CFD Study of the Relationship Between Wall Shear Stress and Aspect Ratio in Elastase Induced Rabbit Aneurysm Models

2008 ◽  
Author(s):  
Zijing Zeng ◽  
Hasballah Zakaria ◽  
Ramanathan Kadirvel ◽  
Yong-Hong Ding ◽  
Debra A. Lewis ◽  
...  
Keyword(s):  
Shear Stress ◽  
Aspect Ratio ◽  
Wall Shear Stress ◽  
Maximum Diameter ◽  
Altered Expression ◽  
Aneurysm Neck ◽  
Aspect Ratios ◽  
Risk Of Rupture ◽  
Wall Shear

Hemodynamic factors are thought to play an important role in the initiation, growth, and rupture of cerebral aneurysms. In-vitro studies have demonstrated a correlation between the magnitude and distribution of wall shear stress (WSS) and biological response of both endothelial cells and smooth muscle cells [1–3]. In elastase induced saccular aneurysms, low WSS (below 0.5 Pa) was found to have a correlation with altered expression of biological markers [4]. Localized regions of rapid aneurysm growth in-vivo have been shown to be associated with regions where WSS is below a critical value of 0.1 Pa [5]. Further, aspect ratio (AR), the ratio of the maximum diameter of the aneurysm to the width of the aneurysm neck, has been correlated with elevated risk of rupture [6]. The purpose of the current study is to explore the possibility of creating elastase induced aneurysms in rabbits with a range of aspect ratios (ratio of aneurysm height/neck) and evaluate the existence of a correlation between aspect ratio and WSS distribution. Aneurysms with ARs from 0.98 to 2.8 were created at the origin of the right common carotid artery (n = 30). Qualitative differences in WSS distribution were found in the high AR aneurysms (HARA) (AR>1.6) and low AR aneurysms (LARA) (AR<1.6) [7].

scholarly journals Investigation of Wall Shear Stress in Cardiovascular Research and in Clinical Practice—From Bench to Bedside

2021 ◽  
Vol 22 (11) ◽  
pp. 5635
Author(s):  
Katharina Urschel ◽  
Miyuki Tauchi ◽  
Stephan Achenbach ◽  
Barbara Dietel
Keyword(s):  
Endothelial Cells ◽  
Shear Stress ◽  
Wall Shear Stress ◽  
Cell Function ◽  
Computational Techniques ◽  
Apical Surface ◽  
Cardiovascular Research ◽  
Endothelial Cell Function ◽  
Wall Shear

In the 1900s, researchers established animal models experimentally to induce atherosclerosis by feeding them with a cholesterol-rich diet. It is now accepted that high circulating cholesterol is one of the main causes of atherosclerosis; however, plaque localization cannot be explained solely by hyperlipidemia. A tremendous amount of studies has demonstrated that hemodynamic forces modify endothelial athero-susceptibility phenotypes. Endothelial cells possess mechanosensors on the apical surface to detect a blood stream-induced force on the vessel wall, known as “wall shear stress (WSS)”, and induce cellular and molecular responses. Investigations to elucidate the mechanisms of this process are on-going: on the one hand, hemodynamics in complex vessel systems have been described in detail, owing to the recent progress in imaging and computational techniques. On the other hand, investigations using unique in vitro chamber systems with various flow applications have enhanced the understanding of WSS-induced changes in endothelial cell function and the involvement of the glycocalyx, the apical surface layer of endothelial cells, in this process. In the clinical setting, attempts have been made to measure WSS and/or glycocalyx degradation non-invasively, for the purpose of their diagnostic utilization. An increasing body of evidence shows that WSS, as well as serum glycocalyx components, can serve as a predicting factor for atherosclerosis development and, most importantly, for the rupture of plaques in patients with high risk of coronary heart disease.

In-Vitro Wall Shear Stress Measurements for Microfluid Flows by Using Second-Order SPE Micro-PIV

2007 ◽  
Author(s):  
Han-Sheng Chuang ◽  
Steven T. Wereley
Keyword(s):  
Shear Stress ◽  
Wall Shear Stress ◽  
Measurement Errors ◽  
Pearson Correlation ◽  
Second Order ◽  
Bias Error ◽  
Central Difference ◽  
Micro Piv ◽  
Wall Shear

