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Advanced Computational Models for Disturbed and Turbulent Flow in Stenosed Human Carotid Artery Bifurcation

F.P.P. Tan1, G. Soloperto1, N.B. Wood1, S. Thom2, A. Hughes2, X.Y. Xu1


2 1 Department of Chemical Engineering, Imperial College London, South Kensington Campus, London, SW7 2AZ, UK National Heart and Lung Institute, International Centre for Circulatory Health, Imperial College London, London, W2 1LA, UK

Abstract In this study, newly developed two-equation transitional and turbulence models are employed for the prediction of blood flow patterns in diseased carotid artery where the growth, progression and structure of plaque at rupture are closely linked to low and oscillating wall shear stresses. Moreover, laminar-turbulent transition in the post-stenotic zone can alter the separation zone length, wall shear stress and pressure distribution over the plaque, with potential implications for stresses within the plaque. A separate validation study was carried out with well established experimental measurements and numerical studies. Laminar flow, Menter's hybrid k- /kShear Stress Transport model and its transitional version were implemented in pulsatile simulations from which analyses of velocity profiles, wall shear stress and turbulence intensity were conducted. It was found that the transitional version of SST gave better overall agreement with experimental data for pulsatile flow in an axisymmetric stenosed tube and this is further highlighted in the patient-specific geometry simulation results. A magnetic-resonance (MR) image based model of the carotid bifurcation with 70% stenosis was reconstructed and simulated using patient-specific boundary conditions. The laminar flow assumption was found to be inadequate when the differences occurred in the wall shear stress analysis of the patient-derived model. Keywords Computational fluid dynamics, turbulence modeling, carotid artery, wall shear stress, atherosclerosis.

I. INTRODUCTION Atherosclerosis is the scourge of modern man in the Western world and has long been related to way of life. Resulting from accumulation of cholesterol-laden plaque in arterial walls, atherosclerosis causes a narrowing or stenosis and a loss of elasticity at the focal sites in the arteries. This disease often leads to heart attack and stroke. Stroke is the second most common cause of death in the world, after heart disease [1]. Often, the major cause of stroke is blood vessel blockage or plaque rupture. Narrowing of an arterial lumen tends to occur in regions of disturbed flow and low wall shear stress (WSS) and, once plaque develops and encroaches into the lumen, further flow disturbances are established [2]. Hemodynamically significant stenoses experience increased shear stress in the entrance region. In the post-stenotic region, the flow decelerates and tends to be-

come unstable, with separation, recirculation and, generally for the more severe constrictions, transition to turbulence [3]. Disturbance and turbulence in blood flow influence physiological parameters and processes, such as flow resistance, shear stress, pressure, mass transport from the blood to the vessel wall and wall remodeling [4]. Of potential interest here are the effects of disordered and turbulent flow on the resultant forces acting on and within the stenosed vessel wall and its neighborhood. Low or oscillating WSS can enhance expression of plaque inducing factors leading to progression of the disease [5] while high WSS can enhance matrix degradation, destabilizing the plaque cap hence causing rupture [6]. Also, regions prone to atherosclerosis are exposed to low and oscillating stress values (between -0.4 and +0.4 Pa), such as bends and bifurcations [5]. Low and random alignment of endothelial cells could actually increase monocytes circulation and platelet aggregation on vessel walls. Various studies have been conducted to investigate flow patterns in physiologically realistic conditions. Experimental studies were carried out to investigate the effects of different degree of stenosis and flow pulsatility (spatial and temporal effects) that could lead to transitional and turbulent flow (e.g. [7-10]). In numerical studies, flow and WSS patterns in stenoses have commonly been analyzed using computational fluid dynamics (CFD) under the laminar flow assumption. Although such analyses have known shortcomings for severe stenoses, most numerical hemodynamics studies to date (e.g. [11-12]) have employed steady or unsteady Reynolds-averaged Navier-Stokes (RANS) CFD codes, in which transition to turbulence cannot generally be taken into account. Other limitations include geometries used for simulations that were too idealized and simulation results not being validated. The objective of this study was to evaluate newly developed transitional and turbulence models for prediction of disturbed blood flow patterns in patient-specific diseased carotid arteries. Since there have been no detailed flow measurements in models based on patient-specific stenotic carotid bifurcations for quantitative comparison, steady and pulsatile flows in an axisymmetric stenosed tube were first separately studied and comparisons were made with available experimental data [16].

