scholarly journals The effect of stenosis rate and Reynolds number on local flow characteristics and plaque formation around the atherosclerotic stenosis

2021 ◽  
Vol 23 (1) ◽  
Author(s):  
Xueping Chen ◽  
Yiyi Zhan ◽  
Yi Fu ◽  
Jiangguo Lin ◽  
Yanru Ji ◽  
...  
Keyword(s):  
Reynolds Number ◽  
Shear Stress ◽  
Wall Shear Stress ◽  
Atherosclerotic Plaque ◽  
Recirculation Zone ◽  
Plaque Formation ◽  
Catch Bond ◽  
Stenosis Rate ◽  
Wall Shear ◽  
Bond Region

Purpose: Atherosclerosis causes plaque to build-up in arteries. Effect of the specific local hemodynamic environment around an atherosclerotic plaque on the thrombosis formation does not remain quite clear but is believed to be crucial. The aim of this study is to uncover the flow effects on plaques formation. Methods: To study the mechanically regulated plaque formation, the flow fields in artery blood vessels with different stenosis rates at various Reynolds numbers were simulated numerically with the two-dimensional axisymmetric models, and the hemodynamic characteristics around the plaque were scaled with stenosis rate and Reynolds number. Results: The results showed that increases of both Reynolds number and stenosis rate facilitated the occurrence of flow separation phenomenon, extended recirculation zone, and upregulated the maximum normalized wall shear stress near the plaque throat section while downregulated the minimal normalized wall shear stress at the front shoulder of plaque, as it should be; in the atherosclerotic plaque leeside of the recirculation zone, an obvious catch bond region of wall shear stress might exist especially under low Reynolds number with stenosis rate smaller than 30%. This catch bond region in the plaque leeside might be responsible for the LBF (low blood flow)-enhanced formation of the atherosclerotic plaque. Conclusions: This work may provide a novel insight into understanding the biomechanical effects behind the formation and damage of atherosclerotic plaques and propose a new strategy for preventing atherosclerotic diseases.

Characterization of a Sudden Expansion Flow Chamber to Study the Response of Endothelium to Flow Recirculation

1995 ◽  
Vol 117 (2) ◽  
pp. 203-210 ◽  
Author(s):  
George A. Truskey ◽  
Kevin M. Barber ◽  
Thomas C. Robey ◽  
Lauri A. Olivier ◽  
Marty P. Combs
Keyword(s):  
Reynolds Number ◽  
Shear Stress ◽  
Wall Shear Stress ◽  
Recirculation Zone ◽  
Numerical Solutions ◽  
Flow Chamber ◽  
Sudden Expansion ◽  
Shear Stresses ◽  
Stress Gradients ◽  
Wall Shear

In order to simulate regions of flow separation observed in vivo, a conventional parallel plate flow chamber was modified to produce an asymmetric sudden expansion. The flow field was visualized using light reflecting particles and the size of the recirculation zone was measured by image analysis of the particles. Finite element numerical solutions of the two and three-dimensional forms of the Navier-Stokes equation were used to determine the wall shear stress distribution and predict the location of reattachment. For two different size expansions, numerical estimates of the reattachment point along the centerline of the flow chamber agreed well with experimental values for Reynolds numbers below 473. Even at a Reynolds number of 473, the flow could be approximated as two-dimensional for 80 percent of the chamber width. Peak shear stresses in the recirculation zone as high as 80 dyne/cm2 and shear stress gradients of 2500 (dyne/cm2)/cm were produced. As an application of this flow chamber, subconfluent bovine aortic endothelial cell shape and orientation were examined in the zone of recirculation during a 24 h exposure to flow at a Reynolds number of 267. After 24 h, gradients in cell orientation and shape were observed within the recirculation zone. At the location of reattachment, where the wall shear stress was zero but the shear stress gradients were large, cells plated at low density were still aligned with the direction of flow. No preferred orientation was observed at the gasket edge where the wall shear stress and shear stress gradients were zero. At higher cell densities, no alignment was observed at the separation point. The results suggest that endothelial cells can respond to spatial gradients of wall shear stress.

scholarly journals Temporal and spatial changes in wall shear stress during atherosclerotic plaque progression in mice

