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Transient blood flow in elastic coronary arteries

with varying degrees of stenosis and dilatations: CFD
modelling and parametric study
a bc b a ad
Jianhuang Wu , Guiying Liu , Wenhua Huang , Dhanjoo N. Ghista & Kelvin K.L. Wong
a
Shenzhen Institutes of Advanced Technology, Chinese Academy of Sciences, 1068 Xueyuan
Boulevard, Xili Nanshan, Shenzhen 518055, P.R. China
b
Guangdong Provincial Key Laboratory of Medical Biomechanics, Department of Anatomy,
School of Basic Medicine Science, Southern Medical University, No. 1838, Guangzhou Avenue
North, Guangzhou 510515, Guangdong, P.R. China
c
Click for updates Department of Cardiology, The Fifth Affiliated Hospital of Southern Medical University, No.
566, Congcheng Avenue, Conghua District, Guangzhou 510900, Guangdong, P.R. China
d
School of Computer Science and Software Engineering, The University of Western
Australia, 35 Stirling Highway, Crawley, WA 6009, Australia
Published online: 14 Nov 2014.

To cite this article: Jianhuang Wu, Guiying Liu, Wenhua Huang, Dhanjoo N. Ghista & Kelvin K.L. Wong (2014): Transient
blood flow in elastic coronary arteries with varying degrees of stenosis and dilatations: CFD modelling and parametric study,
Computer Methods in Biomechanics and Biomedical Engineering, DOI: 10.1080/10255842.2014.976812

To link to this article: http://dx.doi.org/10.1080/10255842.2014.976812

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 Computer Methods in Biomechanics and Biomedical Engineering, 2014
http://dx.doi.org/10.1080/10255842.2014.976812

Transient blood flow in elastic coronary arteries with varying degrees of stenosis and dilatations:
CFD modelling and parametric study
Jianhuang Wua, Guiying Liub,c, Wenhua Huangb, Dhanjoo N. Ghistaa and Kelvin K.L. Wonga,d*
a
Shenzhen Institutes of Advanced Technology, Chinese Academy of Sciences, 1068 Xueyuan Boulevard, Xili Nanshan, Shenzhen 518055,
P.R. China; bGuangdong Provincial Key Laboratory of Medical Biomechanics, Department of Anatomy, School of Basic Medicine
Science, Southern Medical University, No. 1838, Guangzhou Avenue North, Guangzhou 510515, Guangdong, P.R. China;
c
Department of Cardiology, The Fifth Affiliated Hospital of Southern Medical University, No. 566, Congcheng Avenue, Conghua District,
Guangzhou 510900, Guangdong, P.R. China; dSchool of Computer Science and Software Engineering, The University of Western
Australia, 35 Stirling Highway, Crawley, WA 6009, Australia
(Received 27 May 2014; accepted 12 October 2014)
Downloaded by [Archives & Bibliothèques de l'ULB] at 05:19 12 January 2015

In this paper, we have analysed pulsatile flow through partially occluded elastic arteries, to determine the haemodynamic
parameters of wall shear stress (WSS), wall pressure gradient and pressure drops (DP), contributing to enhanced flow resistance
and myocardial ischaemic regions which impair cardiac contractility and cause increased work load on the heart. In summary, it
can be observed that stenoses in an artery significantly influence the haemodynamic parameters of wall shear stress and pressure
drop in contrast to dilatations case. This deduces that stenosis plays a more critical role in plaque growth and vulnerability in
contrast to dilatation, and should be the key element in cardiovascular pathology and diagnosis. Through quantitative analysis of
WSS and DP, we have provided a clearer insight into the haemodynamics of atherosclerotic arteries. Determination of these
parameters can be helpful to cardiologists, because it is directly implicated in the genesis and development of atherosclerosis.
Keywords: atherosclerosis; fluid –structure interaction; elastic artery; stenosis; dilatations