N.A. Abu Osman, F. Ibrahim, W.A.B. Wan Abas, H.S. Abd Rahman, H.N. Ting (Eds.): Biomed 2008, Proceedings 21, pp. 390394, 2008 www.springerlink.com Springer-Verlag Berlin Heidelberg 2008

Advanced Computational Models for Disturbed and Turbulent Flow in Stenosed Human Carotid Artery Bifurcation

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II. METHODOLOGY A. 3D Model Reconstruction A patient-specific diseased carotid artery bifurcation was reconstructed for CFD simulations. A patients neck was scanned using a MRI 1.5T GE Signa machine. A contrast enhanced-2D-bright blood Time-of-Flight (TOF) MRI sequence was used with the following parameters: TE 6.9 s, Flip Angle 60, FOV 20 cm, matrix size 160 x 256 pixels and 2 mm thick contiguous slices. The images were acquired as a set of trans-axial images throughout the length of interest. The lumen area was extracted from the MR images using a segmentation algorithm based on pixel values. The 2D lumen boundary coordinates were stacked to build sets of 3D coordinates and exported into a mesh generation package, ANSYS ICEM CFD (Figure 1). Initial flow simulation results were mesh independent after using a grid of 1180k hexahedral elements. B. Flow Simulation A commercially available package, ANSYS CFX 11 which is based on Finite Volume Method (FVM) was used. The NS equations were spatially discretized using the highresolution upwind scheme. Temporal discretisation was by the second order implicit backward Euler scheme [13]. Solution was by the SIMPLEC algorithm [14]. All simulations were run using a UNIX workstation (HP Intel Core2 Extreme 2.66GHz 6GDDRAM). In order to investigate the prediction of turbulent flow, Menters hybrid k- /k- Shear Stress Transport (SST) [15] and transitional SST (SST Tran) were validated. A separate validation work was carried out using an idealized stenosed tube model [16] and comparison with experimental data from Ahmed and Giddens [17-19]. The model formulations are available in ANSYS CFX manual. SST model utilizes the original kmodel of Wilcox [20] in the inner region of the boundary layer and switches to the standard k- model in the outer region and in free shear flows. The transition model, developed by Langtry et al. [21] and ANSYS CFX has a locally formulated transport equation, intermittency and transition onset criteria in terms of momentum thickness Reynolds number. This full model utilizes a new empirical correlation to cover the standard transition mechanisms and has been validated together with the SST turbulence model. Blood was treated as incompressible and Newtonian fluid with a density of 1176 kg/m3 and viscosity of 3.34 mPa.s. The flow rate ratio for ICA and ECA at the outlet was set as 60%:40% of the inlet flow rate. Timestep independence test was also conducted. Each model was simulated for 3 cardiac cycles with uniform 0.01 s timestep.

Fig. 1 Reconstructed patient-specific carotid artery bifurcation. CCA represents the common carotid artery, ICA the internal carotid artery and ECA the external carotid artery. Arrow shows blood flow direction.

Fig. 2 Patient-specific velocity waveform used as inlet boundary condition. C. Boundary Conditions Introduction of disturbances into the flow mimics features of real disturbance patterns, allowing transition to occur realistically. Turbulence intensity, Tu, is defined as the ratio of the RMS of the turbulent velocity fluctuations to the mean velocity. Low Tu (1.5%) was specified at the inlet. Cine Phase Contrast MRI technique used to obtain the velocity waveform of the patient had the following parameters: TR 24 s, Flip Angle 30, FOV 18 x 18 cm, 256 x 256 pixels and 4 mm thick slices. Womersleys method was used to define the CCA inlet pulsatile velocity waveform [22-23]. The transient inflow velocity waveform is illustrated in Figure 2. The inlet boundary conditions are summarized in Table 1.

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Table 1 Summary of inlet boundary conditions for simulations. *Calculations were based on a non-stenosed section of the ICA, downstream of the throat. Time Duration (one cardiac cycle) Initial Velocity Peak Reynolds number Minimum Reynolds number Mean Reynolds number 0.91 s 0.0552 m/s 600* 150* 375*

F.P.P. Tan, G. Soloperto, N.B. Wood, S. Thom, A. Hughes, X.Y. Xu

D. Visualization of Results All flow simulation results were visualized using CEI Ensight 8. Time-averaged wall shear stress (TAWSS) was used to evaluate the total shear stress exerted on the wall throughout a cardiac cycle and it is governed by,

Fig. 3 Front (L) and back (R) views showing TAWSS profiles of P1

TAWSS

1 T

T 0

dt

(1)

where T is the cardiac cycle period and is the instantaneous WSS. The cyclic variation of WSS is expressed in terms of oscillatory hear index (OSI) which has a range between 0 and 0.5 where 0.5 indicates purely oscillatory flow. OSI is defined as [23],

Fig. 4 Front (L) and back (R) views showing iso-surfaces of flow
separation zone and possible reattachment points of P1.

