Wall Shear Stress Gradient Research Articles

Minimisation of the wall shear stress gradients in bypass grafts anastomoses using meshless CFD and genetic algorithms optimisation

The wall shear stress (WSS) spatial and temporal gradients are two hemodynamics parameters correlated with endothelial damage. Those two gradients become well pronounced in a bypass graft anastomosis geometry where the blood flow patterns are quite disturbed. The WSS gradient minimisation on the host artery floor can be achieved by optimising the anastomosis shape and hence may lead to an improved long-term post-surgical performance of the graft. The anastomosis shape optimisation can be executed via an integrated computational tool comprised of a meshless computational fluid dynamics (CFD) solver and a genetic algorithm (GA) shape optimiser. The meshless CFD solver serves to evaluate the WSS gradients and the GA optimiser serves to search for the end-to-side distal anastomosis (ETSDA) optimal shape that best minimises those gradients. We utilise a meshless CFD method to resolve hemodynamics and a GA for the purpose of optimisation. We consider three different anastomotic models: the conventional ETSDA, the Miller Cuff ETSDA and the hood ETSDA. The results reported herein demonstrate that the graft calibre should always be maximised whether a conventional or Miller Cuff ETSDA model is utilised. Also, it was noted that the Miller Cuff height should be minimised. The choice of an optimal anastomotic angle should be optimised to achieve a compromise between the concurrent minimisations of both the spatial WSS gradient and the temporal WSS gradient.

Mapping vascular response to in vivo Hemodynamics: application to increased flow at the basilar terminus

Hemodynamic forces play critical roles in vascular pathologies such as atherosclerosis, aneurysms, and stenosis. However, detailed relationships between the specific in vivo hemodynamic microenvironment and vascular responses leading to the triggering or exacerbation of pathological remodeling of the vessel remain elusive. We have developed a hemodynamics-biology co-mapping technique that enables in situ correlation between the in vivo blood flow field and vascular changes secondary to hemodynamic insult. The hemodynamics profile is obtained from computational fluid dynamics simulation within the vascular geometry reconstructed from three-dimensional in vivo images, whereas the vascular response is obtained from histology or immunohistochemistry on harvested vascular tissue. The hemodynamics field is virtually sectioned in the histological slicing planes and digitally co-mapped with the histological images, thereby enabling correlation of the specific local vascular responses with the inciting hemodynamic stresses. We demonstrate application of this technique to rabbit basilar terminus subjected to elevated flow. Morphological changes at the basilar terminus 5 days after the flow increase were co-mapped with the initial wall shear stress and wall shear stress gradient distributions, from which localization of destructive remodeling in a specific hemodynamic zone was noticed. This method paves the way for further investigations to determine the connection between in vivo mechanical stimuli and biological responses, such as initiation of aneurysmal remodeling.

A full-range, multi-variable, CFD-based methodology to identify abnormal near-wall hemodynamics in a stented coronary artery

The benefit of coronary stent implantation is reduced by excessive intimal hyperplasia which re-narrows the artery and the prevention of which is still a primary concern for clinicians. Abnormal hemodynamics create non-physiological viscous stress on the artery wall, one of the root causes of intimal hyperplasia following stent implantation. A methodology to comprehensively evaluate the viscous stress on the artery wall following stent implantation would be useful to evaluate a stent's hemodynamic performance.The proposed methodology employs 3D computational fluid dynamics, the variables wall shear stress (WSS), WSS gradient (WSSG), WSS angle gradient (WSSAG) and a statistical analysis to evaluate the viscous stress. The methodology is demonstrated and compared to a commonly used "threshold technique" for evaluating a stent's hemodynamic performance.It is demonstrated that the threshold technique is not adequate to fully analyse the viscous stress on the artery wall and can even be misleading. Furthermore, all three of the aforementioned variables should be considered as each provides a different perspective on the abnormalities that can arise in the arterial viscous stress.The hemodynamic performance of a stent can be assessed more comprehensively than with previously used methods by examining the arterial viscous stresses using the proposed methodology.

