Flow patterns and wall shear stress in arteries

1980 ◽  
pp. 126-159 ◽  
Keyword(s):  
Shear Stress ◽  
Wall Shear Stress ◽  
Flow Patterns ◽  
Wall Shear

The Effect of Wall Distensibility on Flow in a Two-Dimensional End-to-Side Anastomosis

1994 ◽  
Vol 116 (3) ◽  
pp. 294-301 ◽  
Author(s):  
D. A. Steinman ◽  
C. Ross Ethier
Keyword(s):  
Shear Stress ◽  
Wall Shear Stress ◽  
Intimal Hyperplasia ◽  
Bypass Graft ◽  
Numerical Approach ◽  
Flow Patterns ◽  
Temporal Variations ◽  
Model Studies ◽  
Wall Shear ◽  
Wall Distensibility

The development of intimal hyperplasia at the distal anastomosis is the major cause of long-term bypass graft failure. To evaluate the suspected role of hemodynamic factors in the pathogenesis of distal intimal hyperplasia, an understanding of anastomotic flow patterns is essential. Due to the complexity of arterial flow, model studies typically make simplifying assumptions, such as treating the artery and graft walls as rigid. In the present study this restriction is relaxed to consider the effects of vessel wall distensibility on anastomotic flow patterns. Flow was simulated in an idealized 2-D distensible end-to-side anastomosis model, using parameters appropriate for the distal circulation and assuming a purely elastic artery wall. A novel numerical approach was developed in which the wall velocities are solved simultaneously with the fluid and pressure fields, while the wall displacements are treated via an iterative update. Both the rigid and distensible cases indicated the presence of elevated temporal variations and low average magnitudes of wall shear stress at sites known to be susceptible to the development of intimal hyperplasia. At these same sites, large spatial gradients of wall shear stress were also noted. Comparison between distensible-walled and corresponding rigid-walled simulations showed moderate changes in wall shear stress at isolated locations, primarily the bed, toe and heel. For example, in the case of a distensible geometry and a physiologic pressure waveform, the heel experienced a 38 percent increase in cycle-averaged shear stress, with a corresponding 15 percent reduction in shear stress variability, both relative to the corresponding values in the rigid-walled case. However, other than at these isolated locations, only minor changes in overall wall shear stress patterns were observed. While the physiological implications of such changes in wall shear stress are not known, it is suspected that the effects of wall distensibility are less pronounced than those brought about by changes in arterial geometry and flow conditions.

Investigation of the Effects of Dynamic Change in Curvature and Torsion on Pulsatile Flow in a Helical Tube

2012 ◽  
Vol 134 (7) ◽  
Author(s):  
N. K. C. Selvarasu ◽  
Danesh K. Tafti
Keyword(s):  
Shear Stress ◽  
Coronary Artery ◽  
Wall Shear Stress ◽  
Secondary Flow ◽  
Pulsatile Flow ◽  
Flow Patterns ◽  
Shear Stresses ◽  
Wall Shear ◽  
Vorticity Flux ◽  
Curvature And Torsion

Cardiovascular diseases are the number one cause of death in the world, making the understanding of hemodynamics and the development of treatment options imperative. The effect of motion of the coronary artery due to the motion of the myocardium is not extensively studied. In this work, we focus our investigation on the localized hemodynamic effects of dynamic changes in curvature and torsion. It is our objective to understand and reveal the mechanism by which changes in curvature and torsion contribute towards the observed wall shear stress distribution. Such adverse hemodynamic conditions could have an effect on circumferential intimal thickening. Three-dimensional spatiotemporally resolved computational fluid dynamics (CFD) simulations of pulsatile flow with moving wall boundaries were carried out for a simplified coronary artery with physiologically relevant flow parameters. A model with stationary walls is used as the baseline control case. In order to study the effect of curvature and torsion variation on local hemodynamics, this baseline model is compared to models where the curvature, torsion, and both curvature and torsion change. The simulations provided detailed information regarding the secondary flow dynamics. The results suggest that changes in curvature and torsion cause critical changes in local hemodynamics, namely, altering the local pressure and velocity gradients and secondary flow patterns. The wall shear stress (WSS) varies by a maximum of 22% when the curvature changes, by 3% when the torsion changes, and by 26% when both the curvature and torsion change. The oscillatory shear stress (OSI) varies by a maximum of 24% when the curvature changes, by 4% when the torsion changes, and by 28% when both the curvature and torsion change. We demonstrate that these changes are attributed to the physical mechanism associating the secondary flow patterns to the production of vorticity (vorticity flux) due to the wall movement. The secondary flow patterns and augmented vorticity flux affect the wall shear stresses. As a result, this work reveals how changes in curvature and torsion act to modify the near wall hemodynamics of arteries.

scholarly journals Effects of Disturbed Flow on Vascular Endothelium: Pathophysiological Basis and Clinical Perspectives

2011 ◽  
Vol 91 (1) ◽  
pp. 327-387 ◽  
Author(s):  
Jeng-Jiann Chiu ◽  
Shu Chien
Keyword(s):  
Blood Flow ◽  
Shear Stress ◽  
Wall Shear Stress ◽  
Flow Patterns ◽  
Arterial Tree ◽  
Disturbed Flow ◽  
Hemodynamic Forces ◽  
Venous Diseases ◽  
Wall Shear

