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.

Hemodynamic Factors at the Distal End-to-Side Anastomosis of a Bypass Graft With Different POS:DOS Flow Ratios

2000 ◽  
Vol 123 (3) ◽  
pp. 270-276 ◽  
Author(s):  
Xue-Mei Li ◽  
Stanley E. Rittgers
Keyword(s):  
Shear Stress ◽  
Statistical Analysis ◽  
Wall Shear Stress ◽  
Intimal Hyperplasia ◽  
Bypass Graft ◽  
Stress Gradient ◽  
Great Influence ◽  
Flow Patterns ◽  
The Mean ◽  
Wall Shear

A pulsatile flow in vitro model of the distal end-to-side anastomosis of an arterial bypass graft was used to examine the effects that different flow ratios between the proximal outlet segment (POS) and the distal outlet segment (DOS) have on the flow patterns and the distributions of hemodynamic factors in the anastomosis. Amberlite particles were tracked by flow visualization to determine overall flow patterns and velocity measurements were made with Laser Doppler anemometry (LDA) to obtain detailed hemodynamic factors along the artery floor and the graft hood regions. These factors included wall shear stress (WSS), spatial wall shear stress gradient (WSSG), and oscillatory index (OSI). Statistical analysis was used to compare these hemodynamic factors between cases having different POS:DOS flow ratios (Case 1—0:100, Case 2—25:75, Case 3—50:50). The results showed that changes in POS:DOS flow ratios had a great influence on the flow patterns in the anastomosis. With an increase in proximal outlet flow, the range of location of the stagnation point along the artery floor decreased, while the extent of flow separation along the graft hood increased. The statistical results showed that there were significant differences p<0.05 for the mean WSS between cases along the graft hood, but no significant differences were detected along the artery floor. There were no significant differences for the spatial WSSG along both the artery floor and the graft hood. However, there were significant differences p<0.05 in the mean OSI between Cases 1 and 2 and between Cases 1 and 3 both along the artery floor and along the graft hood. Comparing these mechanical factors with histological findings of intimal hyperplasia formation obtained by previous canine studies, the results of the statistical analysis suggest that regions exposed to a combination of low mean WSS and high OSI may be most prone to the formation of intimal hyperplasia.

A Review On the Effect of Temporal Geometric Variations of the Coronary Arteries On the Wall Shear Stress and Pressure Drop

2021 ◽  
Author(s):  
Navid Freidoonimehr ◽  
Rey Chin ◽  
Anthony C. Zander ◽  
Maziar Arjomandi
Keyword(s):  
Shear Stress ◽  
Pressure Drop ◽  
Wall Shear Stress ◽  
Coronary Arteries ◽  
Cardiac Cycle ◽  
Temporal Variations ◽  
Hemodynamic Parameters ◽  
Clinical Environment ◽  
Cross Sectional ◽  
Wall Shear

Abstract Temporal variations of the coronary arteries during a cardiac cycle are defined as the superposition of the changes in the position, curvature, and torsion of the coronary artery axis markers and the variations in the lumen cross-sectional shape due to the distensible wall motion induced by the pulse pressure and contraction of the myocardium in a cardiac cycle. This review discusses whether the modelling the temporal variations of the coronary arteries is needed for the investigation of the hemodynamics specifically in time critical applications such as a clinical environment. The numerical modellings in the literature which model or disregard the temporal variations of the coronary arteries on the hemodynamic parameters are discussed. The results in the literature show that neglecting the effects of temporal geometric variations is expected to result in about 5\% deviation of the time-averaged pressure drop and wall shear stress values and also about 20\% deviation of the temporal variations of hemodynamic parameters, such as time-dependent wall shear stress and oscillatory shear index. This review study can be considered as a guide for the future studies to outline the conditions in which temporal variations of the coronary arteries can be neglected, while providing a reliable estimation of hemodynamic parameters.

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.

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.

Hemodynamics of the Rat Aortic Arch

2012 ◽  
Author(s):  
David S. Molony ◽  
Andrew Nencka ◽  
Zhixin Li ◽  
Ming Zhao ◽  
Don P. Giddens
Keyword(s):  
Shear Stress ◽  
Wall Shear Stress ◽  
Vascular Disease ◽  
Molecular Level ◽  
In Vivo Studies ◽  
Mechanical Stimuli ◽  
Model Studies ◽  
Plaque Development ◽  
Wall Shear

Hemodynamics have been linked to the genesis and progress of vascular disease in humans and animals1. Disturbed flow patterns such as stagnant flow or flow reversal lead to low or oscillating wall shear stress (WSS). Several in-vivo studies have correlated these types of WSS with disease formation1, 2. The desire to find correlations between markers of vascular disease and mechanical stimuli and because of their easier availability has led to an increasing number of animal model studies. The mouse, in particular, is a commonly used animal for investigating vascular disease formation and progression. Suo et al., were one of the first to relate findings on the molecular level with WSS1. They found increased VCAM and ICAM expression in areas of low WSS. More recently Hoi et al.2, have shown a correlation between atherosclerotic plaque development and hemodynamic parameters such as low time averaged wall shear stress (TAWSS) and Oscillatory Shear Index (OSI).

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