Conventional single pixel evaluation (SPE) significantly improves the spatial resolution of PIV measurements to the physical limit of a CCD camera based on the forward difference interrogation (FDI). This paper further enhances the computational algorithm to second-order accuracy by simply modifying the numerical scheme with the central difference interrogation (CDI). The proposed central difference scheme basically superposes the forward-time and the backward-time correlation domains, thus resulting in reduced bias error as well as rapid background noise elimination. An assessment of the CDI SPE algorithm regarding the measurement errors was achieved via numerous synthetic images subject to a four-roll mill flow. In addition, preliminary wall shear stress (WSS) measurements regarding different algorithms are also evaluated with an analytical turbulent boundary flow. CDI scheme showed a 0.32% error deviated from the analytical solution and improved the same error in FFT-based correlation correlation (FFT-CC) by 32.35%. To demonstrate the performance in practice, in-vitro measurements were implemented in a serpentine microchannel made of polydimethyl siloxane (PDMS) for both CDI SPE and spatial cross-correlation. A series of steady-state flow images at five specified regions of interest were acquired using micro-PIV system. Final comparisons of the WSS regarding the Pearson correlation coefficient, R2, between the numerical schemes and the simulations showed that an overall result was improved by CDI SPE due to the fine resolution and the enhanced accuracy.

Design and Analysis of a Shear Stress Sensor for Microcirculation Investigations (Invited Paper)

2003 ◽  
Author(s):  
Risa Robinson ◽  
Lynn Fuller ◽  
Harvey Palmer ◽  
Mary Frame
Keyword(s):  
Blood Flow ◽  
Shear Stress ◽  
Wall Shear Stress ◽  
Computational Technique ◽  
Flow Modification ◽  
Stress Sensors ◽  
Shear Stress Sensors ◽  
Wall Shear

Blood flow regulation in the microvascular network has been investigated by means of computational fluid dynamics, in vivo particle tracking and microchannel models. It is evident from these studies that shear stress along the wall is a key factor in the communication network that results in blood flow modification, yet current methods for shear stress determination are acknowledged to be imprecise. Micromachining technology allows for the development of implantable shear stress sensors that will enable us to monitor wall shear stress at multiple locations in arteriole bifurcations. In this study, a microchannel was employed as an in vitro model of a microvessel. Thermal shear stress sensors were used to mimic the endothelial cells that line the vessel wall. A three dimensional computational model was created to simulate the system’s thermal response to the constant temperature control circuit and related wall shear stress. The model geometry included a silicon wafer section with all the fabrication layers — silicon dioxide, poly silicon resistor, silicon nitride — and a microchannel with cross section 17 μm × 17 μm. This computational technique was used to optimize the dimensions of the system for a 0.01 Reynolds number flow at room temperature in order to reduce the amount of heat lost to the substrate and to predict and maximize the signal response. Results of the design optimization are presented and the fabrication process discussed.

Inflammatory Response of Endothelial Cells to Wall Shear Stress in Three Dimensional Stenotic Models

2009 ◽  
Author(s):  
Leonie Rouleau ◽  
Joanna Rossi ◽  
Jean-Claude Tardif ◽  
Rosaire Mongrain ◽  
Richard L. Leask
Keyword(s):  
Endothelial Cells ◽  
Shear Stress ◽  
Wall Shear Stress ◽  
Three Dimensional ◽  
Realistic Model ◽  
In Vitro Models ◽  
Steady Flows ◽  
Wall Shear

Endothelial cells (ECs) are believed to respond differentially to hemodynamic forces in the vascular tree. Once atherosclerotic plaque has formed in a vessel, the obstruction creates complex spatial gradients in wall shear stress (WSS). In vitro models have used mostly unrealistic and simplified geometries, which cannot reproduce accurately physiological conditions. The objective of this study was to expose ECs to the complex WSS pattern created by an asymmetric stenosis. Endothelial cells were grown and exposed for different times to physiological steady flows in straight dynamic controls and in idealized asymmetric stenosis models. Cell morphology was noticeably different in the regions with spatial WSS gradients, being more randomly oriented and of cobblestone shape. Inflammatory molecule expression was also altered by exposure to shear and endothelial nitric oxide synthase (eNOS) was upregulated by its presence. A regional response in terms of inflammation was observed through confocal microscopy. This work provides a more realistic model to study endothelial cell response to spatial and temporal WSS gradients that are present in vivo and is an important advancement towards a better understanding of the mechanisms involved in coronary artery disease.

scholarly journals Combined In Silico and In Vitro Approach Predicts Low Wall Shear Stress Regions in a Hemofilter that Correlate with Thrombus Formation In Vivo

ASAIO Journal ◽  
2018 ◽  
Vol 64 (2) ◽  
pp. 211-217 ◽  
Author(s):  
Amanda K. W. Buck ◽  
Joseph J. Groszek ◽  
Daniel C. Colvin ◽  
Sara B. Keller ◽  
Clark Kensinger ◽  
...  
Keyword(s):  
Shear Stress ◽  
Wall Shear Stress ◽  
In Silico ◽  
Thrombus Formation ◽  
Wall Shear

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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