Numerical Simulation of Wall Shear Stress Conditions and Platelet Localization in Realistic End-to-Side Arterial Anastomoses

2003 ◽  
Vol 125 (5) ◽  
pp. 671-681 ◽  
Author(s):  
P. Worth Longest ◽  
Clement Kleinstreuer
Keyword(s):  
Shear Stress ◽  
Wall Shear Stress ◽  
Bypass Graft ◽  
Self Regulation ◽  
Suture Line ◽  
Cellular Level ◽  
Vascular Surface ◽  
Wall Shear ◽  
Wall Interactions ◽  
Near Wall

Research studies over the last three decades have established that hemodynamic interactions with the vascular surface as well as surgical injury are inciting mechanisms capable of eliciting distal anastomotic intimal hyperplasia (IH) and ultimate bypass graft failure. While abnormal wall shear stress (WSS) conditions have been widely shown to affect vascular biology and arterial wall self-regulation, the near-wall localization of critical blood particles by convection and diffusion may also play a significant role in IH development. It is hypothesized that locations of elevated platelet interactions with reactive or activated vascular surfaces, due to injury or endothelial dysfunction, are highly susceptible to IH initialization and progression. In an effort to assess the potential role of platelet-wall interactions, experimentally validated particle-hemodynamic simulations have been conducted for two commonly implemented end-to-side anastomotic configurations, with and without proximal outflow. Specifically, sites of significant particle interactions with the vascular surface have been identified by a novel near-wall residence time (NWRT) model for platelets, which includes shear stress-based factors for platelet activation as well as endothelial cell expression of thrombogenic and anti-thrombogenic compounds. Results indicate that the composite NWRT model for platelet-wall interactions effectively captures a reported shift in significant IH formation from the arterial floor of a relatively high-angle (30 deg) graft with no proximal outflow to the graft hood of a low-angle graft (10 deg) with 20% proximal outflow. In contrast, other WSS-based hemodynamic parameters did not identify the observed system-dependent shift in IH formation. However, large variations in WSS-vector magnitude and direction, as encapsulated by the WSS-gradient and WSS-angle-gradient parameters, were consistently observed along the IH-prone suture-line region. Of the multiple hemodynamic factors capable of eliciting a hyperplastic response at the cellular level, results of this study indicate the potential significance of platelet-wall interactions coinciding with regions of low WSS in the development of IH.

Relative Contribution of Wall Shear Stress and Injury in Experimental Intimal Thickening at PTFE End-to-Side Arterial Anastomoses

2001 ◽  
Vol 124 (1) ◽  
pp. 44-51 ◽  
Author(s):  
Francis Loth ◽  
Steven A. Jones ◽  
Christopher K. Zarins ◽  
Don P. Giddens ◽  
Raja F. Nassar ◽  
...  
Keyword(s):  
Shear Stress ◽  
Wall Shear Stress ◽  
Bypass Graft ◽  
Suture Line ◽  
Computer Assisted ◽  
Ptfe Graft ◽  
Intimal Thickening ◽  
Relative Contribution ◽  
Wall Shear

Background : Intimal hyperplastic thickening (IHT) is a frequent cause of prosthetic bypass graft failure. Induction and progression of IHT is thought to involve a number of mechanisms related to variation in the flow field, injury and the prosthetic nature of the conduit. This study was designed to examine the relative contribution of wall shear stress and injury to the induction of IHT at defined regions of experimental end-to-side prosthetic anastomoses. Methods and Results: The distribution of IHT was determined at the distal end-to-side anastomosis of seven canine Iliofemoral PTFE grafts after 12 weeks of implantation. An upscaled transparent model was constructed using the in vivo anastomotic geometry, and wall shear stress was determined at 24 axial locations from laser Doppler anemometry measurements of the near wall velocity under conditions of pulsatile flow similar to that present in vivo. The distribution of IHT at the end-to-side PTFE graft was determined using computer assisted morphometry. IHT involving the native artery ranged from 0.0±0.1 mm to 0.05±0.03 mm. A greater amount of IHT was found on the graft hood (PTFE) and ranged from 0.09±0.06 to 0.24±0.06 mm. Nonlinear multivariable logistic analysis was used to model IHT as a function of the reciprocal of wall shear stress, distance from the suture line, and vascular conduit type (i.e. PTFE versus host artery). Vascular conduit type and distance from the suture line independently contributed to IHT. An inverse correlation between wall shear stress and IHT was found only for those regions located on the juxta-anastomotic PTFE graft. Conclusions: The data are consistent with a model of intimal thickening in which the intimal hyperplastic pannus migrating from the suture line was enhanced by reduced levels of wall shear stress at the PTFE graft/host artery interface. Such hemodynamic modulation of injury induced IHT was absent at the neighboring artery wall.

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.

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).

Preliminary Near Wall Hemodynamic Evaluation of a Coronary Artery Bypass Graft Model With a Flow Streamlining Implant

2002 ◽  
Author(s):  
Pedro D. Pedroso ◽  
Andreas S. Anayiotos ◽  
Brad L. Hershey ◽  
Evangelos Eleftheriou ◽  
William L. Holman
Keyword(s):  
Shear Stress ◽  
Coronary Artery ◽  
Wall Shear Stress ◽  
Coronary Artery Bypass Graft ◽  
Coronary Artery Bypass ◽  
Saphenous Vein ◽  
Artery Bypass ◽  
Bypass Graft ◽  
Artery Bypass Graft ◽  
Wall Shear

