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ISSN 1 746-7233, England, UK World Journal of Modelling and Simulation Vol. 7 (2011) No. 2, pp.

113-122

Effect of increased severity in patient specic stenosis of common carotid artery using CFDa case study
S. M. Abdul Khader1 , B. Satish Shenoy1 , Raghuvir Pai1 , S. Ganesh Kamath2 , Nabeel Md Sharif3 , V. R. K. Rao3
2 3

Department of Mechanical Engineering, MIT, Manipal University, Manipal 575001, India Department of Cardio-Thoracic Surgery, KMC, Manipal University, Manipal 575001, India, Department of Radio-Diagnosis & Imaging, KMC, Manipal University, Manipal 575001, India (Received July 18 2009, Accepted May 1 2010)

Abstract. The prevailing vascular uid dynamics plays an important role in the development of atherosclerosis which is one of the most wide spread disease in humans. The recent advances in computational uid dynamics (CFD) can be useful in observing the ow behavior downstream of the stenosis. The present study investigates a simple case of 66% eccentric stenosis of an approximate model generated from Doppler scan. The blood is assumed to be incompressible, homogenous and Newtonian, while artery is assumed to be a rigid wall. The transient analysis is performed using ANSYS-10.0, commercially available Finite Element Software. The ow pattern, Wall Shear Stress (WSS) and pressure contours are observed at pre-stenotic, throat and post-stenotic regions. In an attempt to predict the ow changes with varying the severity of stenosis, the percentage of stenosis is varied from 66% to 75%, 80%, 85%, 90%, 95% and analyzed. Comparison of results concludes that, with the increase in severity of stenosis, the ow changes abruptly causing an increase in velocity and WSS at throat region. The ow is highly turbulent in downstream leading to formation of eddies. The effect of back pressure is observed during late diastole which alters the ow behavior considerably in the downstream region. Keywords: common carotid artery, ANSYS APDL, stenosis, CFD of blood ow, Newtonian ow

Introduction

A study of stenosis, which is a constriction in the blood vessels, and a leading cause of stroke and even fatal death in most of the countries can be helpful in understanding the biomechanics of vascular diseases. In such diseases, the affected arteries get hardened as a result of accumulation of fatty substances inside the lumen or because of formation of plaques as a result of hemorrhage[1] . As the disease progresses, the arteries/arteriole gets constricted. The ow behavior in the stenosed artery is quite different than one in the normal arteries. Also, stresses and resistance to ow are much higher in stenosed arteries in comparison to the normal ones. After the plaque cap ruptures, the contents of the atheroma stimulate a blood clotting reaction called thrombosis. The thrombosis is initiated by the adherence of platelets at the surface with rapid accumulation of additional platelets. The concepts of uid dynamics can be applied to study the interesting aspects of generation, detection and the treatment of stenosis[9] . The stenotic geometry is highly complex, but in the preliminary study it can be simplied as a constriction in a cylindrical tube. Generally the ow through the constricted tube is characterized by high velocity jet generated in constricted section and ow separation downstream to the stenosis[2] . The constriction can be broadly classied as symmetric-concentric and asymmetric-eccentric conditions. In case of concentric condition, a high speed jet of uid extends downstream along the centerline of model, whereas in case of eccentric condition, the ow pattern is almost stagnant and forces the vorticity against the wall while owing in downstream causing high ow separation.