1. Introduction fatty deposits within arterial walls; however, this is unable

1.1 Motivation of CFD haemodynamic modelling for
understanding the mechanism of atherosclerotic plaque
formation and aggravation
The thickening of an artery wall has long been understood
as an early process in the formation of atherosclerosis, and
is one of the most widespread diseases in humans leading
to the malfunction of the peripheral vascular system
(Nerem 1992; Worthley et al. 2000, 2002). The gradual
built-up of cholesterol plaque in the artery wall and
eventual rupture of the plaque can cause immediate
occlusion of the artery and lead to sudden death. The
causes of atherosclerosis may be high blood pressure,
tobacco smoking, excessive drinking, high cholesterol,
diabetes, as well as physical inactivity and obesity.
Atherosclerosis is a major clinical problem and the
disease leads patients to experience strokes and heart
failures. To prevent such harm from occurring, stents are
inserted into the affected regions of plaque or atheroma
depositions to enhance the area of flow. The haemody-
namics in stenotic elastic arteries can be usefully
investigated by means of computational fluid dynamics
(CFD) modelling, to investigate the regions of low wall
shear stresses, wall pressure gradient (WPG) and pressure
drops that contribute to atherosclerotic plaques formation.
Medical imaging can be used to visualise the regions of
to provide numerical data like the CFD simulation models.
Computational simulations, on the other hand, can provide
an in-depth analysis on flow resistance due to shear stress
on walls, flow rates and pressure drops as illustrated by
Kompatsiaris et al. (2000) and Liu et al. (2014). The CFD
results obtained by modelling the vessels in their affected
regions can be deemed to be equivalent to the accuracy of
mathematical data standards. By combining the knowl-
edge of clinicians and the information extracted from
accurate CFD computational models, we can obtain a
reliable procedure for medical diagnosis and treatment..
The CFD computational results obtained by modelling
the vessels in their affected regions can be used to assess
the disease (Soulis et al. 2006; Prosia et al. 2007).
As stated earlier, by combining the knowledge of
clinicians based on the information extracted from medical
images with the haemodynamic parametric information
derived from CFD modelling, a patient-specific method-
ology can be developed for diagnosis of the severity of the
condition of atherosclerotic arteries in order to then
determine the optimal treatment recourse. In fact, even the
treatment procedure such as by stenting can be analysed in
advance of actually carrying it out, so as to determine the
optimal treatment recourse, be it coronary arterial stenting
or grafting (CABG) based on the assessment of abnormal

*Corresponding author. Email: kelvin.wong@siat.ac.cn, kelvin.wong@uwa.edu.au

q 2014 Taylor & Francis
 2 J. Wu et al.
flow conditions in the stented vessel and the distal
anastomosis of the CABG (Moore et al. 1999; Torii et al.
2009; Chaichana et al. 2013a, 2013b).
Experimental methods of in vitro and in vivo
investigation of the flow field are not representative and
reliable due to small size of the vessel. Hence, the
enhancement in software development along with
computer performance provides CFD as an alternative to
such experimental methods.
The muscular fibres of the heart contract and relax in
order to control the blood flow supply volume through the
vessels, and thereby serve the function of regulating blood
to the different regions of the heart. As such, it is of clinical
importance to understand how constriction and dilatations
at the various arterial segments can affect the blood flow
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dynamics. In this paper, the idealistic arterial vessel
geometry can sufficiently represent the unique flow
behaviour of the stenosed and curved arteries, in terms
of the values of the haemodynamic parameters mentioned
earlier. By using CFD based on physiological boundary
conditions, we can somewhat realistically characterise
atherosclerosis and provide an extensive parametric study
of this disease.
1.2 Implementation of CFD approach and
haemodynamics parameters used
This investigation entails modelling of fluid flow through
the arteries under stenotic conditions, causing athero-
sclerotic plaque. The blood can be treated to be a
generalised Newtonian fluid, and the arterial wall can be
considered to be having different degrees of stenosis in its
lumen, arising from various types of abnormal growth or
plaque formation. The nonlinear unsteady pulsatile flow
phenomenon is governed by the Navier –Stokes equations
combined with the Continuity equation. In an attempt to
derive physiologically significant and accurate quantities,
the governing equations of motion need to be accompanied
by the appropriate choice of boundary conditions.
The necessary checking for numerical stability of the
computational procedure has been incorporated into the
algorithms for better precision of the results computed.
The quantitative analysis results include the profiles of
the flow field, the temperature and the mass concen-
tration, along with their individual distributions over the
entire arterial segment as well. The key haemodynamic
factors such as the wall shear stress (WSS) and the WPG
are also examined for further qualitative insight into the
blood flow through the arterial stenosis. The results are
found to portray consistency with several existing results
in the literature, which substantiate sufficiently to validate
the clinical applicability of the model under
consideration.
In this paper, we are concerned with pulsatile flow
through partially occluded curved arteries, to determine
the haemodynamic parameters of WSS and WPG
contributory to enhanced flow resistance and myocardial
ischaemic regions which impair cardiac contractility and
cause increased work load on the heart. The investigation
is undertaken by working on a set of equations describing
the blood flow in an artery containing deformities and
curvatures in all shapes and sizes. The flow conditions,
structural variation and multiple abnormal segments
all have influence on the resistance to flow ratio. The
theoretical framework examines the variability in curvi-
linear arterial wall geometry on the blood flow resistance
and investigates the haemodynamic disturbances associ-
ated with the two main causes of death due to coronary
artery disease: one is the slowly increasing build-up of
cholesterol plaque in the artery and the other being the
rupture of the plaque causing sudden occlusion of the
artery. Tang et al. (2005) have explored CFD modelling to
provide a non-invasive method of studying plaque rupture
in carotid bifurcation arteries.The main aim of harnessing
computational models is to provide vascular surgeons with
more flow disturbance parameters for cardiac diagnosis.
Based on WSS and WPG, the CFD simulation of blood
flow through an atherosclerotic artery can generate the
characteristics of flow through the abnormal segments of
the artery for varying shape parameter and the degree of
flow resistance, to thereby serve as a guide in clinical
diagnosis.
2. Methodology
2.1 Describing the arterial wall geometry and material
property
The independent variables that influence the resistance to
flow ratio are the characteristics of the blood, the geometry
of the artery and its wall flexibility characteristics. The
dimensional parameters of the typical arterial segment
serve as inputs for determining the flow properties and
characteristics.
The axial geometry is characterised by the non-occluded
wall height H0 for an atherosclerotic lesion of length l0
through an artery of diameter D0. We allow for both
constriction (stenosis) and dilation (aneurysm) of the lumen.
Then, the normalised diseased height is given by:
Di 2 H i
hi ¼ for 2 0:5 # hi # 0:5; i ¼ 1; 2: ð1Þ
Di
The geometrical model of a three-dimensional artery is
shown in Figure 1. The cylindrical domain has a total
length of L ¼ 45 mm, wherein L1 ¼ 5 mm from the inlet
segment, and the first diseased segment (stenosis) has a
length of L2 ¼ 7.5 mm. Then after a length of L3 ¼ 5 mm,
the second diseased segment (dilatation) is located having
the length L4 ¼ 7.5 mm and at a distance L5 ¼ 5 mm from
the outlet segment. The non-diseased sections have
 Computer Methods in Biomechanics and Biomedical Engineering 3

