsEndothelial EPAS1 attenuates atherosclerosis at sites of disturbed flow by maintaining EC proliferative via fatty acid uptake and metabolism. This endothelial repair pathway is inhibited in obesity, suggesting a novel triglyceride-PHD3 modulation pathway suppressing EPAS1 expression. These findings have implications for therapeutic strategies addressing vascular dysfunction in obesity.

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“…Yet, no viscosity model specifically tailored for VAD gap flows at high Reynolds numbers exists, since the available models are derived for significantly smaller Reynolds numbers (

) [ 20 , 21 ]. Hence, we aim to address this research gap by deriving a viscosity model for high

based on our previously assessed experimental results.…”

Section: Introductionmentioning

confidence: 99%

Viscosity Modeling for Blood and Blood Analog Fluids in Narrow Gap and High Reynolds Numbers Flows

Knüppel,

Malchow,

Sun

et al. 2024

Micromachines

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For the optimization of ventricular assist devices (VADs), flow simulations are crucial. Typically, these simulations assume single-phase flow to represent blood flow. However, blood consists of plasma and blood cells, making it a multiphase flow. Cell migration in such flows leads to a heterogeneous cell distribution, significantly impacting flow dynamics, especially in narrow gaps of less than 300 μm found in VADs. In these areas, cells migrate away from the walls, forming a cell-free layer, a phenomenon not usually considered in current VAD simulations. This paper addresses this gap by introducing a viscosity model that accounts for cell migration in microchannels under VAD-relevant conditions. The model is based on local particle distributions measured in a microchannels with a blood analog fluid. We developed a local viscosity distribution for flows with particles/cells and a cell-free layer, applicable to both blood and analog fluids, with particle volume fractions of up to 5%, gap heights of 150 μm, and Reynolds numbers around 100. The model was validated by comparing simulation results with experimental data of blood and blood analog fluid flow on wall shear stresses and pressure losses, showing strong agreement. This model improves the accuracy of simulations by considering local viscosity changes rather than assuming a single-phase fluid. Future developments will extend the model to physiological volume fractions up to 40%.

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Continuum Scale Non Newtonian Particle Transport Model for Hæmorheology

Cited by 5 publications

References 35 publications

Integrating particle tracking with computational fluid dynamics to assess haemodynamic perturbation by coronary artery stents

Integrating particle tracking with computational fluid dynamics to assess haemodynamic perturbation by coronary artery stents

EPAS1 Attenuates Atherosclerosis Initiation at Disturbed Flow Sites through Endothelial Fatty Acid Uptake

Viscosity Modeling for Blood and Blood Analog Fluids in Narrow Gap and High Reynolds Numbers Flows

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