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 ◽  
...  

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.

2003 ◽  
Vol 125 (5) ◽  
pp. 671-681 ◽  
Author(s):  
P. Worth Longest ◽  
Clement Kleinstreuer

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.


2005 ◽  
Vol 127 (7) ◽  
pp. 1087-1098 ◽  
Author(s):  
S. Giordana ◽  
S. J. Sherwin ◽  
J. Peiró ◽  
D. J. Doorly ◽  
J. S. Crane ◽  
...  

We consider the effect of geometrical configuration on the steady flow field of representative geometries from an in vivo anatomical data set of end-to-side distal anastomoses constructed as part of a peripheral bypass graft. Using a geometrical classification technique, we select the anastomoses of three representative patients according to the angle between the graft and proximal host vessels (GPA) and the planarity of the anastomotic configuration. The geometries considered include two surgically tunneled grafts with shallow GPAs which are relatively planar but have different lumen characteristics, one case exhibiting a local restriction at the perianastomotic graft and proximal host whilst the other case has a relatively uniform cross section. The third case is nonplanar and characterized by a wide GPA resulting from the graft being constructed superficially from an in situ vein. In all three models the same peripheral resistance was imposed at the computational outflows of the distal and proximal host vessels and this condition, combined with the effect of the anastomotic geometry, has been observed to reasonably reproduce the in vivo flow split. By analyzing the flow fields we demonstrate how the local and global geometric characteristics influences the distribution of wall shear stress and the steady transport of fluid particles. Specifically, in vessels that have a global geometric characteristic we observe that the wall shear stress depends on large scale geometrical factors, e.g., the curvature and planarity of blood vessels. In contrast, the wall shear stress distribution and local mixing is significantly influenced by morphology and location of restrictions, particular when there is a shallow GPA. A combination of local and global effects are also possible as demonstrated in our third study of an anastomosis with a larger GPA. These relatively simple observations highlight the need to distinguish between local and global geometric influences for a given reconstruction. We further present the geometrical evolution of the anastomoses over a series of follow-up studies and observe how the lumen progresses towards the faster bulk flow of the velocity in the original geometry. This mechanism is consistent with the luminal changes in recirculation regions that experience low wall shear stress. In the shallow GPA anastomoses the proximal part of the native host vessel occludes or stenoses earlier than in the case with wide GPA. A potential contribution to this behavior is suggested by the stronger mixing that characterizes anastomoses with large GPA.


2010 ◽  
Vol 30 (11) ◽  
pp. 2099-2102 ◽  
Author(s):  
Nick J. Willett ◽  
Robert C. Long ◽  
Kathryn Maiellaro-Rafferty ◽  
Roy L. Sutliff ◽  
Richard Shafer ◽  
...  

Stroke ◽  
1997 ◽  
Vol 28 (5) ◽  
pp. 993-998 ◽  
Author(s):  
Agostino Gnasso ◽  
Concetta Irace ◽  
Claudio Carallo ◽  
Maria Serena De Franceschi ◽  
Corradino Motti ◽  
...  

Blood ◽  
1993 ◽  
Vol 82 (4) ◽  
pp. 1165-1174 ◽  
Author(s):  
SM Buttrum ◽  
R Hatton ◽  
GB Nash

Abstract Interaction between neutrophils and platelets at the site of vascular damage or in ischaemic tissue may promote thrombosis and/or vascular occlusion. To study this interaction, we have developed a novel technique that allows visualization of adhesion of flowing neutrophils to immobilized, activated platelets. The total number of adherent neutrophils decreased with increasing wall shear stress in the range 0.05 to 0.4 Pa. Although a proportion of the adherent neutrophils were stationary, most were rolling with a velocity greater than 0.4 micron/s. The percentage of rolling cells increased with increasing wall shear stress, but the mean rolling cell velocity was nearly independent of shear stress. Adhesion of neutrophils was nearly abolished by treatment of the platelets with antibody to P-selectin, or by treatment of neutrophils with either neuraminidase, dextran sulfate, or EDTA. Studies with a series of antibodies to L-selectin (TQ-1, Dreg- 56, LAM1–3, and LAM1–10) suggested that this molecule was one neutrophil ligand for rolling adhesion. Thus, sialylated carbohydrate on neutrophils appears essential for P-selectin-mediated adhesion, and a proportion of this ligand may be presented by L-selectin. Treatment of the neutrophils with N-formyl-methionyl-leucyl-phenylalanine decreased the number of rolling cells, and increased the rolling velocity, possibly due to shedding of neutrophil ligand(s) and/or cell shape change. In vivo, immobilized platelets could play an important role in promoting attachment of neutrophils to vessel walls, eg, by slowing neutrophils so that integrin-mediated immobilization could occur.