Coronary artery disease (CAD) is the leading cause of death in the world today. According to the American Heart Association 529,659 people in 1999 died as a result of CAD [1]. Starting in the 1960’s, surgeons have used Coronary Artery Bypass Graft (CABG) techniques in order to reestablish blood flow to the heart. Today, the procedure remains the same, using autologous grafts, such as the mammary artery and the saphenous vein. An unresolved problem, is that a significant number of CABGs reocclude months to years postoperatively. In the case of Saphenous Vein Grafts (SVGs) typically 50% of these bypasses are totally occluded months to years after the procedure, the remaining half being more than 50% occluded [2]. The re-occlusion of CABGs is due to a process labeled intimal hyperplasia (IH). Investigators have shown that IH, believed by some to be a remodeling process, occurs at branch sites, regions of curvature, and anastomotic junctions [3,4]. At these sites there are low residence times, slow secondary structures, disturbed flow, and areas of recirculation, therefore the onset of IH is believed to be hemodynamically linked. Most recently, floor IH has been attributed to four variables: time averaged wall shear stress (WSS), oscillating shear index (OSI), spatial wall shear stress gradients (WSSG), and temporal WSSG [5]. Adverse values of these parameters, in the case of SVGs, are believed to be caused by impedance mismatch at the anastomosis site. Over time this characteristic causes a bulge at the sinus. Such a morphology additionally contributes to disturbed flows which tend to propagate down the CABG and are believed to play a major role in the development of IH and the eventual failure of the graft.

The Law of the Wall for Swirling Flow in Annular Ducts

1989 ◽  
Vol 111 (2) ◽  
pp. 160-164 ◽  
Author(s):  
R. J. Kind ◽  
F. M. Yowakim ◽  
S. A. Sjolander
Keyword(s):  
Shear Stress ◽  
Wall Shear Stress ◽  
Swirling Flow ◽  
Tangential Velocity ◽  
Wall Region ◽  
Law Of The Wall ◽  
Resultant Velocity ◽  
The Law ◽  
Wall Shear ◽  
Near Wall

Expressions for the logarithmic portion of the law of the wall are derived for the axial and tangential velocity components of swirling flow in annular ducts. These expressions involve new shear-velocity scales and curvature terms. They are shown to agree well with experiment over a substantial portion of the flow near both walls of an annulus. The resultant velocity data also agree with the law of the wall. The success of the proposed logarithmic expressions implies that the mixing-length model used in deriving them correctly describes flow-velocity behavior. This model indicates that the velocity gradient at any height y in the near-wall region is determined by the wall shear stress, not by the local shear stress. This suggests that the influence of wall shear stress is dominant and that it determines the near-wall wall flow even in flows with curvature and pressure gradient. A physical explanation is suggested for this.

scholarly journals Effect of reverse flow on the pattern of wall shear stress near arterial branches

2011 ◽  
Vol 8 (64) ◽  
pp. 1594-1603 ◽  
Author(s):  
A. Kazakidi ◽  
A. M. Plata ◽  
S. J. Sherwin ◽  
P. D. Weinberg
Keyword(s):  
Shear Stress ◽  
Wall Shear Stress ◽  
Steady Flow ◽  
Stokes Equations ◽  
Reverse Flow ◽  
Side Branch ◽  
Navier Stokes ◽  
Wall Region ◽  
Wall Shear ◽  
Near Wall

Atherosclerotic lesions have a patchy distribution within arteries that suggests a controlling influence of haemodynamic stresses on their development. The distribution near aortic branches varies with age and species, perhaps reflecting differences in these stresses. Our previous work, which assumed steady flow, revealed a dependence of wall shear stress (WSS) patterns on Reynolds number and side-branch flow rate. Here, we examine effects of pulsatile flow. Flow and WSS patterns were computed by applying high-order unstructured spectral/hp element methods to the Newtonian incompressible Navier–Stokes equations in a geometrically simplified model of an aorto-intercostal junction. The effect of pulsatile but non-reversing side-branch flow was small; the aortic WSS pattern resembled that obtained under steady flow conditions, with high WSS upstream and downstream of the branch. When flow in the side branch or in the aortic near-wall region reversed during part of the cycle, significantly different instantaneous patterns were generated, with low WSS appearing upstream and downstream. Time-averaged WSS was similar to the steady flow case, reflecting the short duration of these events, but patterns of the oscillatory shear index for reversing aortic near-wall flow were profoundly altered. Effects of reverse flow may help explain the different distributions of lesions.

Characterizing Flow in the Vertebro-Basilar System Using MR in Conjunction With Subject-Specific Computational Models

2010 ◽  
Author(s):  
Amanda K. Wake ◽  
John C. Gore ◽  
J. Christopher Gatenby
Keyword(s):  
Shear Stress ◽  
Wall Shear Stress ◽  
Vascular Graft ◽  
Graft Failure ◽  
Computational Models ◽  
Artery Bypass ◽  
Bypass Graft ◽  
Arterial Graft ◽  
Vessel Patency ◽  
Wall Shear

Coronary artery bypass graft failure is often a consequence of intimal hyperplasia (IH), which correlates with hemodynamic factors (e.g., wall shear stress); this relationship has been used to evaluate arterial graft design [e.g., 1–4]. The vertebro-basilar system is a native arterial merge (i.e., two arteries, the vertebrals, converge into a single artery, the basilar artery); thus, characterizing the flow field of this system in healthy subjects could be useful for early detection of anomalies (e.g., aneurysms) or for vascular graft design improvements to ensure graft/vessel patency. This study uses high field MR and phase contrast MR (PCMR) to investigate the hemodynamics of the vertebro-basilar system in a healthy, adult subject for predicting pathophysiologically-relevant flow patterns (e.g., low wall shear stress) that are related to IH and subsequent graft failure.

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