Corresponding author. Tel.: E-mail address: smak.quadri@gmail.com. Published by World Academic Press, World Academic Union

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S. Khader & B. Shenoy & et al.: Effect of increased severity in patient specic stenosis

The application of CFD in the study of stenosis has developed recently as it lays the basis for further study of association between haemodynamic variables and atherosclerosis, which has received considerable attention in the recent past[14] . Currently there is no standardized procedure to grade the physical severity of the stenosis. Doctors often judge severity based on a patients physical symptoms as well as growth rate, constriction size and pressure drop often at high risk to patient lives[2] . Also the knowledge of ow parameters, such as velocity, ow rate, pressure drop will aid bio-medical engineers in developing bio-medical instruments for treatment(surgical) modalities[6] . The results of numerical simulation can be better than MR/CT/Doppler Ultrasound imaging techniques in analyzing, as it provides an accurate picture of the haemodynamics especially in stenosed zones. It also provides high resolution, time-resolved models of 3D ow elds[12] . This is also backed by several experimental studies which also help in evaluating the detailed ow dynamics in downstream of stenosis[2] . Further the comparison of stenosed ow conditions with the normal case provides the proper understanding of underlying mechanism behind the development of atherosclerosis. The investigation of plaque rupture in carotid bifurcation reveals high dynamic pressure and WSS proximal to throat. This variation is signicant throughout the ow cycle with the severe vortex shedding in downstream of stenosis[16] . Another study on moderately stenosed carotid bifurcation model indicates that the ow in downstream of stenosis is highly disturbed and demonstrates the risk of embolism and plaque rupture[21] . In case of subject-specic anatomically realistic stenosed carotid bifurcation subjected to pulsatile inlet condition, the simulation results demonstrates the rapid uctuation of velocity and pressure in post-stenotic region[8] . Similar investigation of instability in pulsatile ow through 3D stenosis revealed that the presence of stenosis leads to large ow variations in cross-sectional planes and swirling motion in post-stenotic region[11, 13] . In another interesting study, the stenoses having different geometric proles like trapezium, semi-ellipse and triangle are analyzed considering the non-Newtonian behavior[10] . They investigated that the length of ow disturbance is due to stenotic shape and height, downstream disturbance is due to the stenotic walls and peak velocity depends on the shape and height of stenosis. Some of the above mentioned previous experimental and computational studies have analyzed the ow aspects in proximal and distal end of stenosis including a detailed observation into rupture potential of plaque. Apart from this, the ow patterns with the increase in severity have been investigated extensively for idealized geometry alone but the realistic physiological model is yet to be analyzed. An attempt has been made

Fig. 1. CFD model highlighting stenosed region

Fig. 2. Section description of CFD model

in the present study to demonstrate the signicant changes for various severities considering a realistic case. The patient has an eccentric stenosis of 66% in left common carotid artery and transient analysis has been performed for several pulse cycles. This study focuses on detailed investigation of ow parameters like velocity, WSS, pressure contours. A similar analysis is performed with various stenosis percentages starting from 66% in steps of 5% till occlusion. The comparison of results obtained for various severities reveals the high
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WSS zones on the far wall of downstream of the throat causing degradation of wall tissue. Also shear layer dissipates more quickly due to formation of high eddies in downstream. The ow behavior changes abruptly with the increase in velocity at throat and large recirculation in the downstream of stenosis. Moreover it is also observed that severity less than 75% is considered as mild and anything greater than this is termed as critical. This type of study will be useful to predict the outcome of severity of stenosis, and aids the physicians with better insight into ow dynamics.

Methodology and model description

In the present study, the blood is assumed to be incompressible, homogeneous and Newtonian as this approximate assumption is acceptable in large arteries where relatively high shear rates occurs[20] . However, when the shear rate is lower than 100s1 , blood behaves as a non-Newtonian uid and the stresses depend nonlinearly on the deformation rate[19, 20] . Many models assume blood ow to be Newtonian and the instantaneous shear rate over a cardiac cycle may vary from zero to over 1000s1 depending on the circumstance[22] ). 2.1 Governing equation for cfd solution

In the uid ow computations, arterial wall is assumed to be rigid and the governing equation for incompressible, Newtonian study is dened by the modied continuity & momentum equations shown below[4, 5] . = 0, ( + ) = p + 2 , t where is the density, p is the pressure, is velocity vector and is the dynamic viscosity. 2.2 Model description

