Effects of The Inlet Conditions and Blood Models On Accurate Prediction of Hemodynamics in The Stented Coronary Arteries

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Effects of the inlet conditions and blood models on accurate prediction of

hemodynamics in the stented coronary arteries
Article in AIP Advances · May 2015

DOI: 10.1063/1.4919937
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Effects of the inlet conditions and blood models on accurate prediction of
hemodynamics in the stented coronary arteries
Yongfei Jiang, Jun Zhang, and Wanhua Zhao
Citation: AIP Advances 5, 057109 (2015); doi: 10.1063/1.4919937

View online: http://dx.doi.org/10.1063/1.4919937
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AIP ADVANCES 5, 057109 (2015)
Effects of the inlet conditions and blood models

on accurate prediction of hemodynamics in the stented
coronary arteries
Yongfei Jiang,1,2 Jun Zhang,1,2 and Wanhua Zhao1,2,a
1
School of Mechanical Engineering, Xi’an Jiaotong University, Xi’an, 710049,
People’s Republic of China
2
State Key Laboratory for Manufacturing Systems Engineering, Room 405 West Building5,
99# Yanxiang Road, Yanta District, 710054, Xi’an, Shaanxi, People’s Republic of China
(Received 2 April 2015; accepted 28 April 2015; published online 5 May 2015)
Hemodynamics altered by stent implantation is well-known to be closely related

to in-stent restenosis. Computational fluid dynamics (CFD) method has been used
to investigate the hemodynamics in stented arteries in detail and help to analyze
the performances of stents. In this study, blood models with Newtonian or non-
Newtonian properties were numerically investigated for the hemodynamics at steady
or pulsatile inlet conditions respectively employing CFD based on the finite volume
method. The results showed that the blood model with non-Newtonian property
decreased the area of low wall shear stress (WSS) compared with the blood model
with Newtonian property and the magnitude of WSS varied with the magnitude and
waveform of the inlet velocity. The study indicates that the inlet conditions and blood
models are all important for accurately predicting the hemodynamics. This will be
beneficial to estimate the performances of stents and also help clinicians to select
the proper stents for the patients. C 2015 Author(s). All article content, except where
otherwise noted, is licensed under a Creative Commons Attribution 3.0 Unported
License. [http://dx.doi.org/10.1063/1.4919937]
I. INTRODUCTION
Endovascular stent implantation is an effective treatment for stenosis lesion arteries, but in-stent
restenosis is still an inevitable concern that urgently needs to be resolved. In-stent restenosis is a
potentially life threatening for the success of artery disease. Since the work of Caro et al.,1 hemody-
namic parameters have been considered as important determinants for predicting the development
of in-stent restenosis. Among the hemodynamic parameters, wall shear stress (WSS) induced by
stent implantation is a well-known quantity related to the initiation and progression of neointimal
formation in in-stent restenosis.2–6
Computational fluid dynamics method (CFD) is often used to obtain detailed flow patterns
for estimating of WSS in stented arteries. This method requires some information about the blood
flow fields, except for the 3D geometry of the arteries, it still preferably needs to acquire some
hemodynamic data, such as boundary conditions at the inlet of the arteries and the properties
of blood models. Much work has been carried on the effects of Newtonian and non-Newtonian
properties of blood on WSS predictions under steady or pulsatile inlet conditions separately. In the
previous hemodynamic studies about stents,7–10 blood often was modeled as a Newtonian fluid with
a viscosity equal to blood’s viscosity at very high shear strain rates. Actually blood is a suspension
of formed elements, red blood cells, white blood cells and platelets in a Newtonian liquid (plasma).
Blood should be considered as a non-Newtonian fluid at normal concentrations. Therefore, some
further studies11–15 concerning stents have modeled blood as a non-Newtonian fluid to analyze and
a Author to whom correspondence should be addressed. Electronic mail: whzhao@mail.xjtu.edu.cn. Tel.:+86-029-