Realistic Temporal Variations of Shear Stress Modulate MMP-2 and MCP-1 Expression in Arteriovenous Vascular Access

Venous neointimal hyperplasia (VNH) lesions are prone to localized development within the vascular access junction (VAJ) and efferent vein of arteriovenous (AV) fistulae and grafts. The creation of VAJ dramatically alters the local venous hemodynamics with high pulsatile flow velocities enter the vein resulting in blood-flow separation, recirculation and flow reversal. This study conducted a computational hemodynamic investigation of an idealized AV graft and realistic AV fistula which demonstrated a complex hemodynamic environment within the VAJ, producing elevated wall shear stress (WSS) magnitudes and significant spatial and temporal WSS gradients in the VAJ. These hemodynamic patterns and non-physiological WSSs are postulated to initiate VNH development at the transcriptional level. Human umbilical vein endothelial cells (HUVEC) were exposed to elevated temporal WSS waveforms obtained from the aforementioned computational analysis, using a cone-and-plate bioreactor. Using real-time RT-PCR, early induction of MMP-2 and delayed transcriptional upregulation of MCP-1 was observed following EC exposure to VAJ high wall shear forces. These results indicate that MMP-2 and MCP-1 may be induced by high WSS present in the VAJ, suggesting a link between elevated WSS magnitudes and temporal gradients, extracellular matrix decomposition, smooth muscle cell migration and proliferation, and the subsequent VNH development in AV VAJs.

Optimization of anastomotic configuration in CABG surgery

AbstractThe geometric factors have prominent impacts on the success rate of coronary artery bypass graft (CABG). In order to clarify how to choose suitable graft‐host diameter ratio and junction angle, ANSYS9.0 was used to simulate CABG, then response surface methodology was applied to construct mathematical model, finally theory of optimization was performed to determine the optimum graft‐host diameter ratio and junction angle that could make the main factor influencing the success rate of CABG, i.e. wall shear stress gradients, smallest. The result indicates that the model of large graft‐host diameter ratio and small junction angle has better hemodynamics. It can be concluded that adopting large graft‐host diameter ratio and small junction angle with the help of clinical experiences is advisable in CABG surgery. Copyright © 2009 John Wiley & Sons, Ltd.

MOLECULAR ALTERATIONS ASSOCIATED WITH ANEURYSMAL REMODELING ARE LOCALIZED IN THE HIGH HEMODYNAMIC STRESS REGION OF A CREATED CAROTID BIFURCATION

Although elevated hemodynamics has been speculated to play a key role in intracranial aneurysm (IA) initiation, little is known about the specific hemodynamic microenvironment that triggers aneurysmal vascular degradation. We previously demonstrated maladaptive remodeling characteristic of IA initiation occurring in hemodynamic regions of combined high wall shear stress (WSS) and high WSS gradient near the apex of an experimentally created carotid bifurcation. This study examines whether this remodeling recapitulates the molecular changes found in IAs and whether molecular changes also correspond to specific hemodynamic environments. De novo bifurcations were surgically created using both native common carotid arteries in each of 6 dogs. Bifurcations were imaged 2 weeks or 2 months after surgery by high-resolution 3-dimensional angiography, from which flow fields were obtained by computational fluid dynamics simulations. Subsequently, harvested tissues, demonstrating early aneurysmal changes near the apex, were immunostained for interleukin-1beta, endothelial and inducible nitric oxide synthases, nitrotyrosine, and matrix metalloproteinase-2 and -9. Spatial distributions of these molecules were comapped with computational fluid dynamics results. The aneurysmal wall showed decreased endothelial nitric oxide synthase expression compared with surrounding segments, the feeding artery, and native controls, whereas all other markers increased. Anti-CD68 staining indicated the absence of inflammatory cells in the aneurysmal wall. Comapping molecular marker distributions with flow fields revealed confinement of these molecular changes within the hemodynamic region of high WSS and high, positive WSS gradient. Aneurysm-initiating remodeling induced by combined high WSS and high, positive WSS gradient is associated with molecular changes implicated in IAs.