An eccentric stenosed CCA model is generated in ANSYS-10.0 with the required details obtained from the Duplex scan performed on a patient. The necessary data was taken at different sections depending upon the convenience using M-mode scan for velocity and B-mode scan for diastolic diameter[14, 19] . The geometry of generated model in this study has a length of 15D. Fig. 1 shows the CFD model with stenosed region. The various sections considered at different lengths along the model to observe the ow parameters is depicted[7] in Fig. 2. In order to analyze the effect of severity, the initial 66% eccentric stenosis is increased and separate models are generated for 75%, 80%, 85%, 90% and 95% stenosis and the rest of the parameters remain same for all the later cases. This will yield useful simulation data when the stenotic severity progresses. It will be helpful for doctors to decide when an intervention is required and prognosis of the clinical cases and further useful in quantifying haemodynamic factors that indicates plaque rupture potential.

Analysis

The CFD model generated contains approximately 45000 hexahedral elements[17, 22] . The normalized velocity waveform as shown in Fig. 3 at the inlet, constant pressure boundary conditions at outlet and noslip condition along the length of model are the only boundary conditions applied for CFD model[16, 20] . In the present case, one pulse cycle is discretized into 30 time steps to simulate the ow behavior accurately. The density and dynamic viscosity of the blood considered are 1050 kg/m3 and 0.004N sec/m2 respectively[19, 22] . An APDL written in ANSYS generates geometry, performs transient solution and post processing of results. The parameters considered in the analysis includes ow separation zone (FSZ), wall shear stress behaviour and velocity pattern at specied instants of pulse cycle, which are early systole, peak systole and diastole[3, 15, 18] . In the present analysis, the changes in ow variation have been observed for various percentages of stenosis, which is highly turbulent in the downstream of the stenosis. An accurate prediction of such turbulent ow still remains a challenging task since the ow is turbulent for only a part of the domain and is time dependent. The increase in percentage of stenosis reduces the lumen diameter causing an occlusion at 100% as seen from Fig. 4, which compares the reduction in lumen diameter due to increased severity.
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S. Khader & B. Shenoy & et al.: Effect of increased severity in patient specic stenosis

Fig. 3. Input velocity wave form

Fig. 4. Change in lumen diameter due to severity

Results & discussions

The computational results are conducted to study the inuence of stenosis on the ow behavior. The ow parameters like velocity, pressure, WSS, ow separation, vortices are observed from transverse and longitudinal contours at specic instants of pulse cycle for comparing the ow variation. The following discussion has been categorized with the observations of ow variation starting from early systole, peak systole and diastole. Further the inuence of stenotic jet in various cases has been discussed followed by changes in WSS due to increase in severity. The results reveal that the ow pattern changes abruptly in all cases from section-3 onwards in the downstream, whereas no signicant changes are observed in the upstream. Fig. 5 depicts the

Fig. 5. Velocity prole at 66% during early systole

Fig. 6. Velocity prole at section-2 during early systole

velocity contour during early systole at 66%. It is observed that the ow behavior is uniform in upstream and there is a slight increase in velocity at Section 3 due to the presence of throat. Another illustration of transverse velocity contour at Section 2 depicts the uniform ow behavior in the upstream of stenosis at 85%. Fig. 7 and Fig. 8 compares the normalized velocity variation at different sections for 80% and 90% during early systole. It is observed that there is an increase in velocity at the throat region i.e. Section 3, but at Section 1 & 2, the ow behavior appears to be normal in all the cases. The ow disturbance is observed from Section 3 onwards in all cases with the initiation of recirculation in the downstream. Due to the eccentric stenosis, the streamlines are denser adjacent to the throat than in outlet region and similar behavior aggravates with increase in severity. The maximum velocity in pulse cycle will be during peak systole. But due to the presence of stenosis, the velocity instantaneously increases at Section 3 as seen from Fig. 9 for 66%. The transverse velocity
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Fig. 7. Velocity comparison at 80% in early systole