1994 ◽  
Vol 116 (3) ◽  
pp. 294-301 ◽  
Author(s):  
D. A. Steinman ◽  
C. Ross Ethier

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.


2012 ◽  
Vol 134 (9) ◽  
Author(s):  
Matthew D. Ford ◽  
Ugo Piomelli

Cerebral aneurysms are a common cause of death and disability. Of all the cardiovascular diseases, aneurysms are perhaps the most strongly linked with the local fluid mechanic environment. Aside from early in vivo clinical work that hinted at the possibility of high-frequency intra-aneurysmal velocity oscillations, flow in cerebral aneurysms is most often assumed to be laminar. This work investigates, through the use of numerical simulations, the potential for disturbed flow to exist in the terminal aneurysm of the basilar bifurcation. The nature of the disturbed flow is explored using a series of four idealized basilar tip models, and the results supported by four patient specific terminal basilar tip aneurysms. All four idealized models demonstrated instability in the inflow jet through high frequency fluctuations in the velocity and the pressure at approximately 120 Hz. The instability arises through a breakdown of the inflow jet, which begins to oscillate upon entering the aneurysm. The wall shear stress undergoes similar high-frequency oscillations in both magnitude and direction. The neck and dome regions of the aneurysm present 180 deg changes in the direction of the wall shear stress, due to the formation of small recirculation zones near the shear layer of the jet (at the frequency of the inflow jet oscillation) and the oscillation of the impingement zone on the dome of the aneurysm, respectively. Similar results were observed in the patient-specific models, which showed high frequency fluctuations at approximately 112 Hz in two of the four models and oscillations in the magnitude and direction of the wall shear stress. These results demonstrate that there is potential for disturbed laminar unsteady flow in the terminal aneurysm of the basilar bifurcation. The instabilities appear similar to the first instability mode of a free round jet.


Author(s):  
Risa Robinson ◽  
Lynn Fuller ◽  
Harvey Palmer ◽  
Mary Frame

Blood flow regulation in the microvascular network has been investigated by means of computational fluid dynamics, in vivo particle tracking and microchannel models. It is evident from these studies that shear stress along the wall is a key factor in the communication network that results in blood flow modification, yet current methods for shear stress determination are acknowledged to be imprecise. Micromachining technology allows for the development of implantable shear stress sensors that will enable us to monitor wall shear stress at multiple locations in arteriole bifurcations. In this study, a microchannel was employed as an in vitro model of a microvessel. Thermal shear stress sensors were used to mimic the endothelial cells that line the vessel wall. A three dimensional computational model was created to simulate the system’s thermal response to the constant temperature control circuit and related wall shear stress. The model geometry included a silicon wafer section with all the fabrication layers — silicon dioxide, poly silicon resistor, silicon nitride — and a microchannel with cross section 17 μm × 17 μm. This computational technique was used to optimize the dimensions of the system for a 0.01 Reynolds number flow at room temperature in order to reduce the amount of heat lost to the substrate and to predict and maximize the signal response. Results of the design optimization are presented and the fabrication process discussed.


Author(s):  
Pedro D. Pedroso ◽  
Andreas S. Anayiotos ◽  
Brad L. Hershey ◽  
Evangelos Eleftheriou ◽  
William L. Holman

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.


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