with fluid viscosity and density of m ¼ 0.035 Pa s and

Stenosis
H1= 2 mm
r ¼ 1050 kg m 3, and the flow is assumed to be
H1= 3.2 mm
L1
h1= 0.5 h1= 0.3 Newtonian (Johnston et al. 2004). The arterial wall is
L2
modelled as a no-slip wall and is elastic in nature. At the
L3 H1= 3.6 mm
inlets and outlets, we have interpolated the velocity and
10 mm 1
L4
h1= 0.1 pressure waveforms that were simultaneously acquired
5 mm
L5
with an electrocardiography-gated intravascular ultra-
2
7.5 mm sound Doppler and pressure probe (Combo Wire, Volcano
H2= 4.4 mm 5 mm
h2= –0.1 TM Corporation) in the proximal and distal RCA of a
7.5 mm hw= 0.2 mm suspected patient with confirmation of unobstructed
5 mm
coronary artery (Hadjiloizou et al. 2008). Then as regards
H2= 5.2 mm H2= 6 mm
h2= –0.3 h2= –0.5 the boundary conditions, the time-varying velocity was
20 mm
applied at the inlet cross section, while the time-varying
4 mm
pressure was applied at all the outlets for all the simulated
Dilatation vessels (as illustrated in Figure 2). For the solution setting,
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the incompressible Navier – Stokes equations were