2018 ◽  
Vol 5 (3) ◽  
pp. 171447 ◽  
Author(s):  
R. Xing ◽  
A. M. Moerman ◽  
Y. Ridwan ◽  
M. J. Daemen ◽  
A. F. W. van der Steen ◽  
...  
Keyword(s):  
Shear Stress ◽  
Wall Shear Stress ◽  
Mouse Model ◽  
Atherosclerotic Plaque ◽  
Proximal Part ◽  
Plaque Progression ◽  
Plaque Composition ◽  
Spatial Changes ◽  
Temporal And Spatial ◽  
Wall Shear

Wall shear stress (WSS) is involved in atherosclerotic plaque initiation, yet its role in plaque progression remains unclear. We aimed to study (i) the temporal and spatial changes in WSS over a growing plaque and (ii) the correlation between WSS and plaque composition, using animal-specific data in an atherosclerotic mouse model. Tapered casts were placed around the right common carotid arteries (RCCA) of ApoE −/− mice. At 5, 7 and 9 weeks after cast placement, RCCA geometry was reconstructed using contrast-enhanced micro-CT. Lumen narrowing was observed in all mice, indicating the progression of a lumen intruding plaque. Next, we determined the flow rate in the RCCA of each mouse using Doppler Ultrasound and computed WSS at all time points. Over time, as the plaque developed and further intruded into the lumen, absolute WSS significantly decreased. Finally at week 9, plaque composition was histologically characterized. The proximal part of the plaque was small and eccentric, exposed to relatively lower WSS. Close to the cast a larger and concentric plaque was present, exposed to relatively higher WSS. Lower WSS was significantly correlated to the accumulation of macrophages in the eccentric plaque. When pooling data of all animals, correlation between WSS and plaque composition was weak and no longer statistically significant. In conclusion, our data showed that in our mouse model absolute WSS strikingly decreased during disease progression, which was significantly correlated to plaque area and macrophage content. Besides, our study demonstrates the necessity to analyse individual animals and plaques when studying correlations between WSS and plaque composition.

Flow and Thermal Fields in a Pendant Droplet Moving on Lyophobic Surface

2010 ◽  
Author(s):  
Basant Singh Sikarwar ◽  
K. Muralidhar ◽  
Sameer Khandekar
Keyword(s):  
Heat Transfer ◽  
Contact Angle ◽  
Reynolds Number ◽  
Shear Stress ◽  
Heat Transfer Coefficient ◽  
Wall Shear Stress ◽  
Transfer Coefficient ◽  
Maximum Shear Stress ◽  
Computational Domain ◽  
Wall Shear

Clusters of liquid drops growing and moving on physically or chemically textured lyophobic surfaces are encountered in drop-wise mode of vapor condensation. As opposed to film-wise condensation, drops permit a large heat transfer coefficient and are hence attractive. However, the temporal sustainability of drop formation on a surface is a challenging task, primarily because the sliding drops eventually leach away the lyophobicity promoter layer. Assuming that there is no chemical reaction between the promoter and the condensing liquid, the wall shear stress (viscous resistance) is the prime parameter for controlling physical leaching. The dynamic shape of individual droplets, as they form and roll/slide on such surfaces, determines the effective shear interaction at the wall. Given a shear stress distribution of an individual droplet, the net effect of droplet ensemble can be determined using the time averaged population density during condensation. In this paper, we solve the Navier-Stokes and the energy equation in three-dimensions on an unstructured tetrahedral grid representing the computational domain corresponding to an isolated pendant droplet sliding on a lyophobic substrate. We correlate the droplet Reynolds number (Re = 10–500, based on droplet hydraulic diameter), contact angle and shape of droplet with wall shear stress and heat transfer coefficient. The simulations presented here are for Prandtl Number (Pr) = 5.8. We see that, both Poiseuille number (Po) and Nusselt number (Nu), increase with increasing the droplet Reynolds number. The maximum shear stress as well as heat transfer occurs at the droplet corners. For a given droplet volume, increasing contact angle decreases the transport coefficients.