Viscous, cohesive, non-Newtonian, depositing, radial slurry flow

Mining induced subsidence can significantly affect mining costs where major surface facilities and natural environment need to be protected. Overburden grout injection is a technology used to control coal mine subsidence by injecting the mine waste material extracted from the coal back into the inter-burden rock during longwall mining. The flowing slurry is here categorised as a nonlinear viscous cohesive (Bingham plastic) fluid. During longwall mining the grout slurry is pumped into the separated beds of the rock mass through a central vertical borehole, which is drilled deep into the inter-burden rock strata above the coal seam. However, a blockage can occur in the injection system when the slurry velocity falls below a certain critical threshold velocity, indicating a material phase change from cohesive-viscous to cohesive-frictional. In situ field injection tests through boreholes have been simulated at a smaller scale at the CSIRO laboratory in Brisbane by pumping the slurry through a radial disk (gap = 4 mm) from its centre. Laboratory experiments indicate a general, nonlinear, cohesive, viscous, frictional model for shear behaviour of the slurry, in which the material shear parameters are functions of the disk radial distance. Complete dimensional and dimensionless analytical solutions have been developed based on an approach related to Bingham–Herschel–Bulkley fluid mechanics. The derived formulae include relations for minimum pump pressure, local pressure and pressure gradient, wall shear stress, volume rate, velocity and velocity gradient. The theoretical results match the experimental measurements. The experiments covered slurries with maximum particle sizes of 0.5 to 2 mm with about 50% being larger than 100 µm. The viscosities at the various solids concentrations were measured with a standard torsion viscometer. This study differs from the previous research in several distinct aspects, namely, consideration of the variable shear parameters rather than fixed values, inclusion of total nonlinear behaviour, and implementation of a friction function to mimic behaviour of the deposited and consolidating stiff slurry, which can cause a significant pressure rise as a result of the increased shear resistance.

Comparison of Near-Wall Hemodynamic Parameters in Stented Artery Models

Four commercially available stent designs (two balloon expandable-Bx Velocity and NIR, and two self-expanding-Wallstent and Aurora) were modeled to compare the near-wall flow characteristics of stented arteries using computational fluid dynamics simulations under pulsatile flow conditions. A flat rectangular stented vessel model was constructed and simulations were carried out using rigid walls and sinusoidal velocity input (nominal wall shear stress of 10+/-5 dyn/cm2). Mesh independence was determined from convergence (<10%) of the axial wall shear stress (WSS) along the length of the stented model. The flow disturbance was characterized and quantified by the distributions of axial and transverse WSS, WSS gradients, and flow separation parameters. Normalized time-averaged effective WSS during the flow cycle was the smallest for the Wallstent (2.9 dyn/cm2) compared with the others (5.8 dyn/cm2 for the Bx Velocity stent, 5.0 dyn/cm2 for the Aurora stent, and 5.3 dyn/cm2 for the NIR stent). Regions of low mean WSS (<5 dyn/cm2) and elevated WSS gradients (>20 dyn/cm3) were also the largest for the Wallstent compared with the others. WSS gradients were the largest near the struts and remained distinctly nonzero for most of the region between the struts for all stent designs. Fully recirculating regions (as determined by separation parameter) were the largest for the Bx Velocity stent compared with the others. The most hemodynamically favorable stents from our computational analysis were the Bx Velocity and NIR stents, which were slotted-tube balloon-expandable designs. Since clinical data indicate lower restenosis rates for the Bx Velocity and NIR stents compared with the Wallstent, our data suggest that near-wall hemodynamics may predict some aspects of in vivo performance. Further consideration of biomechanics, including solid mechanics, in stent design is warranted.

Effects of stent sizing on endothelial and vessel wall stress: potential mechanisms for in-stent restenosis

Stent sizing and apposition have been shown to be important determinants of clinical outcome. This study evaluates the mechanical effects of undersizing and oversizing of stents on endothelial wall shear stress (WSS) and vessel wall stress to determine a possible biomechanical mechanism of in-stent restenosis and thrombosis. Three-dimensional computational models of stents, artery, and internal fluid were created in a computer-assisted design package, meshed, and solved in finite element and computational fluid dynamic packages. The simulation results show that the effects of various degrees of undersizing on WSS, WSS gradient, and oscillatory shear index were highly nonlinear. As the degree of undersizing increased, the heterogeneity of WSS became smaller. The WSS distribution for the 20% undersizing was smooth and uniform, whereas the 5% case was very heterogeneous. The combination of lower WSS and higher WSS gradient and oscillatory shear index in the 5% undersized case may induce neointimal hyperplasia or thrombosis. Additionally, the oversizing simulation results show that the maximum intramural wall stress of the 20% oversizing case is significantly larger than the maximum stress for the 10% and zero oversizing cases. Edge stress concentration was observed, consistent with the restenosis typically observed in this region. This study demonstrates that proper sizing of stent is important for reducing the hemodynamic and mechanical disturbances to the vessel wall. Furthermore, the present findings may be used to improve stent design to reduce endothelial flow disturbances and intramural wall stress concentrations.