Figure 1. Different degrees of stenotic heights and lengths of
the arterial sections. The wall heights vary at different sections
(L1 – L5) of the cylindrical tube of the specific thickness
representing an artery. The inlet and outlet of the tube are
extended to enable the parabolic flow profile to be developed fully
prior to entering the artery. The flow parameters are extracted at
the beginning of L1 and the end of L5 surfaces, and averaged.
constant diameter of D0 ¼ 4.0 mm. The variational h1 and
h2 localised at the throats of the artery represent the heights
of the diseased segments. The wall thickness hw ¼ 0.2 mm
with density of r ¼ 1150 kg m3. The compliant vessel is
modelled as an isotropic material with Poisson ratio of
v ¼ 0.499 and Young modulus E ¼ 5 MPa of the solid
structure (Liu et al. 2014).
2.2 CFD modelling of arterial flow
The fluid flow is considered to be laminar, three-
dimensional, transient, isothermal and incompressible.
The blood fluid is modelled as an incompressible fluid,
employed as the governing equations, and a high
resolution for advection and second-order backward
Euler for transient scheme were used.
2.3 Configuration of numerical simulation
Numerical analyses using CFD techniques have been
performed on various structural configurations of the
artery. Over the decade, with the rapid advancement of
computer technology, CFD has been widely adopted to
investigate the haemodynamic parameters inside various
stenosed arteries as portrayed by Poiseuille (1836).
Although the method requires considerably long compu-
tational time, it is well accepted as one of the more
accurate approaches for a detailed haemodynamic
analysis. In our study, we have analysed a sample of 36
geometrical configurations, with the diseased to normal
wall length ratio; different combinations of disease heights
(h1 and h2), ranging from dilatation with value of 2 0.5 to
stenosis with value of 0.5 (Wong et al. 2006), have been

Figure 2. Physiological waveforms for velocity at the inlet and pressure at the outlet of an artery. The waveforms present the velocity
(left axis) and pressure variations (right axis) at the entrance and exit of the vessel in one cardiac cycle. The velocity waveform is
measured in m/s, while that of the pressure is measured in mmHg.
 4 J. Wu et al.

Table 1. Geometrical parameters and boundary conditions where P is the wall static pressure, and x, y and z are the 3D
adopted in the CFD simulations. coordinates in space.
Parameter Value
The ratio l1 of average wall shear stress WSS
pertaining to the entire wall of artery at peak systole is
Normalised diseased height, h1 [2 0.5, 2 0.3, given by:
2 0.1, 0.1, 0.3, 0.5]
Normalised diseased height, h2 [2 0.5, 2 0.3,
2 0.1, 0.1, 0.3, 0.5] WSS1
l1 ¼ ; ð5Þ
Normalised wall length, l0/L [1/6, 1/4, 1/6, 1/4] WSS2
Reynolds number, Re 122– 692
Number of mesh elements 28,782
where WSS1 and WSS2 are the average WSS in the
atherosclerotic artery and in the normal artery,
generated and imported into a generic CFD package – respectively.
ANSYS CFX 14.5. The flow resistance ratio (Wong et al. 2006) is defined
Within the CFD code, the finite volume method is used as
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to solve the detailed blood flow structure that is

represented by the Navier– Stokes equations. At the DP1
l2 ¼ ; ð6Þ
inlet, we have stipulated fully developed parabolic DP2
velocity profiles corresponding to the Reynolds number,
Re ¼ rVL=y , having a range of 122 – 692; a constant where DP1 and DP2 are the pressure differences pertaining
static pressure is employed at the outlet of the tube. Details to the atherosclerotic artery and to the normal artery,
of the boundary conditions and geometrical parameters respectively.
adopted are summarised in Table 1.

2.5 Mathematics of fluid structure interaction

2.4 Measured fluid dynamics properties In fluid –structure interaction (FSI) simulations, the fluid is
This paper places its focus on the two critical flow modelled using an appropriate Navier– Stokes equation
parameters: WSS and WPG for arteries with stenosis and that includes energy equation, continuity equation and the
dilatations locations at the diseased segments. momentum equation. These equations are then coupled
It is of interest to examine the WSS, as endothelial with the governing equation for the solid domain. When
cells of the vessel wall tend to be aligned along the site of solving FSI, the coupling between fluid and solid solvers is
local WSS at the throat of the artery (as indicated by the governed by a set of conditions that ensure that the
stenosis located at section 1 of the artery in Figure 1). The dynamic and kinematic relationships of the two sub-
WSS is calculated as domains are properly represented.
These two conditions are employed for FSI coding,


›ut

which generally adopt the partitioned approach. For
tw ¼ 2m
wall; ð2Þ following the kinematic condition, the fluid nodes on the
›n
FSI interface are updated according to their corresponding
solid nodes. In the dynamic condition, equilibrium of
where m (kg/m s) is the dynamic viscosity, velocity ut (m/s)
stress on FSI interface is maintained, and the fluid pressure
is the tangential to the wall and n is the unit vector
is integrated into fluid force that is applied onto the solid
perpendicular to the wall.
nodes at the FSI interface. In FSI simulation, the governing
The average WSS is calculated as
equations involved can be derived in Lagrangian, Eulerian
ÐÐÐ and Arbitrary Lagrangian – Eulerian (ALE) frame of
D tw ðx; y; zÞd x d y d z references. The governing equations for the fluid and
WSS ¼ ; ð3Þ
kDk solid domains are given below.

