Assessment of fluid wall shear stress and vessel wall stress in an ‘ideal’ atherosclerotic plaque model

2005 ◽  
Vol 8 (sup1) ◽  
pp. 91-92
Author(s):  
K. Dumont ◽  
P. Impellizeri ◽  
J. Ricotta ◽  
Y. Alemu ◽  
D. Bluestein
Keyword(s):  
Shear Stress ◽  
Wall Shear Stress ◽  
Atherosclerotic Plaque ◽  
Vessel Wall ◽  
Wall Stress ◽  
Wall Shear ◽  
Fluid Wall Shear Stress

scholarly journals Mis-sizing of stent promotes intimal hyperplasia: impact of endothelial shear and intramural stress

2011 ◽  
Vol 301 (6) ◽  
pp. H2254-H2263 ◽  
Author(s):  
Henry Y. Chen ◽  
Anjan K. Sinha ◽  
Jenny S. Choy ◽  
Hai Zheng ◽  
Michael Sturek ◽  
...  
Keyword(s):  
Shear Stress ◽  
Wall Shear Stress ◽  
Coronary Arteries ◽  
Vessel Wall ◽  
Solid Mechanics ◽  
Linear Regression Analysis ◽  
Wall Stress ◽  
Linear Relations ◽  
Flow Disturbances ◽  
Wall Shear

Stent can cause flow disturbances on the endothelium and compliance mismatch and increased stress on the vessel wall. These effects can cause low wall shear stress (WSS), high wall shear stress gradient (WSSG), oscillatory shear index (OSI), and circumferential wall stress (CWS), which may promote neointimal hyperplasia (IH). The hypothesis is that stent-induced abnormal fluid and solid mechanics contribute to IH. To vary the range of WSS, WSSG, OSI, and CWS, we intentionally mismatched the size of stents to that of the vessel lumen. Stents were implanted in coronary arteries of 10 swine. Intravascular ultrasound (IVUS) was used to size the coronary arteries and stents. After 4 wk of stent implantation, IVUS was performed again to determine the extent of IH. In conjunction, computational models of actual stents, the artery, and non-Newtonian blood were created in a computer simulation to yield the distribution of WSS, WSSG, OSI, and CWS in the stented vessel wall. An inverse relation ( R2 = 0.59, P < 0.005) between WSS and IH was found based on a linear regression analysis. Linear relations between WSSG, OSI, and IH were observed ( R2 = 0.48 and 0.50, respectively, P < 0.005). A linear relation ( R2 = 0.58, P < 0.005) between CWS and IH was also found. More statistically significant linear relations between the ratio of CWS to WSS (CWS/WSS), the products CWS × WSSG and CWS × OSI, and IH were observed ( R2 = 0.67, 0.54, and 0.56, respectively, P < 0.005), suggesting that both fluid and solid mechanics influence the extent of IH. Stents create endothelial flow disturbances and intramural wall stress concentrations, which correlate with the extent of IH formation, and these effects were exaggerated with mismatch of stent/vessel size. These findings reveal the importance of reliable vessel and stent sizing to improve the mechanics on the vessel wall and minimize IH.

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.

On the Effects of a Flexible Structure on Boundary Layer Stability and Transition

2011 ◽  
Vol 133 (7) ◽  
Author(s):  
Ashraf Al Musleh ◽  
Abdelkader Frendi
Keyword(s):  
Boundary Layer ◽  
Shear Stress ◽  
Wall Shear Stress ◽  
Young Modulus ◽  
Boundary Layer Transition ◽  
Beam Equation ◽  
Flexible Structure ◽  
Boundary Layer Stability ◽  
Wall Shear ◽  
Fluid Wall Shear Stress

Delaying the onset of boundary layer transition has become a major research area in the last few years. This delay can be achieved by either active or passive control techniques. In the present paper, the effects of flexible or compliant structures on boundary layer stability and transition is studied. The Orr-Sommerfeld equation coupled to a beam equation representing the flexible structure is solved for a Blasius type boundary layer. A parametric study consisting of the beam thickness and material properties is carried out. In addition, the effect of fluid wall shear stress on boundary layer stability is analyzed. It is found that high density and high Young modulus materials behave like rigid structures and therefore do not alter the stability characteristic of the boundary layer. Whereas low density and low Young modulus materials are found to stabilize the boundary layer. High values of fluid wall shear stress are found to destabilize the boundary layer. Our results are in good agreement with those published in the literature.