OSI

1 mean 1 TAWSS 2

(2)

mean

1 T

T 0

dt

(3)

where mean represents the mean shear stress to express the magnitude of the time-averaged surface traction vector. III. RESULTS AND DISCUSSION Results from the separate validation study indicated that the transitional model faired better than the fully turbulent, SST model. Therefore, the SST transitional model was used for the patient-specific carotid artery geometry, P1, flow simulation. For comparison and completeness, laminar flow was also simulated. Time-averaged WSS (TAWSS) contours were plotted to show WSS distribution throughout a cardiac cycle. A peak value of 16.3 Pa was predicted by laminar flow whilst SST Tran predicted peak value of 18.7 Pa. Regions of high TAWSS occurred at the throat of the stenosis and on the inner wall of the ICA immediately downstream of the throat. A larger zone of higher TAWSS in the mid ICA region was predicted by laminar flow shown in the back view of Figure 3 (indicated by *). Laminar slow also predicted bands of lower TAWSS values farther downstream as compared to SST Tran (indicated by **). ECA branches showed distribution of low TAWSS due to lower velocities.

Fig. 5 Front (L) and back (R) views of OSI contour plots of P1. Figure 4 shows iso-surfaces outlining regions where the axial TAWSS (TAWSS-Z) values of zero or less indicate flow reattachments points and possible flow separation regions. The laminar flow predicted a slightly narrower flow separation zone than SST Tran. Magnitude wise, the laminar flow predicted a lower minimum TAWSS-Z value (-3.3 Pa) while SST Tran predicted -2.96 Pa. In the back view immediately after the throat of Figure 4, intense and low TAWSS-Z region predicted by laminar flow is indicated by *. Oscillatory shear index (OSI) was another parameter investigated and is shown in the contours in Figure 5. A common feature that can be seen was that the areas of high OSI lie within areas of low TAWSS indicating lo-

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calized slow reversal or varying flow direction. Shown in the front and back view of ICA far downstream after the throat, the laminar flow predicted a larger area of high OSI than SST Tran. Downstream of the throat, regions high OSI values up to 0.5 were found. A helical flow pattern in the region of high OSI and low TAWSS occurred from the outer wall immediately after the throat towards the inner wall downstream of the throat. Throughout the cardiac cycle, TAWSS distribution corresponded to velocity gradient, where areas of high WSS such as the throat were due to high velocity and low WSS regions indicated flow separation and reversal zones. Recirculation zones on the outer wall of the ICA corresponded to low TAWSS values and high shear stress temporal oscillation (OSI). High OSI values occurred where the jet impinges on the wall, probably suggesting very unsteady reattachment. Even during high velocity (e.g. during peak systole) the WSS values in this flow recirculation region remained relatively low. Low WSS spots were due to sudden changes in cross-sectional area or curvature causing increased localised adverse pressure gradient. As many previous studies, such as of Ku et al. [24] had shown, distribution pattern of low and oscillating WSS is closely related to development of atherosclerotic lesions. IV. CONCLUSIONS In this study, the suitability of turbulence flow models to predict the possible onset of turbulent flow and relaminarization throughout the cardiac cycle for accurate prediction of flow patterns and resultant forces in a moderate to severe stenosis was investigated. The validation work carried out separately [16] had shown that difference exist between laminar flow assumption and turbulent flow. Through comparison with past experimental studies, it was found that the transitional model fared better than laminar flow assumption. The validation results presented for the present application give credence to the comprehensive engineering correlations incorporated in the transition model. Flow simulations for the patient specific carotid artery resulted in the transitional model predicting higher TAWSS values and larger flow separation zones (TAWSS 0) compared to laminar flow. This study highlighted a possible suitable transitional flow model in capturing flow phenomena in the stenosed carotid artery. Future work will include experimental work on similar patient-specific geometries to enable validation of the flow models and the implementation of fluid-solid interaction to take into account arterial wall compliance and its effects on wall shear stresses.

ACKNOWLEDGMENT
The author acknowledges fundings from the Foundation for Circulatory Health, St Marys Hospital and the Overseas Research Students Awards Scheme (ORSAS), Imperial College London.

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22. Womersley J R (1955) Method for the calculation of velocity, rate of flow and viscous drag in arteries when the pressure gradient is known. J Physiol 127: 553-563 23. Taylor C A et al. (1998) Finite element modelling of three dimensional pulsatile flow in the abdominal aorta: relevance to atheroscleorsis. Ann Bio Med 26: 975-987 24. Ku et al. (1985) Pulsatile flow and atherosclerosis in the human carotid bifurcation. Positive correlation between plaque location and low oscillating shear stress. Arterioscler Thromb Vasc Biol 5(3): 293302

F.P.P. Tan, G. Soloperto, N.B. Wood, S. Thom, A. Hughes, X.Y. Xu


Author: Felicia P P Tan Institute: Chemical Engineering Department, Imperial College London Street: South Kensington Campus City: London Country: United Kingdom Email: felicia.tan05@ic.ac.uk

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