A Dynamic Procedure for Wall-Modeled Large-Eddy Simulation of High Reynolds Number Flows

2011 ◽  
Author(s):  
Soshi Kawai
Keyword(s):  
Reynolds Number ◽  
Shear Stress ◽  
Wall Shear Stress ◽  
Large Eddy Simulation ◽  
High Reynolds Number ◽  
Eddy Simulation ◽  
Large Eddy ◽  
Wall Shear ◽  
High Reynolds ◽  
Near Wall

This paper addresses the error in large-eddy simulation with wall-modeling (i.e., when the wall shear stress is modeled and the viscous near-wall layer is not resolved): the error in estimating the wall shear stress from a given outer-layer velocity field using auxiliary near-wall RANS equations where convection is not neglected. By considering the behavior of turbulence length scales near a wall, the cause of the errors is diagnosed and solutions that remove the errors are proposed based solidly on physical reasoning. The resulting method is shown to accurately predict equilibrium boundary layers at very high Reynolds number, with both realistic instantaneous fields (without overly elongated unphysical near-wall structures) and accurate statistics (both skin friction and turbulence quantities).

Evolution of wall shear stress with Reynolds number in fully developed turbulent channel flow experiments

2019 ◽  
Vol 4 (7) ◽  
Author(s):  
Pierre-Alain Gubian ◽  
Jordan Stoker ◽  
James Medvescek ◽  
Laurent Mydlarski ◽  
B. Rabi Baliga
Keyword(s):  
Reynolds Number ◽  
Shear Stress ◽  
Wall Shear Stress ◽  
Channel Flow ◽  
Turbulent Channel Flow ◽  
Wall Shear ◽  
Flow Experiments

Endothelial Cell Morphologic Response to Asymmetric Stenosis Hemodynamics: Effects of Spatial Wall Shear Stress Gradients

2010 ◽  
Vol 132 (8) ◽  
Author(s):  
Leonie Rouleau ◽  
Monica Farcas ◽  
Jean-Claude Tardif ◽  
Rosaire Mongrain ◽  
Richard L. Leask
Keyword(s):  
Endothelial Cells ◽  
Shear Stress ◽  
Endothelial Cell ◽  
Wall Shear Stress ◽  
Atherosclerotic Plaque ◽  
Morphological Changes ◽  
Stress Gradients ◽  
Spatial Gradients ◽  
Wall Shear

Endothelial cells are known to respond to hemodynamic forces. Their phenotype has been suggested to differ between atheroprone and atheroprotective regions of the vasculature, which are characterized by the local hemodynamic environment. Once an atherosclerotic plaque has formed in a vessel, the obstruction creates complex spatial gradients in wall shear stress. Endothelial cell response to wall shear stress may be linked to the stability of coronary plaques. Unfortunately, in vitro studies of the endothelial cell involvement in plaque stability have been limited by unrealistic and simplified geometries, which cannot reproduce accurately the hemodynamics created by a coronary stenosis. Hence, in an attempt to better replicate the spatial wall shear stress gradient patterns in an atherosclerotic region, a three dimensional asymmetric stenosis model was created. Human abdominal aortic endothelial cells were exposed to steady flow (Re=50, 100, and 200 and τ=4.5 dyn/cm2, 9 dyn/cm2, and 18 dyn/cm2) in idealized 50% asymmetric stenosis and straight/tubular in vitro models. Local morphological changes that occur due to magnitude, duration, and spatial gradients were quantified to identify differences in cell response. In the one dimensional flow regions, where flow is fully developed and uniform wall shear stress is observed, cells aligned in flow direction and had a spindlelike shape when compared with static controls. Morphological changes were progressive and a function of time and magnitude in these regions. Cells were more randomly oriented and had a more cobblestone shape in regions of spatial wall shear stress gradients. These regions were present, both proximal and distal, at the stenosis and on the wall opposite to the stenosis. The response of endothelial cells to spatial wall shear stress gradients both in regions of acceleration and deceleration and without flow recirculation has not been previously reported. This study shows the dependence of endothelial cell morphology on spatial wall shear stress gradients and demonstrates that care must be taken to account for altered phenotype due to geometric features. These results may help explain plaque stability, as cells in shoulder regions near an atherosclerotic plaque had a cobblestone morphology indicating that they may be more permeable to subendothelial transport and express prothrombotic factors, which would increase the risk of atherothrombosis.

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