83399520.
2158-3226/2015/5(5)/057109/9 5, 057109-1 © Author(s) 2015
057109-2 Jiang, Zhang, and Zhao AIP Advances 5, 057109 (2015)
compare WSS in stented arteries. These results indicate that a proper model of blood properties,
as well as properly assumed boundary conditions all exerts a direct influence on the quality and
accuracy of computational results. However, few studies have been reported on the comprehensive
comparisons about the effects of different combinations of inlet conditions and blood models on
accurate predictions of WSS in CFD. In this paper, steady and pulsatile inlet conditions, blood
models with Newtonian or non-Newtonian properties were all proposed to comprehensively analyze
how they affected the prediction of WSS in the stented artery under different combined conditions.
II. COMPUTATIONAL MODEL AND METHODS
A. Computational flow model

The stented artery is assumed to be a straight single-layer cylindrical tube with an internal
diameter of 3 mm and the stent-to-artery ratio is 1:1. Considering the calculation time, stent struc-
ture is only composed of six supports in the axial direction and six sinusoidal parts of each support
in the circumferential direction. Also, three connectors in the circumferential direction are used to
link two adjacent supports to guarantee the mechanical flexibility of stents. Stent structure and cor-
responding flow model are depicted in Fig. 1(a). The strut cross-section is assumed to be rectangular
with strut width and thickness of 0.1 mm. Moreover, additional lengths are added to the proximal
and distal regions of the stented segment for a fully developed flow, so the flow model is shown in
Fig. 1(a) with a total length of 79 mm.
The flow model is imported into the commercial code Gambit2.3 (ANSYS, Inc.) to generate
the computational grids for the fluid domain. It is divided into three segments firstly, such as the
inlet segment, the stented segment and the exit segment. A mixed grid method with hex/wedge and
TGrid is employed to generate grids in stented segment. And grid refining of the stented segment
is generated by the size-function for the flow model (Fig. 1(b)). A cooper grid method is employed
to generate uniform grids in the other two segments for the flow model (Fig. 1(c)). Furthermore,
considering the dependence of calculation results on the number of grids, repeated simulations are
carried out by refining the grids. When the relative error of WSS for two adjacent grids of flow
model is less than 5%,8 it can be considered as grid-independence.
B. Blood models
This paper aims to evaluate the effects of constitutive model choice of blood on the resulting
WSS within a stented artery. Newtonian and non-Newtonian properties of blood models are all used
in numerical simulations. For the Newtonian model, blood is assumed to be an incompressible,
FIG. 1. Stent structure, flow model and computational grids.
FIG. 2. Rheological blood properties and useful shear rate range for in-stent flow.
homogeneous and Newtonian viscous fluid16 with a density of 1060 kg/m3 and with a viscosity of
3.5 × 10−3 kg/m·s. Moreover, it is well-known that blood behaves as a non-Newtonian fluid, particu-
larly at low shear rates (less than 100 s−1).17,18 And the instantaneous shear rate over a cardiac cycle
varies from zero to approximately 1000 s−1 in several large arterial vessels19 as shown in Fig. 2.
For the non-Newtonian model, the viscosity is modeled using the Carreau-Yasuda model which
mathematically is given by
µ = µ∞ + (µ0 − µ∞) [1 + (λγ̇)2](n−1)/2, (1)