Pulsatile flow in a coronary artery using multiphase kinetic theory

Pulsatile flow in a model of a right coronary artery (RCA) was previously modeled as a single-phase fluid and as a two-phase fluid using experimental rheological data for blood as a function of hematocrit and shear rate. Here we present a multiphase kinetic theory model which has been shown to compute correctly the viscosity of red blood cells (RBCs) and their migration away from vessel walls: the Fahraeus–Lindqvist effect. The computed RBC viscosity decreases with shear rate and vessel size, consistent with measurements. The pulsatile computations were performed using a typical cardiac waveform until a limit cycle was well established. The RBC volume fractions, shear stresses, shear stress gradients, granular temperatures, viscosities, and phase velocities varied with time and position during each cardiac cycle. Steady-state computations were also performed and were found to compare well with time-averaged transient results. The wall shear stress and wall shear stress gradients (both spatial and temporal) were found to be highest on the inside area of maximum curvature. Potential atherosclerosis sites are identified using these computational results.

Can temporal fluctuation in spatial wall shear stress gradient initiate a cerebral aneurysm? A proposed novel hemodynamic index, the gradient oscillatory number (GON)

We propose a new hemodynamic index for the initiation of a cerebral aneurysm, defined by the temporal fluctuations of tension/compression forces acting on endothelial cells. We employed a patient-specific geometry of a human internal carotid artery (ICA) with an aneurysm, and reconstructed the geometry of the ICA before aneurysm formation by artificially removing the aneurysm. We calculated the proposed hemodynamic index and five other hemodynamic indices (wall shear stress (WSS) at peak systole, time-averaged WSS, time-averaged spatial WSS gradient, oscillatory shear index (OSI), and potential aneurysm formation indicator (AFI)) for the geometry before aneurysm formation using a computational fluid dynamics technique. By comparing the distribution of each index at the location of aneurysm formation, we discussed the validity of each. The results showed that only the proposed hemodynamic index had a significant correlation with the location of aneurysm formation. Our findings suggest that the proposed index may be useful as a hemodynamic index for the initiation of cerebral aneurysms.

The role of fluid dynamics in plaque excavation and rupture in the human carotid bifurcation: a computational study

A 3D computational fluid dynamics model of the human carotid bifurcation has been created to explore plaque excavation and plaque rupture. The model considers different degrees of atherosclerotic stenosis, the form of which is determined using computerised tomography scans of a patient with moderate plaque stenosis. The results suggest that 70% stenosis will diminish blood flow to the brain from 245 ml/min to 71 ml/min. Pressure in the 50% stenosis model is increased by only 3.3%, while pressure in the 70% and 80% stenosis models are increased by 8.8% and 15.4%, respectively. Starting at 30% stenosis, each increase of 10% stenosis increases the peak wall shear stress value by a factor of two. Severely elevated magnitudes in the product of the pressure and the wall shear stress gradient were found on the upstream face of the stenosis. In specific cases, these peaks can be correlated to excavation points observed clinically.

The mechanical triggers of plaque rupture: shear stressvspressure gradient

The aim of this study was to evaluate the mechanical triggers that may cause plaque rupture. Wall shear stress (WSS) and pressure gradient are the direct mechanical forces acting on the plaque in a stenotic artery. Their influence on plaque stability is thought to be controversial. This study used a physiologically realistic, pulsatile flow, two-dimensional, cine phase-contrast MRI sequence in a patient with a 70% carotid stenosis. Instead of considering the full patient-specific carotid bifurcation derived from MRI, only the plaque region has been modelled by means of the idealised flow model. WSS reached a local maximum just distal to the stenosis followed by a negative local minimum. A pressure drop across the stenosis was found which varied significantly during systole and diastole. The ratio of the relative importance of WSS and pressure was assessed and was found to be less than 0.07% for all time phases, even at the throat of the stenosis. In conclusion, although the local high WSS at the stenosis may damage the endothelium and fissure plaque, the magnitude of WSS is small compared with the overall loading on plaque. Therefore, pressure may be the main mechanical trigger for plaque rupture and risk stratification using stress analysis of plaque stability may only need to consider the pressure effect.