Fig. 8. Velocity comparison at 90% in early systole

Fig. 9. Velocity prole during peak systole at 66%

Fig. 10. Velocity prole at section-3 during peak systole at 80%

contour at section-3 for 75% depicts the fully developed ow during peak systole as shown in Fig. 10. As the severity increases, the peak systolic velocity increases as shown in Fig. 11 and Fig. 12 for 90% and 95% respectively[3, 20] . The ow behavior signicantly varies from Section 3 onwards in the downstream and it becomes more severe from 75% leading to large recirculation zones in downstream. The normalized systolic

Fig. 11. Velocity prole during peak systole at 90%

Fig. 12. Velocity prole during peak systole at 95%

comparison of velocity at various sections is shown in the Fig. 13 and Fig. 14 for 66% and 90% respectively.
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S. Khader & B. Shenoy & et al.: Effect of increased severity in patient specic stenosis

Fig. 13. Velocity comparison at 66% in peak systole

Fig. 14. Velocity comparison at 90% in peak systole

An interesting change in the ow pattern is observed at Section 4. Due to eccentric stenosis there is an instant rise in velocity at Section 3 and the ow continues to grow as a jet in the downstream. Because of this reason, there is a sharp rise in top half at Section 4 and sudden decline in the lower half. Similar behavior is observed at Section 4 for all the various cases. The formation of jet subsides by the time it reaches the Section 5 and uniform ow is observed similar to that of Section 1 and 2. The uniform ow behavior persists throughout the pulse cycle till it approaches early diastole. The ow deceleration during diastole contains large recircu-

Fig. 15. Velocity prole at during diastole at 66%

Fig. 16. Velocity prole at section-3 during diastole

lation zones and high vorticity causing the disturbance in the downstream of stenosis. Fig. 15 and 16 show the velocity prole at 66% and transverse velocity contour at section-3 at 80% respectively. It is observed that there is a uniform ow in the upstream and the instant increase in velocity as observed at the throat during peak systole has subsided. The ow in downstream region is more complicated and vortex shedding occurs as shown in Fig. 17. The vortex emerges from near wall region adjacent to the throat and it becomes more severe from 80% onwards. The magnitude of deceleration increases abruptly in the downstream of stenosis with the increase in severity. The recirculation zone with the increase in severity still grows as a jet as shown in Fig. 18 for 95%. The jet subsides after travelling a certain length and leads to the formation of large eddies causing turbulence as depicted in Fig. 17. The normalized diastole velocity comparison is shown in Fig. 19 and Fig. 20 for 80% and 95% respectively. The highest variation in ow behavior is observed in this part of pulse cycle than compared to others due to back ow. The throat region has prevented the smooth ow causing the disturbance due to back ow as it obstructs the smooth ow of streamlines. The ow velocity is similar at Section 1 and 2, but highest variation is observed at Section 4 for all cases. This is due to subsiding ow jet during early diastole leading to sudden disturbance in ow pattern and streamlines[3, 22] . However, in cases
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Fig. 17. Velocity prole during diastole at 90%

Fig. 18. Velocity prole at section-4 during diastole

Fig. 19. Velocity comparison at 80% in diastole

Fig. 20. Velocity comparison at 95% in diastole

with 80% stenosis and above, at Section 4, the ow path rises sharply, drops down at top-half of lumen area and continues to decline at bottom half. This is because of the ow jet, which extends to a greater length as percentage of stenosis becomes severe. This is the main reason for sudden sharp peak of ow observed for top-half of lumen area. Also at Section 5 variation is almost similar for all sections for entire period of pulse cycle. The main region of interest is the Section 3 as the consequences are very critical due to sudden changes