where tw is the WSS on the wall, and x, y and z are the 3D

coordinates in space. D is the volume while d is the 2.5.1 Fluid domain
infinitisimal distance. The Continuity equation is based on the idea that any mass
The WPG is defined as in the system has to be conserved. This means that the rate
of change of mass within the control volume is equivalent
ffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffi
s     2  2 to the mass flux crossing the surface S of volume V. After
›P 2 ›P 2 ›P ›P
WPG ¼ þ þ ; ð4Þ some mathematical manipulations, a general form of
›x ›x ›y ›z continuity equation in the Eulerian frame can be written as
 Computer Methods in Biomechanics and Biomedical Engineering
Continuity equation:
›P
þ V
7r ¼ 2r7
V:
›t
The Energy equation is formulated on the physical
principle that energy in the system has to be conserved.
A general form of energy equation in the Eulerian frame
can be written as
›E
r þ rðV
7ÞE ¼ 7
ðs
VÞ þ V
rb:
›t
The Momentum equation can be formulated based on
the physical principle that momentum in the system has to
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be conserved. A general form of momentum equation in
the Eulerian frame can be written as
›V
r þ rðV
7ÞV ¼ 7
s þ rb:
›t
2.5.2 Solid domain
The governing equation for the solid domain is formulated
in the Lagrangian reference frame shown as follows:
›2 d G ›2 d G
rs hs þ a 0 d G 2 b ¼ PG ;
›t 2 ›X 2
where a0 ¼ Ehs =r 2 ð1 2 y 2 Þ; b ¼ K T Bhs . Note that KT
denotes the Timoshenko shear correction factor and PG is
structural load on the interface G due to the external
forcing term from the fluid, dG is displacement at the
interface, X is position in space and t is position in time.
The solid domain is constructed in the ANSYS solver,
while the fluid domain is modelled in the CFX solver. The
in-between coupling is from the ‘setup’ of the two solvers.
Once the simulation is run in the ‘solution’ window, it first
begins computing iterations for the solid domain by
initiating the ANSYS solver, and then progresses onto the
fluid domain in the CFX solver.
3. Results
3.1 Contour plots of WSS and WPG
The study of flow of a viscous incompressible fluid through a
compliant tube has many applications. One major appli-
cation is blood flow through human arteries. Understanding
wave propagation in arterial walls, local haemodynamics,
temporal WSS and WPG are important in understanding the
mechanisms leading to various complications in cardiovas-
cular function. Many clinical treatments can be studied in
detail only if a reliable model describing the response of
arterial walls to the pulsatile blood flow is considered.
From Figures 3 and 4, it can be seen that both WSS and
WPG properties are shown to demonstrate significant
5
increments at segments where the artery is more stenosed.
The opposite occurs for dilatations but at much lower
magnitudes. For the narrowest sections (i.e. at the maximum
ð7Þ
h1 and h2), the WSS and WPG values are significant.
However, for the widest sections (i.e. at the minimum h1 and
h2), these parameter values are not changing as significantly
as in the narrowest sections. We note that the values of WSS
and DP for normal (non-stenosed and non-dilated) arterial
segments, whereby h1 ¼ 0 and h2 ¼ 0, are 5.601 Pa and
425.806 Pa, respectively.
ð8Þ
3.2 Surface response graphs of WSS and WPG
The effect of additional flow resistance can be further
ascertained based on the velocity variation in an artery. For
example, as the dilation increases, the vessel cross-sectional
area enlarges and the flow velocity gradually decreases
while the pressure increases; for this case, the flow resistance
ð9Þ will be minimal. However, the re-circulating motion of the
fluid induces additional energy and pressure loss to flow,
causing extra flow resistance. In our study, due to the small
arterial dilatation implemented, the flow separations are
assumed to be negligible. As such, the flow resistance will
still show a decline when there is dilatation.
As depicted in Figure 5, the predicted average wall
shear stress WSS and pressure drop DP (or flow resistance
ratio) surface response from CFD simulations illustrate a
surface response trend that is identical with each other.
In particular, for the cases with dilation (i.e. where h1 and h2
are of negative value), the elastic artery has generated 3D
flow response results of WSS and DP values that are shown
to decline. However, this decline is not significant. The
decline is also dissimilar in magnitude for the two WSS and
DP cases. The minimum average wall shear stress ratio, l1
falls much below a value of one at 0.667, whereas the
minimum flow resistance ratio l2 is very much closer to one
at 0.987. With reference to this trend, dilatations can be
observed to have an influence on reducing WSS values with
respect to the normal and healthy artery, and may also have
some implications on the plaque growth. In addition, it is
also observed that a longer diseased segment (based on a
ratio of 2:1 for diseased to non-diseased sections) tends to
increase the WSS magnitude, which can be explained by the
greater narrowing resulting from a larger extension of the
stenosis. However, this does not affect DP since the pressure
across the inlet and outlet is not dependent on the
geometrical variation in between.
On the other hand, for those stenosis cases (i.e. where
h1 and h2 are of positive value), both WSS and DP are
higher in values. The increment in these flow values with
respect to the increasing stenosis is much more significant.
However, the maximum ratio l1 rises to a value of 2.956,
whereas that of l2 is very much higher at 6.842. While
both the l1 and l2 surface plots of Figure 5 demonstrate
similar trends, we can see that pressure drop ratio gives a
 6 J. Wu et al.