Hemodynamics for Asymmetric Inlet Axial Velocity Profile in Carotid Bifurcation Model

The asymmetric inlet velocity profile has been observed in phantom model using LDA and in health subjects using Magnet Resonance (MR). The effects of asymmetric inlet axial velocity profile on the flow field and the Wall Shear Stress (WSS) of carotid bifurcation were numerically studied herein with the TF-AHCB model. The results show that the Wall Shear Stress Gradient (WSSG) in the front part of the sinus for inward-tilting inlet axial velocity profile is nearly 2 times of that for the symmetric one in the beginning of systole, the end of systole, and diastole, respectively. The area of WSS below 5×10 −3 Pa at the outer wall of the sinus for outward-tilting inlet axial velocity profile is 1.5 times of that for the inward-tilting one during diastole of the cardiac cycle. The asymmetric inlet velocity profiles can reduce the flow velocity near the inner wall of the sinus, which has been normally considered a high velocity region. It is concluded that besides bifurcation geometry and flow waveform, the asymmetry of inlet velocity profile is probably a factor influencing atherosclerosis.

Noninvasive determination of spatial distribution and temporal gradient of wall shear stress at common carotid artery

Wall shear stress (WSS) has been proved to play a critical role in formation and development of atherosclerotic plaques. Our objective was to quantify local WSS in vivo in normal subjects, and to analyze spatial distribution patterns and determine the temporal gradient of WSS. Seventy-eight CCAs of 42 healthy volunteers at common carotid arteries (CCAs) were studied. Cine phase-contrast MR sequence was used to acquire the flow velocity information. Three-dimensional paraboloid modeling was applied to fit the velocity profiles and WSS values were calculated. Mean WSS value for CCAs was 0.783±0.209, with the range of WSS value from −0.541 to 3.464 N/m 2. The 95% confidence interval for mean WSS value in CCA was (0.736–0.830) N/m 2. Different WSS spatial distribution patterns were classified into three types according to the location of low WSS values during a cardiac cycle. Mean value of maximum temporal gradient of WSS was 14.12±5.46, with the range from 5.87 to 33.23 N/m 2 s −1. Skewed velocity profiles were displayed in most CCAs, indicating the flow patterns in CCA were more complicated than commonly assumed. Obvious inter-subject variation were found in magnitude, spatial distribution and the temporal gradient of WSS in CCAs, and the blood flow patterns as well.

Rheological Effects of Blood in a Nonplanar Distal End-to-Side Anastomosis

This study investigates rheological effects of blood on steady flows in a nonplanar distal end-to-side anastomosis. The shear-thinning behavior of blood is depicted by a Carreau-Yasuda model and a modified power-law model. To explore effects of nonplanarity in vessel geometry, a curved bypass graft is considered that connects to the host artery with a 90 deg out-of-plane curvature. Navier-Stokes equations are solved using a finite volume method. Velocity and wall shear stress (WSS) are compared between Newtonian and non-Newtonian fluids at different flow rates. At low flow rate, difference in axial velocity profiles between Newtonian and non-Newtonian fluids is significant and secondary flows are weaker for non-Newtonian fluids. At high flow rate, non-Newtonian fluids have bigger peak WSS and WSS gradient. The size of the flow recirculation zone near the toe is smaller for non-Newtonian fluids and the difference is significant at low flow rate. The nonplanar bypass graft introduces helical flow in the host vessel. Results from the study reveal that near the bed, heel, and toe of the anastomotic junction where intimal hyperplasia occurs preferentially, WSS gradients are all very big. At high flow rates, WSS gradients are elevated by the non-Newtonian effect of blood but they are reduced at low flow rates. At these locations, blood rheology not only affects the WSS and its gradient but also secondary flow patterns and the size of flow recirculation near the toe. This study reemphasizes that the rheological property of blood is a key factor in studying hemodynamic effects on vascular diseases.

ESTIMATION OF WALL SHEAR STRESS DYNAMIC FLUCTUATIONS IN INTRACRANIAL ATHEROSCLEROTIC LESIONS USING COMPUTATIONAL FLUID DYNAMICS