A New Ultrasonographic Instrument for Measuring Vessel Wall Shear Stress: Comparison to a Mathematical Model in Essential Hypertensives

1996 ◽  
pp. 403-407 ◽  
Author(s):  
Moreno Bardelli ◽  
Renzo Carretta ◽  
Domenico Dotti ◽  
Bruno Fabris ◽  
Fabio Fischetti ◽  
...  
Keyword(s):  
Mathematical Model ◽  
Shear Stress ◽  
Wall Shear Stress ◽  
Vessel Wall ◽  
Measuring Vessel ◽  
Wall Shear

Differential Gene Expression of Endothelial Cells Under High Wall Shear Stress and Spatial Gradients

2010 ◽  
Author(s):  
Jennifer Dolan ◽  
Song Liu ◽  
Hui Meng ◽  
John Kolega
Keyword(s):  
Shear Stress ◽  
Wall Shear Stress ◽  
Vessel Wall ◽  
Cerebral Aneurysms ◽  
In Vivo Studies ◽  
Spatial Gradient ◽  
Flow Acceleration ◽  
Spatial Gradients ◽  
Wall Shear

In both human and animal models, cerebral aneurysms tend to develop at the apices of bifurcations in the cerebral vasculature. Due to the focal nature of aneurysm development it has long been speculated that hemodynamics are an important factor in aneurysm susceptibility. The local hemodynamics of bifurcations are complex, being characterized by flow impingement causing a high frictional force on the vessel wall known as wall shear stress (WSS) and significant flow acceleration or deceleration, manifested as the positive or negative spatial gradient of WSS (WSSG). In vivo studies have recently identified that aneurysm initiation occurs at areas of the vessel wall that experience a combination of both high WSS and positive WSSG [1,2]

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.

Positive and Negative Wall Shear Stress Gradients Have Different Effects on Endothelial Phenotype Under High Wall Shear Stress

2011 ◽  
Author(s):  
Jennifer Dolan ◽  
Frasier Sim ◽  
Hui Meng ◽  
John Kolega
Keyword(s):  
Shear Stress ◽  
Wall Shear Stress ◽  
Vessel Wall ◽  
Cerebral Aneurysms ◽  
In Vivo Studies ◽  
Spatial Gradient ◽  
Cerebral Vasculature ◽  
High Wall Shear Stress ◽  
Wall Shear

In both human and animal models, cerebral aneurysms tend to develop at the apices of bifurcations in the cerebral vasculature where the blood vessel wall experiences complex hemodynamics. In vivo studies have recently revealed that the initiation of cerebral aneurysms is confined to a well-defined hemodynamic microenvironment [1,2]. Metaxa et al. [2] found that early aneurysm remodeling initiates where the vessel wall experiences high wall shear stress (WSS) and flow is accelerating, thus creating a positive spatial gradient in WSS (WSSG). Closer examination of such in vivo studies reveals that exposure of the vessel wall to equally high WSS in the presence of decelerating flow, that is, negative WSSG, does not result in aneurysm-like destruction.

A Numerical Multiscale Study of the Haemodynamics in an Image-Based Model of Human Carotid Artery Bifurcation

2009 ◽  
Author(s):  
Diego Gallo ◽  
Raffaele Ponzini ◽  
Filippo Consolo ◽  
Diana Massai ◽  
Luca Antiga ◽  
...  
Keyword(s):  
Fluid Dynamics ◽  
Blood Flow ◽  
Shear Stress ◽  
Wall Shear Stress ◽  
Cardiovascular System ◽  
Vessel Wall ◽  
3D Model ◽  
Carotid Bifurcation ◽  
Wall Shear ◽  
Flow Division

The initiation and progression of vessel wall pathologies have been linked to disturbances of blood flow and altered wall shear stress. The development of computational techniques in fluid dynamics, together with the increasing performances of hardware and software allow to routinely solve problems on a virtual environment, helping to understand the role of biomechanics factors in the healthy and diseased cardiovascular system and to reveal the interplay of biology and local fluid dynamics nearly intractable in the past, opening to detailed investigation of parameters affecting disease progression. One of the major difficulties encountered when wishing to model accurately the cardiovascular system is that the flow dynamics of the blood in a specific vascular district is strictly related to the global systemic dynamics. The multiscale modelling approach for the description of blood flow into vessels consists in coupling a detailed model of the district of interest in the framework of a synthetic description of the surrounding areas of the vascular net [1]. In the present work, we aim at evaluating the effect of boundary conditions on wall shear stress (WSS) related vessel wall indexes and on bulk flow topology inside a carotid bifurcation. To do it, we coupled an image-based 3D model of carotid bifurcation (local computational domain), with a lumped parameters (0D) model (global domain) which allows for physiological mimicking of the haemodynamics at the boundaries of the 3D carotid bifurcation model here investigated. Two WSS based blood-vessel wall interaction descriptors, the Time Averaged WSS (TAWSS), and the Oscillating Shear Index (OSI) were considered. A specific Lagrangian-based “bulk” blood flow descriptor, the Helical Flow Index (HFI) [2], was calculated in order to get a “measure” of the helical structure in the blood flow. In a first analysis the effects of the coupled 0D models on the 3D model are evaluated. The results obtained from the multiscale simulation are compared with the results of simulations performed using the same 3D model, but imposing a flow rate at internal carotid (ICA) outlet section equal to the maximum (60%) and the minimum (50%) flow division obtained out from ICA in the multiscale model simulation (the presence of the coupled 0D model gives variable internal/external flow division ratio during the cardiac cycle), and a stress free condition on the external carotid (ECA).

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