Vascular endothelial cells (ECs) are exposed to hemodynamic forces, which modulate EC functions and vascular biology/pathobiology in health and disease. The flow patterns and hemodynamic forces are not uniform in the vascular system. In straight parts of the arterial tree, blood flow is generally laminar and wall shear stress is high and directed; in branches and curvatures, blood flow is disturbed with nonuniform and irregular distribution of low wall shear stress. Sustained laminar flow with high shear stress upregulates expressions of EC genes and proteins that are protective against atherosclerosis, whereas disturbed flow with associated reciprocating, low shear stress generally upregulates the EC genes and proteins that promote atherogenesis. These findings have led to the concept that the disturbed flow pattern in branch points and curvatures causes the preferential localization of atherosclerotic lesions. Disturbed flow also results in postsurgical neointimal hyperplasia and contributes to pathophysiology of clinical conditions such as in-stent restenosis, vein bypass graft failure, and transplant vasculopathy, as well as aortic valve calcification. In the venous system, disturbed flow resulting from reflux, outflow obstruction, and/or stasis leads to venous inflammation and thrombosis, and hence the development of chronic venous diseases. Understanding of the effects of disturbed flow on ECs can provide mechanistic insights into the role of complex flow patterns in pathogenesis of vascular diseases and can help to elucidate the phenotypic and functional differences between quiescent (nonatherogenic/nonthrombogenic) and activated (atherogenic/thrombogenic) ECs. This review summarizes the current knowledge on the role of disturbed flow in EC physiology and pathophysiology, as well as its clinical implications. Such information can contribute to our understanding of the etiology of lesion development in vascular niches with disturbed flow and help to generate new approaches for therapeutic interventions.

scholarly journals Hemodynamic impingement and the initiation of intracranial side-wall aneurysms

2018 ◽  
Vol 24 (3) ◽  
pp. 288-296 ◽  
Author(s):  
Gerald J Riccardello ◽  
Abhinav R Changa ◽  
Fawaz Al-Mufti ◽  
I Paul Singh ◽  
Chirag Gandhi ◽  
...  
Keyword(s):  
Shear Stress ◽  
Carotid Artery ◽  
Wall Shear Stress ◽  
Internal Carotid Artery ◽  
Secondary Flow ◽  
Internal Carotid ◽  
Fluid Dynamic ◽  
Side Wall ◽  
Flow Patterns ◽  
Wall Shear

Objective The natural history intracranial aneurysms (IA) remains poorly understood despite significant morbidity and mortality associated with IA rupture. Hemodynamic impingement resulting in elevations in wall shear stress and wall shear stress gradient (WSSG) has been shown to induce aneurysmal remodeling at arterial bifurcations. We investigate the hemodynamic environment specific to side-wall pre-aneurysmal vasculature. We hypothesize that fluid impingement and secondary flow patterns play a role in side-wall aneurysm initiation. Methods Eight side-wall internal carotid artery aneurysms from the Aneurisk repository were identified. Pre-aneurysmal vasculature was algorithmically reconstructed. Blood flow was simulated with computational fluid dynamic simulations. An indicator of isolated fluid impingement energy was developed by insetting the vessel surface and calculating the impinging component of the fluid dynamic pressure. Results Isolated fluid impingement was found to be elevated in the area of aneurysm initiation in 8/8 cases. The underlying fluid flow for each area of initiation was found to harbor secondary flow patterns known as Dean’s vortices, the result of changes in momentum imparted by bends in the internal carotid artery (ICA). Conclusion Isolated fluid impingement and secondary flow patterns may play a major role in the initiation of side-wall aneurysm initiation. We are unable to determine if this role is through direct or indirect mechanisms but hypothesize that elevations in isolated fluid impingement mark areas of cerebral vasculature that are at risk for aneurysm initiation. Thus, this indicator provides vascular locations to focus future study of side-wall aneurysm initiation.

Wall Deformation, Wall Shear Stress and Atherosclerosis Around the Intercostal Ostia of C57 Mice

2007 ◽  
Author(s):  
Jin Suo ◽  
Dardo E. Ferrara ◽  
Robert E. Guldberg ◽  
Robert W. Taylor ◽  
Don P. Giddens
Keyword(s):  
Blood Flow ◽  
Shear Stress ◽  
Wall Shear Stress ◽  
Flow Patterns ◽  
Laser Scanning Microscopy ◽  
Upstream Region ◽  
Disturbed Flow ◽  
Wall Deformation ◽  
Wall Shear ◽  
Blood Flow Patterns

Dorsal surfaces and upstream regions around ostia of aortic branches are favored sites of atherosclerosis. Both asymmetrical stresses in branch walls and disturbed flow patterns have been suggested as contributing to this localization. In the present study, fluorescence images of the thoracic aortic tree of C57 mice were obtained using quantum dot (Qdot) bioconjugate markers for vascular cell adhesion molecule-1 (VCAM-1) and two-photon excitation laser scanning microscopy. The images show that dorsal surfaces and upstream regions of intercostal ostia have a higher intensity of VCAM-1 than the downstream region. We also investigated blood flow patterns and wall shear stress (WSS) in the descending aorta and proximal intercostal branches of C57 mice using micro-CT imaging and ultrasound velocity measurements, combined with computational fluid dynamics (CFD). The latter investigation showed that dynamical wall deformation caused by pulsatile pressure around the ostia induces blood flow patterns which create lower and oscillating WSS in the upstream region and dorsal surface than in the distal region. Comparisons of the Qdot marker and CFD studies demonstrate that the distribution of greater expression of VCAM-1 corresponds with lower and oscillating WSS around the branch ostia. Thus, local wall deformation may contribute to disturbed flow patterns that are known to be associated with increased VCAM-1 expression.

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