Intracranial stenosis (IS) is associated with significant morbidity and mortality from hypoperfusion and thromboembolism. We used computational fluid dynamic methods to analyze luminal patterns of wall shear stress (WSS), a known critical modulator of endothelial function, within patient-based IS lesions undergoing percutaneous angioplasty and stenting. High-resolution three-dimensional rotational angiographic data sets were reconstructed to yield a fine-resolution computational mesh allowing application of pulsatile computational fluid dynamic analysis with a non-Newtonian realistic model of blood. WSS and its gradient were analyzed spatiotemporally in five IS lesions before and after percutaneous angioplasty and stenting. WSS within the stenosis reached average shear magnitudes of 1870 +/- 783 dyn/cm with rapidly reversing direction to oscillating low values in the recirculation zone. WSS vectors revealed complex dynamic directional and amplitude oscillations not seen in healthy segments with time-dependent convergence and divergence strips sweeping back and forth across the lesion during the cardiac cycle. These areas also underwent extreme temporal WSS oscillation of 2052 +/- 909 dyn/cm over a short time interval. The endothelial mechanotransductive response to such extreme WSS magnitudes and gradients, which were normalized by percutaneous angioplasty and stenting in the current study, remains undefined. Computational fluid dynamic analysis of IS has uncovered a complex and hostile microhemodynamic environment characterized by wide and rapid shear variations in time and space. Characterization of the mechanical forces acting on the wall can help in determining the molecular transduction response of the luminal endothelium to these extreme stresses and may lead to better understanding of the hemodynamic contribution to stenosis pathophysiology.

Endothelial Cell Layer Subjected to Impinging Flow Mimicking the Apex of an Arterial Bifurcation

Little is known about endothelial responses to the impinging flow hemodynamics that occur at arterial bifurcation apices, where intracranial aneurysms usually form. Such hemodynamic environments are characterized by high wall shear stress (WSS >40 dynes/cm(2)) and high wall shear stress gradients (WSSG >300 dynes/cm(3)). In this study, confluent bovine aortic endothelial cells were exposed to impinging flow in a T-shaped chamber designed to mimic a bifurcation. After 24-72 h under flow, cells around the stagnation point maintained polygonal shapes but cell density was reduced, whereas cells in adjacent downstream regions exposed to very high WSS and WSSG were elongated, aligned parallel to flow, and at higher density. Such behavior was not blocked by inhibiting proliferation, indicating that cells migrated downstream from the stagnation point in response to impinging flow. Furthermore, although the area of highest cell density moved downstream and away from the impingement point over time, it never moved beyond the WSS maximum. The accumulation of cells upstream of maximal WSS and downstream of maximal WSSG suggests that positive WSSG is responsible for the observed migration. These results demonstrate a unique endothelial response to aneurysm-promoting flow environments at bifurcation apices.

Direct numerical simulation of transitional flow in a stenosed carotid bifurcation

The blood flow dynamics of a stenosed, subject-specific, carotid bifurcation were numerically simulated using the spectral element method. Pulsatile inlet conditions were based on in vivo color Doppler ultrasound measurements of blood velocity. The results demonstrated the transitional or weakly turbulent state of the blood flow, which featured rapid velocity and pressure fluctuations in the post-stenotic region of the internal carotid artery (ICA) during systole and laminar flow during diastole. High-frequency vortex shedding was greatest downstream of the stenosis during the deceleration phase of systole. Velocity fluctuations had a frequency within the audible range of 100–300 Hz. Instantaneous wall shear stress (WSS) within the stenosis was relatively high during systole (∼25–45 Pa) compared to that in a healthy carotid. In addition, high spatial gradients of WSS were present due to flow separation on the inner wall. Oscillatory flow reversal and low pressure were observed distal to the stenosis in the ICA. This study predicts the complex flow field, the turbulence levels and the distribution of the biomechanical stresses present in vivo within a stenosed carotid artery.

A Study on the Compliance of a Right Coronary Artery and Its Impact on Wall Shear Stress

A computational model incorporating physiological motion and uniform transient wall deformation of a branchless right coronary artery (RCA) was developed to assess the influence of artery compliance on wall shear stress (WSS). Arterial geometry and deformation were derived from modern medical imaging techniques, whereas the blood flow was solved numerically employing a moving-grid approach using a well-validated in-house finite element code. The simulation results indicate that artery compliance affects the WSS in the RCA heterogeneously, with the distal region mostly experiencing these effects. Under physiological inflow conditions, coronary compliance contributed to phase changes in the WSS time history, without affecting the temporal gradient of the local WSS nor the bounds of the WSS magnitude. Compliance does not cause considerable changes to the topology of WSS vector patterns nor to the localization of WSS minima along the RCA. We conclude that compliance is not an important factor affecting local hemodynamics in the proximal region of the RCA while the influence of compliance in the distal region needs to be evaluated in conjunction with the outflow to the myocardium through the major branches of the RCA.