where µ∞ and µ0 are the infinite and zero shear rate limit viscosities respectively, λ is the relaxation
time constant and n is the power law index. The Carreau-Yasuda model is fitted to the experimental
data,20 resulting in the following set of parameters:
µ∞ = 0.25 kg/m·s, µ0 = 0.0035 kg/m·s, λ = 25.00 s and n = 0.25.
C. Boundary conditions
A zero pressure boundary condition is imposed at the outlet of the computational models to be
a steady outlet flow.16 For the flow model, the stent and the arterial wall are assumed to be rigid
and no-slip as the previous CFD study21 by ignoring the influence of very low radial velocity on
flow field. In order to compare the accuracy of WSS predictions, numerical simulations are carried
out under steady and pulsatile inlet conditions separately. Two different flow waveforms of the inlet
velocity are employed in simulations as shown in Fig. 3.
The inlet boundary condition for the numerical simulations under steady-state flow conditions
is as follows:
The blood flow velocity at the inlet is assumed to be steady and the velocity is a mean value
of 0.2 m/s which corresponds to the average velocity of blood flows in human’s arterial lumen. The
averaged inlet velocity is corresponded to the Reynolds number (Re) of 182.
The inlet boundary condition for the numerical simulations under pulsatile flow conditions is as
follows:
A normalized pulsatile flow waveform of the inlet velocity, as a function of flow-time, is shown
in Fig. 1, which is based on the waveform for a right coronary artery taken from the literature.22
Under this flow condition, the peak Re is 330 which correspond to the largest inlet velocity of
0.36 m/s, and the lowest Re is 114 which correspond to the lowest inlet velocity of 0.125 m/s.
The Re is expressed by the following equation:
Re = ρV D/µ, (2)
FIG. 3. The average velocity and the pulsatile velocity waveform in the inlet for blood flow. Dimensionless time t/T is scaled
by the cardiac cycle period, T=0.735 s.
where ρ and V represent the density of the blood and the velocity vector respectively, D is the
diameter of the artery, µ is the viscosity of the blood.
From the above equation of Re, it can be seen that the value of Re decreases with the increase
of the viscosity value. The previous calculations related to Re are based on the minimum viscosity
value of 0.0035 Pa·s and the calculation maximum Re is much less than the critical Re. Therefore,
it is reasonable to assume blood flow to be laminar in the stented artery for all numerical studies in
this paper.
D. Governing equations and numerical methods

The computational grid is imported into the finite-volume-based CFD commercial package
software-Fluent (ANSYS, Inc) to solve numerically the mass continuity and momentum conversa-
tion equations for different combinations of inlet boundary conditions and blood models. The mass
continuity equation for an incompressible fluid is expressed as follows:
∇ · V = 0. (3)
And the momentum conversation equation is decided by the combining forms of inlet boundary
conditions and blood models.
For a steady inlet boundary condition, the momentum conversation equations are expressed
separately as follows for Newtonian or non-Newtonian properties of blood models:
ρV · ∇V = −∇P + µ∇2V. (4)

For a pulsatile inlet boundary condition, the momentum conversation equations are expressed
separately as follows for Newtonian or non-Newtonian properties of blood model:
∂V
( )
ρ + V · ∇V = −∇P + µ∇2V. (5)
∂t
In these equations (3)–(5), V and P represent the blood flow velocity vector and the pressure
respectively, ρ and µ is the density and viscosity of blood respectively.
The fore-mentioned governing equations are discretized by employing a three-dimensional
single-precision, segregated and laminar solver. Default relaxation factors were used to be set as 0.3
for pressure, 1 for density, and 0.7 for momentum. Convergence criterion for continuity and velocity
residuals was set as less than 1 × 10−4, an order of magnitude lower than the recommended value.
As for time step-independence, we used 300 time steps per pulse cycle based on the work
of Dwyer et al.23 who found that 240 time steps per pulse cycle could give very good results
with high resolution. The transient inlet velocity waveforms for the cardiac cycle are programmed
into the Fluent code as UDF profile files. During this simulation, WSS was used to analyze time
step-independence. The computation showed that cyclic independence was achieved at the 4th cy-
cle. And data of some specific time points (see in Fig. 3) in the 4th cardiac cycle are used to analyze
the flow behaviors.
III. RESULTS
A. Effects of the inlet conditions and blood models on blood viscosity

It is obvious that the viscosity of the Newtonian model is constant everywhere independent
of the steady or pulsatile inlet conditions. But the non-Newtonian model shows some interesting
viscosity characteristics. As shown in Fig. 4, for non-Newtonian model, at instants t1, t2 and t3 of
pulsatile conditions (as shown in Fig. 3) and steady conditions there is an increase in viscosity, and
reaches a local maximum along the centerline of the model. In any inlet conditions, the viscosities
in near wall for the non-Newtonian model are all larger than that for the Newtonian model. Espe-
cially, the changes of the viscosity for the non-Newtonian model in the pulsatile inlet conditions
are significant different due to the magnitude of the pulsatile inlet velocity, and the magnitude of
dynamic viscosity is contrary to the magnitude of the inlet velocity. The inlet velocity at instants t2
and t8 of the pulsatile condition is equal to that at the steady condition, but the dynamic viscosity is
still different among them. These results show that the blood models with a non-Newtonian property
and the pulsatile inlet condition all have a strong influence on the blood viscosity, and they can
influence the accurate prediction of hemodynamics in stented arteries.
B. Effects of the inlet conditions and blood models on WSS