Segment 2
H2 2.0 3.2 3.6 4.0 4.4 5.2 6.0
H1 h1,2 0.5 0.3 0.1 0.0 –0.1 –0.3 –0.5

2.0 0.5

3.2 0.3
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3.6 0.1
Segment 1

4.0 0.0

4.4 –0.1

5.2 –0.3

6.0 –0.5

Figure 3. Detailed WSS contour plot showing the development of WSS profiles for diseased segment heights h1 and h2. The normalised
diseased wall heights vary from h1 ¼ 2 0.5 to þ0.5 and h2 ¼ 2 0.5 to þ0.5 at sections L2 and L4. The WSS is shown to demonstrate a
larger variation at these sections when the artery is particularly stenosed, rather than dilated. When the value of h1 and h2 becomes 0.5, the
WSS value increases significantly at the narrowest sections. The colour bar scale representing WSS values varies from 0 to 40 Pa.

stronger indication of variation as than the average WSS
ratio. It is possible that there can be some discrepancy in
the actual WSS and DP values in the event of stenosis due
to the additional flow resistance created by flow separation
at the downstream of the stenosis. Nonetheless, in general,
existing theories agree reasonably well with the results
produced by the FSI framework.
3.3 Velocity contour plots of stenosed artery flow
Based on flow visualisation in the diseased artery obtained
by numerical simulation of haemodynamic analysis, we
have plotted in Figure 6 velocity contours in the of X – Y
plane, at different times in the ideal vessel with stenosis
and dilatations. The blood flows from left to right as shown
in the figure. The nature of blood flow through
atherosclerotic arteries can assist our understanding of
the flow conditions within diseased arteries. For example,
higher velocity flow is observed at the site of stenosis, and
this can cause plaque rupture. Also, sudden pressure
release after stenosis can aggravate dilatations.
3.4 Summary of haemodynamic analysis
In summary, as can be observed in Figures 3– 5, double
stenoses (based on h1 . 0 and h2 . 0) in an artery
 Computer Methods in Biomechanics and Biomedical Engineering 7

Segment 2
H2 2.0 3.2 3.6 4.0 4.4 5.2 6.0
H1 h1,2 0.5 0.3 0.1 0.0 –0.1 –0.3 –0.5

2.0 0.5

3.2 0.3
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3.6 0.1
Segment 1

4.0 0.0

4.4 –0.1

5.2 –0.3

6.0 –0.5

Figure 4. Detailed WPG contour plot showing the development of WPG profiles for diseased segment heights h1 and h2. The normalised
diseased wall heights vary from h1 ¼ 2 0.5 to þ 0.5 and h2 ¼ 2 0.5 to þ 0.5 at sections L2 and L4. However, the WPG is shown to
demonstrate a larger variation at sections L1 and L3 rather than sections L2 and L4 where the stenosis occurs. This may be explained by the
pressure build up at the entrance segment of each stenosis. The colour bar scale representing WPG values varies from 9900 to 12,000 Pa.

significantly influence the parameters that we are
investigating, and this is in contrast to the double
dilatations case (based on h1 , 0 and h2 , 0). This
deduces that stenosis plays a more critical role in plaque
growth and vulnerability in contrast to dilatation, and
should be the key element in cardiovascular diagnosis.
Through qualitative visualisation that is coupled with the
quantitative analysis of WSS and DP, we can gain a clearer
insight into the haemodynamics of atherosclerotic arteries.
Determination of these parameters can be helpful to
cardiologists because it is directly implicated in the
genesis and development of atherosclerosis, which thereby
motivates us to use them as exemplified parameters in our
parametric analysis framework.
4. Discussion
We have carried out CFD haemodynamic analysis of
blood flow through atherosclerotic arteries. The resulting
generation of flow properties and parameters enables us to
understand the mechanisms of cardiovascular athero-
sclerotic pathology due to varying degrees of arterial
 8 J. Wu et al.

