WALL SHEAR STRESS GRADIENT ANALYSIS WITHIN AN IDEALIZED STENOSIS USING NON-NEWTONIAN FLOW

Neurosurgery ◽  
2007 ◽  
Vol 61 (4) ◽  
pp. 853-864 ◽  
Author(s):  
Clemens M. Schirmer ◽  
Adel M. Malek

Abstract OBJECTIVE The endothelium is functionally regulated by the magnitude and spatiotemporal gradients of wall shear stress (WSS). Although flow separation and reversal occur beyond high-grade stenoses, little is known of the WSS pattern within clinically relevant mild to moderate stenoses. METHODS An axisymmetric geometry with 25, 50, and 75% stenosis criteria (quantified in accordance with the North American Symptomatic Carotid Endarterectomy Trial) was used to generate a high-resolution, hybrid, tetrahedral-hexahedral computational mesh with boundary-layer enrichment to improve near-wall shear stress gradient (WSSG) computation. Time-dependent computational fluid dynamic analysis was performed using a non-Newtonian Carreau-Yasuda model of blood to yield the shear-dependent viscosity. RESULTS Transition to secondary flow patterns was demonstrated in stenoses of 25, 50, and 75%. A focal region with near-wall flow reversal and retrograde WSS was identified within the stenosis itself and was found to migrate cyclically during the cardiac pulse. A zone of zero WSS and divergent WSSG that shifts in toward the throat with increasing stenotic severity was identified. Focal zones of high WSSG with converging and/or diverging direction were uncovered within the stenosis itself, as were expected changes in the distal poststenotic region. These zones of divergent WSSG shift over a substantial length of the stenosis during the course of the cardiac cycle. CONCLUSION Luminal WSS demonstrates dynamic direction reversal and high spatial gradients within the distal stenosis throat of even clinically moderate lesions. These findings shed light on the complex vessel wall hemodynamics within clinical stenoses and reveal a mechanical microenvironment that is conducive to perpetual endothelial functional dysregulation and stenosis progression.

1995 ◽  
Vol 117 (3) ◽  
pp. 350-357 ◽  
Author(s):  
M. Lei ◽  
C. Kleinstreuer ◽  
G. A. Truskey

Atherosclerosis, a disease of large- and medium-size arteries, is the chief cause of death in the US and most of the western world. It is widely accepted that the focal nature of the disease in arterial bends, junctions, and bifurcations is directly related to locally abnormal hemodynamics, often labeled “disturbed flows.” Employing the aorto-celiac junction of rabbits as a representative atherosclerotic model and considering other branching blood vessels with their distinctive input wave forms, it is suggested that the local wall shear stress gradient (WSSG) is the single best indicator of nonuniform flow fields leading to atherogenesis. Alternative predictors of susceptible sites are briefly evaluated. The results discussed include transient velocity vector fields, wall shear stress gradient distributions, and a new dimensionless parameter for the prediction of the probable sites of stenotic developments in branching blood vessels. Some of the possible underlying biological aspects of atherogenesis due to locally significant |WSSG|-magnitudes are briefly discussed.


2016 ◽  
Vol 10 (5) ◽  
pp. 054119 ◽  
Author(s):  
Hyung Woo Kim ◽  
Seonjin Han ◽  
Wonkyoung Kim ◽  
Jiwon Lim ◽  
Dong Sung Kim

2011 ◽  
Vol 32 (3) ◽  
pp. 587-594 ◽  
Author(s):  
Z. Kulcsár ◽  
Á. Ugron ◽  
M. Marosfői ◽  
Z. Berentei ◽  
G. Paál ◽  
...  

1997 ◽  
Vol 41 ◽  
pp. 27-27
Author(s):  
Michael D. VanAuker ◽  
Theresa A. Tacy ◽  
Gunnlaugur Sigfusson ◽  
Pedro J. Del Nido ◽  
Edward G. Cape

2004 ◽  
Vol 20 (5) ◽  
pp. 587-596 ◽  
Author(s):  
Thomas M. Farmakis ◽  
Johannes V. Soulis ◽  
George D. Giannoglou ◽  
George J. Zioupos ◽  
George E. Louridas

2006 ◽  
Vol 39 ◽  
pp. S312
Author(s):  
E. Metaxa ◽  
J. Kolega ◽  
M.P. Szymanski ◽  
Z.J. Wang ◽  
D.D. Swartz ◽  
...  

2015 ◽  
Vol 15 (01) ◽  
pp. 1550008 ◽  
Author(s):  
YULIN FU ◽  
AIKE QIAO ◽  
LONG JIN

The further rupture of atherosclerotic ulceration plaque is one of the main triggers of the carotid ischemic stroke. However, the abnormal hemodynamics is not well addressed yet. A lesion-based computational fluid dynamic (CFD) analysis is proposed to investigate the complex hemodynamic change of the ulceration plaque that prevails in patients. The 3D models including eight groups of ulcerations (six groups with single ulceration and two groups with two consecutive ulcerations), were reconstructed based on the computer tomography (CT) images, and the tetrahedral grid was taken to mesh the models with the appropriate numbers. After setting the boundary conditions, numerical simulation was carried out to analyze the pulsatile blood flow in the models. The complex flow in the vicinity of the ulcerations directly leads to a significant effect on the distribution of the wall shear stress (WSS). WSS is respectively from 3.29 to 35.41 Pa at the upstream, from 11.90 to 41.85 Pa at the downstream ulceration, and 18.60 and 30.60 Pa in the area between the two consecutive ulcerations. The rupture from these regions could cause the further rupture of ulceration plaques, particularly at the downstream ulceration and the area between the two consecutive ulcerations. The twisting and the curling of the flow at the ulcerations can lead to thrombosis which may break free later and go through the downstream stenosis by the effect of the flow. The different degrees of WSS in downstream and upstream ulcerations will damage the ulceration on the plaque because of pulling and stretching forces at the ulcerations. Furthermore, high wall shear stress gradient (WSSG) also increases the risk of the further rupture. Our study gives a better understanding in the further rupture mechanism of ulceration plaques and provides the information of the location of thrombosis after aggravated rupturing, which can be referred by surgeons to improve the surgical planning.


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