As shown in Fig. 5, the WSS distributions in the stented artery vary with different combined
conditions. In the pulsatile inlet condition, three different inlet velocities at time points t1, t2 and t3
(as shown in Fig. 3) respectively represent the minimum, average and maximum velocity and they
are selected to analyze the WSS distributions. As a whole, WSS for non-Newtonian blood model
are all larger than that for Newtonian model in the same inlet conditions. However, for a same blood
model (Newtonian or non-Newtonian), the WSS distributions are completely different at a same
inlet velocity of 0.2 m/s (steady and pulsatile (t1)). Moreover, it can be seen that with the increase of
the inlet velocity, the WSS distributions increase without regard to blood models. It seems that the
WSS distributions are strongly dependent on the pulsation of inlet conditions and blood models.
FIG. 4. Viscosity profiles in the cross-section location indicated in Fig. 1 in the middle of the stented segment at different
conditions.
FIG. 5. The WSS distributions for different blood models at the steady and pulsatile conditions (instants t1, t2 and t3) (units:
Pa).
FIG. 6. Distributions of WSS at the stented wall for Newtonian and non-Newtonian models at different inlet conditions with
a same inlet velocity of 0.2 m/s.
The detailed variations of WSS in stented wall are shown in Fig. 6 and Fig. 7. The time points
showed in Fig. 6 and Fig. 7 are displayed in Fig. 3. Figure 6 shows the variations of WSS for
different blood models at a same inlet velocity of 0.2 m/s. At a same inlet conditions, the WSS
distributions for the non-Newtonian model are all higher than that for the Newtonian model. Though
the magnitude of the inlet velocity is same at the pulsatile condition, the WSS distribution is still
different among these times points. The WSS patterns are all similar, but the magnitude of WSS at
the ascending waveform of blood flow for the systole (t2) and diastole (t6) are far greater than that at
the descending waveform for the systole (t4) and diastole (t8). It can be deduced that the magnitude
and pulsatile waveform of inlet velocity is important for calculating the WSS.
Figure 7 shows the variations of WSS for different blood models at different inflexion points of
the inlet velocity waveform. It still can be seen that the WSS distributions for the non-Newtonian
model are all higher than that for the Newtonian model at the same inlet condition, and with the
increases of the inlet velocity, the WSS increase except for the time point t5. From this figure it can
be noted that the acute change of the inlet velocity waveform results in the abnormal changes of
WSS at instant t5.
Some previous studies8,24,25 on blood flow and WSS indicate that low or oscillating WSS gener-
ated by stent implantation is easy to contribute to neointima hyperplasia, especially in some regions
with the WSS value of less than 0.5 Pa. So 0.5 Pa is assumed as a critical WSS value to consider
the regions prone to restenosis in this study. In order to quantitatively compare the effect of different
inlet velocity conditions and blood models on evaluations of WSS, Figure 8 shows the comparison
results of the area percentage of WSS < 0.5 Pa. For the steady condition, the area percentage of
low-WSS (< 0.5 Pa) for the Newtonian model is higher than 7.86% of that for the non-Newtonian
FIG. 7. Distributions of WSS at the stented wall for Newtonian and non-Newtonian models at different inlet conditions.
FIG. 8. Comparison of the area percentage of WSS < 0.5 Pa for Newtonian and non-Newtonian models at steady and
pulsatile inlet conditions.
model. But for the pulsatile condition, the minimum and maximum area percentage differences of
low-WSS between the Newtonian and non-Newtonian models are 11.03% and 27.65% at instants t7
and t5 respectively. Obviously, the resulting differences between the Newtonian and non-Newtonian
models at the steady condition are larger than that at the pulsatile condition.
IV. DISCUSSION
The studies reported in this paper have studied that the effects of different combinations of
blood models and inlet conditions on predictions of WSS. From the Fig. 4, it can be seen that the
viscosity variations mainly appear in the non-Newtonian blood models and are related to the inlet
conditions. It is also well-known that viscosity is an important factor for WSS. Non-homogeneity
of the viscosity fields for the non-Newtonian model would have a direct impact on the prediction of
hemodynamics. It is conventional to neglect the non-Newtonian effects in large arteries where the
shear rates are much above 100 s−1.26 But as shown in Fig. 9, the regions of shear rates < 100 s−1
are always there for various combinations of inlet conditions and blood models and the area of
shear rates < 100 s−1 for non-Newtonian models are always larger than that for Newtonian models.
Therefore, a better blood model that is close to reality would help us to accurately predict the
hemodynamics in stented arteries.
FIG. 9. Comparison of the area percentage of shear rate <100 s−1 for Newtonian and non-Newtonian models at steady and
pulsatile inlet conditions.
As shown in Fig. 6 and Fig. 7, the variations of WSS for Newtonian and non-Newtonian models
are very similar, while the magnitudes of WSS for the non-Newtonian model are all higher than that
for the Newtonian model at any inlet conditions. This result is demonstrated to be reasonable which
is consistent with the findings of Johnston et al.13,14 It is mainly that the non-Newtonian properties
of blood models greatly affect the viscosity of the whole blood flow field, thus changing the results
of WSS. Moreover, it can be concluded that simulations of Newtonian models overestimate the area
of low-WSS in the stented artery, which can potentially lead to an overestimation of the risk of
in-stent restenosis. It is necessary to achieve a proper blood model for predicting WSS.
For a model with a same inlet velocity of 0.2 m/s at steady or pulsatile conditions, there is a
significant difference and not be compared qualitatively and quantitively for the results of WSS.
Even the model with a same inlet velocity at the pulsatile conditions, the magnitude of WSS is still
different and varies with the waveform of the inlet velocity. It is possible that the waveform of the
inlet velocity would be an important determination for predicting WSS. Only the correct waveform
of the inlet velocity was found to obtain the accurate result of WSS.
V. LIMITATIONS AND FUTURE WORKS