∆P
Wall Ratio 1: 1 Wall Ratio 1: 1

Wall Ratio 2: 1 Wall Ratio 2: 1

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h1 –0.5 –0.3 –0.1 +0.1 +0.3 +0.5 h1 –0.5 –0.3 –0.1 +0.1 +0.3 +0.5
Max Max
1.768 1.839 1.992 2.137 2.308 2.956 4.512 4.509 4.566 4.566 4.879 6.842
λ1 λ2
Max Max
WSS 9.903 10.298 11.158 11.968 12.929 16.558 ∆P 1921.38 1919.92 1944.07 1944.07 2077.68 2913.49
(Pa) (Pa)
Min Min
0.667 0.685 0.769 0.850 0.959 1.814 0.987 0.974 0.968 0.985 1.411 4.035
λ1 λ2
Min Min
WSS 3.735 3.836 4.307 4.759 5.370 10.158 ∆P 420.441 414.608 412.393 419.43 600.615 1718.13
(Pa) (Pa)

Figure 5. Flow surface response of elastic arteries based on average WSS and pressure drop flow parameters. The surface response
values pertaining to ratio l1 of average wall shear stress WSS and to ratio l2 of pressure drop DP are normalised with respect to those of
the healthy artery with no wall variation that represents our standard model. Double stenosis is seen to present incremental values of l1 and
l2 ratios, implying larger WSS and WPG distributions, whereas double dilatation indicates otherwise. For the longer diseased segments
(with diseased to non-diseased segment ratio of 2:1), the WSS increases in magnitude, while the change in DP is negligible. As a reference,
the values of WSS and DP for normal arterial segments (h1 ¼ 0 and h2 ¼ 0) are 5.601 Pa and 425.806 Pa, respectively.

stenosis and dilations. We shall now discuss the results
with reference to the implications with atherosclerosis.
4.1 Implications in relevance with atherosclerosis
Research into the cause of atherosclerosis has been
performed for decades (Caro et al. 1971; Ku et al. 1985;
Glagov et al. 1989). There are various schools of thoughts on
its causative mechanism. In this regard, one group believes
that plaque growth is due to low wall and oscillating shear
stress levels (Friedman et al. 1986, 1989; Nerem 1992;
Giddens et al. 1993; Lee and Chiu 1996; Kleinstreuer et al.
2001), whereas high levels of this parameter tends to suppress
it (Ku et al. 1985; Friedman et al. 1986; Giddens et al. 1993).
In addition to the low and oscillating WSS, the intramural
stress of the wall may also contribute to plaque growth at an
advance stage of the disease (Tang et al. 2008). Another
group believes that vessel wall thickening occurs in the event
of high shear stress (as reported by Wentzel et al. (2003) and
Joshi et al. (2004)). It is also believed that von Mises and
principal stress at the apex of the plaque can also be used to
characterise the initialisation and aggravation of its growth
(Salzar et al. 1995; Thubrikar and Robicsek 1995; Delfino
et al. 1997; Lee and Xu 2002; Kaunas et al. 2006; Hariton
et al. 2007; Callaghan et al. 2009). Meanwhile, the search for
other indicators that better describe the causative mechanism
is still on-going. We have shown in our results that the
stenotic part of the arteries experiences high WSS and
demonstrates to be more prone to plaque aggravation. This
has been consistent with the previous experimental studies.
4.2 Elasticity of atherosclerotic arteries and its
implication in atherogenesis
Although there is no direct relationship between
deformation and atherogenesis, the presence and charac-
terisation of high deformation regions at the throat of the
artery has been investigated for inducing plaque rupture.
Atherosclerotic plaque may be categorised into various
types, such as (i) atheromatous plaque that has an
artheroma or lipid pool covered with a fibrous cap, and (ii)
a non-atheromatous plaque that consists of a connective
issue with admixed smooth muscle cells, and the calcified
plaque. We show that the FSI algorithm based on the
 Computer Methods in Biomechanics and Biomedical Engineering 9
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Figure 6. Flow visualisation in atherosclerotic artery with stenosis and dilatations. The plots of axial velocities in a stenosed artery are
presented for the double stenosis and double dilatations conditions. Velocity distribution is taken at the centre plane of a stenosed artery
and may be used to compare the difference in flow due to those stenosis and dilatations. This flow visualisation allows us to understand the
flow condition within a diseased artery effectively by showing the regions of high speed flow qualitatively.