Fig. 21. Comparison of percentages at early systole

Fig. 22. Comparison of percentages at peak systole


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S. Khader & B. Shenoy & et al.: Effect of increased severity in patient specic stenosis

in ow behavior. The velocities are compared at this section for all severities simulated during various phases of the pulse cycle. Fig. 21 and Fig. 22 shows the comparison during early systole and peak systole respectively and the maximum peak velocity is observed at 95%. The variation at 95% is much sharper along the core of the stenosis due to the jet ow. Similar variation is observed for from 80% onwards due to the traces of the jet ow still prevailing at throat region during diastole. All the cases show gradual increase in velocity during peak systole. The ow variation is less during early systole in upstream, but the increase in velocity at the throat begins at this phase and continues throughout the ow cycle. This observation of initial rise increases with severity for all the various cases. Another interesting observation in this study is the comparison of jet

Fig. 23. Velocity prole of stenotic jet at 66%

Fig. 24. Velocity prole of stenotic jet at 80%

length at various severities. The maximum jet formation is usually during early diastole for most of the cases. The jet length contours are shown in Fig. 23, Fig. 24 and Fig. 25 for 66%, 80% and 90% respectively. It is evident that with the increase of severity, the length of jet increases and maximum length is seen at 95%. Also as the jet traverses in downstream, it subsides and the turbulence observed is highest during the whole pulse cycle. Due to asymmetric constriction, the jet is usually in upper side of the model and the formation of eddies and ow separation is highest in immediate vicinity of the throat in downstream section. The normalized wall shear stress comparison for various cases matches well with that of input ow pattern as shown in Fig. 26. As the severity of stenosis increases, the WSS also increase and the maximum variation is dominated by 95%[15, 22] . Also the values considered for plotting is maximum for each time period for entire model. Due to the complexity involved in measuring the calculated values, the variation for each case for the entire model is considered. The result obtained from 66% stenosis agrees well with the clinical

Fig. 25. Velocity prole of stenotic jet at 90%


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Fig. 26. WSS comparison for various percentages

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observations. An instantaneous increase in velocity is observed during the peak systole at throat region and with jet ow extending into the post-stenotic region. Further, the hypothetical cases of increased severity were used in prediction of changes in ow behavior as the percentage of stenosis increases. This can be benecial in the prognosis of the clinical cases.

Conclusions

Numerical simulated results of the present study demonstrate that velocity increases in throat region with the increase in severity. Due to the eccentric constriction, the ow behavior changes abruptly in the downstream of the stenosis. There are no signicant changes in proximal side during early systole for the various severity cases. During peak systole the ow increases at the throat region forming a jet and later disrupts suddenly forming eddies due to pressure drop in downstream side. During diastole, due to ow deceleration, the traces of the jet formed prevail for short period and subsides. But the extent of disruption of the ow behavior is maximum during this period due to constriction in distal side and the ow separation zone reduces slightly. As the severity increase the stenotic jet length increases, thus increasing turbulence in distal side including the ow separation zone. The maximum disruption of the ow occurs in between section 4 and 5.Due to eccentric stenotic condition, the ow will be more in top half than bottom half beginning from throat region towards distal side. It is observed from the velocity prole comparison for various cases at various sections that ow behavior disrupts drastically and is dominated by the higher constriction percentage. WSS comparison shows that as severity increases, shearing of ow also increases and the resulting pattern matches well with that of the input ow prole and the maximum stress is exerted in throat region. Analysis of velocity and wall shear stress shows that the most signicant ow changes are in the post-stenotic region. The results demonstrate that the 3D stenotic CFD model is capable of predicting the changes in ow behavior for increased severity. Also this study can be further extended to various anatomically realistic models of stenosed carotid artery and predict a range of haemodynamic phenomena that are likely to have clinical signicance.

Nomenclature
CCA : Common Carotid Artery; Vmax : Maximum velocity in time period; Vt V : Normalized velocity = Vmax ; Vt : Velocity at time, t; WSSmax : Maximum Wall Shear Stress in time period; WSSt : Wall Shear Stress at time, t; WSSt WSS : Normalized Wall Shear Stress = WSS . max

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