The physical models proposed in this paper are mainly based on simplifying assumptions of
the stents and the vessel walls. There are still some factors which need to be added into the current
models, including the actual vessel structure after stent implantation, viscoelastic properties of
the vessel, cell activities, plaque progression and remodeling. Despite of these simplifications, the
present models also demonstrate the importance of the inlet conditions and the properties of blood
models on hemodynamics.
VI. CONCLUSIONS
In this study, CFD was used to analyze the hemodynamics in the stented artery under different
combinations of inlet conditions and blood models. The effects of blood models with non-Newtonian
property on hemodynamics were significantly higher than that with Newtonian property and blood
models with Newtonian property would overestimate the risk of restenosis. Moreover, WSS was
strongly dependent on the magnitude and waveform of the inlet velocity. It is necessary to compre-
hensively consider the inlet conditions and the properties of blood models for WSS. This will be
beneficial to help predict accurately the performances of stents and assist clinicians in selecting an
appropriate stent for treating stenosis arteries.
ACKNOWLEDGMENTS
This work was supported by National Natural Science Foundation of China under the grant
number: 5775179.
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Effects of the inlet conditions and blood models on accurate prediction of

Article in AIP Advances · May 2015

Yongfei Jiang Jun Zhang

The user has requested enhancement of the downloaded file.

Citation: AIP Advances 5, 057109 (2015); doi: 10.1063/1.4919937

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Hemodynamics altered by stent implantation is well-known to be closely related

a Author to whom correspondence should be addressed. Electronic mail: whzhao@mail.xjtu.edu.cn. Tel.:+86-029-

2158-3226/2015/5(5)/057109/9 5, 057109-1 © Author(s) 2015

II. COMPUTATIONAL MODEL AND METHODS

A. Computational flow model

FIG. 1. Stent structure, flow model and computational grids.

µ = µ∞ + (µ0 − µ∞) [1 + (λγ̇)2](n−1)/2, (1)

D. Governing equations and numerical methods

ρV · ∇V = −∇P + µ∇2V. (4)

A. Effects of the inlet conditions and blood models on blood viscosity

B. Effects of the inlet conditions and blood models on WSS

V. LIMITATIONS AND FUTURE WORKS

C. J. Slager, Circulation 105(23), E185 (2002).

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