Dynamic equations coupled with the Navier –Stokes
equations for a viscous incompressible fluid captures the
experimentally measured viscoelastic properties of arterial
walls in the modelled arterial length. Using estimates
based on an energy inequality, coupled with the
asymptotic analysis and homogenisation theory, it is
possible to derive an effective, closed FSI model and a fast
numerical solver whose solutions capture the viscoelastic
properties of major arteries. The reduced effective model
reveals several interesting features of the coupled FSI
problem.
It is also of interest from the evidence of the 3D surface
plots that elastic boundary conditions seemed to have a
higher resistance to that of the rigid boundary conditions.
This result is because energy is taken to deform the blood
vessel, hence there is a loss of momentum and more
resistance is added due to the loss of momentum and in the
direction of flow. With comparisons between transient and
steady state flows, the transient flow conditions seemed to
have a higher resistance, which corresponds to a higher
flow resistance ratio to that of steady state flow conditions.
This is also due to the scenario in which the energy in the
pulse generated by the pump (heart) begins to lose the
momentum throughout the length of artery due to friction
from the arterial walls. A consistent flow through the
length of the artery will seem to experience mush less
resistance throughout the flow conditions. With the aid of
3D surface plots, strong support can be based on theory
relating to flow behaviour through a length of artery.
To study the coupling between the motion of the vessel
wall and pulsatile blood flow, a detailed description of
the vessel wall biomechanical properties may lead to a
mathematical and numerical problem whose complexity is
beyond today’s computational capabilities. The nonlinear-
ity of the underlying FSI is so severe that even a simplified
description of the vessel wall mechanics assuming
homogeneous linearly elastic behaviour leads to compli-
cated numerical algorithms with challenging stability and
convergence properties. To devise a mathematical model
that will lead to a problem that is agreeable to numerical
methods producing computational solutions in a reason-
able period (time frame), various simplifications need to
be introduced. They can be based on simplifying model
assumptions, capturing only the most important physics of
the problem or on the simplifications utilising special
problem features, such as special geometry, symmetry and
periodicity.
Devising an accurate model for the mechanical
behaviour of arterial walls is more complicated. Arterial
walls are anisotropic and heterogeneous and composed of
layers with different biomechanical characteristics.
A variety of different models has been suggested in the
 10 J. Wu et al.
literature to model the mechanical behaviour of arteries.
They range from the detailed description of each of the
layers to the average description of the total mechanical
response of the vessel wall assuming homogeneous,
linearly elastic behaviour.
5. Conclusion
Medical imaging modalities are able to characterise the
atherosclerotic plaque in terms of their mechanical
properties. Non-invasive imaging not only identifies
flow-limiting vascular stenosis, but also measures athero-
sclerotic plaque burden and its response to treatment, and
differentiates stable plaques from those which tend to
rupture. However, the prediction of high-risk plaque
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rupture still requires a numerical simulation framework for
verification.
In this study, the numerical simulations of variational
stenotic arteries were analysed quantitatively in terms of
WSS and DP. The mechanical interaction between the
vessel wall and fluid is modelled using FSI. Utilisation of a
pulsatile waveform for the physiological inlet velocity and
outlet pressure of the blood brings the simulation closer to
its real physiological state. This can form the basis to
undertake CFD and FSI techniques to find solutions
problems which somewhat may have never been possible a
few decade ago. With the coupling of fluid and structural
solvers by means of an FSI framework, it is possible to
determine the unsteady flow behaviour throughout the
length of an elastic artery. Furthermore, the visualisation
using 3D surface plots of the average WSS and pressure
drop parameters can support theoretical measures that lead
to the determination of flow parameters contributory to
cardiovascular flow pathology.
Conflict of interest statement
We confirm that all authors of this manuscript have no
conflicts of interest to declare.
Funding
This work is supported by the National Natural Science
Foundation of China [grant number 61272328].
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