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

Author(s):  
Amanda K. Wake ◽  
John C. Gore ◽  
J. Christopher Gatenby

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.

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.


Author(s):  
Sethuraman Sankaran ◽  
Alison L. Marsden

Bypass graft (BG) surgeries involve surgical construction of a graft over a blocked blood vessel. The graft can either be native tissue of the patient or a synthetic material. Some commonly performed BG surgeries include aorto-bifemoral, femoro-popliteal, femoro-tibial, and coronary artery bypass (CABG). The operative mortality rate for CABG is around 3%. Around 15 to 30% of bypass grafts occlude within the first year of surgery, increasing to over 50% after 10 years. Graft incompatibility, and hemodynamic factors such as blood recirculation, low wall shear stress, and abnormal wall shear stress gradients play an important role in the onset and development of intimal thickening and plaque deposition (atherogenesis).


2012 ◽  
Vol 2012 ◽  
pp. 1-7 ◽  
Author(s):  
Jinli Ding ◽  
Youjun Liu ◽  
Feng Wang ◽  
Fan Bai

Competitive flow from native coronary artery is considered as a major factor in the failure of the coronary artery bypass grafts. However, the physiological effects are not very clear. The aim is to research the impact of competitive flow caused by different left anterior descending (LAD) artery stenosis degrees on hemodynamics in internal thoracic artery (ITA) bypass graft. An idealized ITA-LAD model was built in CAD tools. The degree of the competitive flow was divided into five classes according to different LAD stenosis degrees: higher (no stenosis), secondary (30% stenosis), reduced (50% stenosis), lower (75% stenosis) and no competitive flow (fully stenosis). Finite volume method was employed for the numerical simulation. The flow velocity distributions, wall shear stress and oscillatory shear index were analyzed. Results showed that higher competitive flow in the bypass graft would produce unbeneficial wall shear stress distribution associating with endothelial dysfunction and subsequent graft failure. The coronary bypass graft surgery was preferred to be carried out when the LAD stenosis was higher than 75%.


Author(s):  
Triona Campbell ◽  
Reena Cole ◽  
Michael O’Donnell

Femoral or femoropopliteal artery bypass graft junctions have a predilection for failure due to restenosis. It has been clinically proven that vascular reconstructions tend to restenose within a short period of time [1]. Extensive studies have cited wall shear stresses as being primarily responsible and definite correlations between hydrodynamic stresses in the arterial wall and arterial disease have been shown [2,3]. However intensive investigations into wall shear stresses have lead to conflicting arguments on the proliferation and propagation of stenoses. It was concluded by Freidman [4] that the intima at sites exposed to relatively high or unidirectional shears thickened initially, but as time progressed the greatest thicknesses were ultimately achieved at sites exposed to lower or more oscillatory shear environments. A contradicting view was expressed by Nazemi [5] that low wall shear stress contributed to the onset of atherosclerotic plaque formation, whilst high wall shear stress encouraging plaque growth. A number of studies have however established a statistically significant correlation between pressure and intimal hyperplasia and concluded that blood pressure and not blood flow is the primary factor responsible for the localization of atherosclerosis [6–8].


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.


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.


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.


Author(s):  
Colin W. Curtis ◽  
Michael L. Calvisi

An axisymmetric model of an intracranial saccular aneurysm is presented and analyzed. The model assumes a simplified spherical geometry for the aneurysm in order to develop insight into the mechanisms that effect wall shear stress and deformation of the membrane. A theoretical model is first developed based on Stokes’ equations for viscous flow in order to derive a stream function that describes vortical flow inside a sphere representative of flow inside a real aneurysm. This flow pattern is implemented in a finite element model of a spherical aneurysm using the software COMSOL Multiphysics. The results indicate close agreement between the theoretical and computational models in terms of the flow streamlines and location of the maximum wall shear stress. Furthermore, the computational model accounts for the deformation and stress of the membrane, showing regions of maximum tension and compression at opposite poles of the saccular membrane. This work elucidates many important results regarding the mechanics of saccular aneurysms and provides a basis for developing more physiologically realistic analyses.


2006 ◽  
Vol 29 (4) ◽  
pp. 473-478 ◽  
Author(s):  
Massimo Lemma ◽  
Andrea Innorta ◽  
Matteo Pettinari ◽  
Andrea Mangini ◽  
Guido Gelpi ◽  
...  

Sign in / Sign up

Export Citation Format

Share Document