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

*Corresponding author. Email: [email protected], [email protected]

q 2014 Taylor & Francis
 2 J. Wu et al.

flow conditions in the stented vessel and the distal the haemodynamic parameters of WSS and WPG
anastomosis of the CABG (Moore et al. 1999; Torii et al. contributory to enhanced flow resistance and myocardial
2009; Chaichana et al. 2013a, 2013b). ischaemic regions which impair cardiac contractility and
Experimental methods of in vitro and in vivo cause increased work load on the heart. The investigation
investigation of the flow field are not representative and is undertaken by working on a set of equations describing
reliable due to small size of the vessel. Hence, the the blood flow in an artery containing deformities and
enhancement in software development along with curvatures in all shapes and sizes. The flow conditions,
computer performance provides CFD as an alternative to structural variation and multiple abnormal segments
such experimental methods. all have influence on the resistance to flow ratio. The
The muscular fibres of the heart contract and relax in theoretical framework examines the variability in curvi-
order to control the blood flow supply volume through the linear arterial wall geometry on the blood flow resistance
vessels, and thereby serve the function of regulating blood and investigates the haemodynamic disturbances associ-
to the different regions of the heart. As such, it is of clinical ated with the two main causes of death due to coronary
importance to understand how constriction and dilatations artery disease: one is the slowly increasing build-up of
at the various arterial segments can affect the blood flow cholesterol plaque in the artery and the other being the
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dynamics. In this paper, the idealistic arterial vessel rupture of the plaque causing sudden occlusion of the
geometry can sufficiently represent the unique flow artery. Tang et al. (2005) have explored CFD modelling to
behaviour of the stenosed and curved arteries, in terms provide a non-invasive method of studying plaque rupture
of the values of the haemodynamic parameters mentioned in carotid bifurcation arteries.The main aim of harnessing
earlier. By using CFD based on physiological boundary computational models is to provide vascular surgeons with
conditions, we can somewhat realistically characterise more flow disturbance parameters for cardiac diagnosis.
atherosclerosis and provide an extensive parametric study Based on WSS and WPG, the CFD simulation of blood
of this disease. 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
1.2 Implementation of CFD approach and flow resistance, to thereby serve as a guide in clinical
haemodynamics parameters used diagnosis.
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 2. Methodology
generalised Newtonian fluid, and the arterial wall can be 2.1 Describing the arterial wall geometry and material
considered to be having different degrees of stenosis in its property
lumen, arising from various types of abnormal growth or
The independent variables that influence the resistance to
plaque formation. The nonlinear unsteady pulsatile flow
flow ratio are the characteristics of the blood, the geometry
phenomenon is governed by the Navier –Stokes equations
of the artery and its wall flexibility characteristics. The
combined with the Continuity equation. In an attempt to
dimensional parameters of the typical arterial segment
derive physiologically significant and accurate quantities,
serve as inputs for determining the flow properties and
the governing equations of motion need to be accompanied
characteristics.
by the appropriate choice of boundary conditions.
The axial geometry is characterised by the non-occluded
The necessary checking for numerical stability of the
wall height H0 for an atherosclerotic lesion of length l0
computational procedure has been incorporated into the
through an artery of diameter D0. We allow for both
algorithms for better precision of the results computed.
constriction (stenosis) and dilation (aneurysm) of the lumen.
The quantitative analysis results include the profiles of
Then, the normalised diseased height is given by:
the flow field, the temperature and the mass concen-
tration, along with their individual distributions over the Di 2 H i
entire arterial segment as well. The key haemodynamic hi ¼ for 2 0:5 # hi # 0:5; i ¼ 1; 2: ð1Þ
Di
factors such as the wall shear stress (WSS) and the WPG
are also examined for further qualitative insight into the The geometrical model of a three-dimensional artery is
blood flow through the arterial stenosis. The results are shown in Figure 1. The cylindrical domain has a total
found to portray consistency with several existing results length of L ¼ 45 mm, wherein L1 ¼ 5 mm from the inlet
in the literature, which substantiate sufficiently to validate segment, and the first diseased segment (stenosis) has a
the clinical applicability of the model under length of L2 ¼ 7.5 mm. Then after a length of L3 ¼ 5 mm,
consideration. the second diseased segment (dilatation) is located having
In this paper, we are concerned with pulsatile flow the length L4 ¼ 7.5 mm and at a distance L5 ¼ 5 mm from
through partially occluded curved arteries, to determine 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
employed as the governing equations, and a high
(L1 – L5) of the cylindrical tube of the specific thickness resolution for advection and second-order backward
representing an artery. The inlet and outlet of the tube are Euler for transient scheme were used.
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.
2.3 Configuration of numerical simulation
Numerical analyses using CFD techniques have been
constant diameter of D0 ¼ 4.0 mm. The variational h1 and performed on various structural configurations of the
h2 localised at the throats of the artery represent the heights artery. Over the decade, with the rapid advancement of
of the diseased segments. The wall thickness hw ¼ 0.2 mm computer technology, CFD has been widely adopted to
with density of r ¼ 1150 kg m3. The compliant vessel is investigate the haemodynamic parameters inside various
modelled as an isotropic material with Poisson ratio of stenosed arteries as portrayed by Poiseuille (1836).
v ¼ 0.499 and Young modulus E ¼ 5 MPa of the solid Although the method requires considerably long compu-
structure (Liu et al. 2014). 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
2.2 CFD modelling of arterial flow geometrical configurations, with the diseased to normal
The fluid flow is considered to be laminar, three- wall length ratio; different combinations of disease heights
dimensional, transient, isothermal and incompressible. (h1 and h2), ranging from dilatation with value of 2 0.5 to
The blood fluid is modelled as an incompressible fluid, 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 5

Continuity equation: increments at segments where the artery is more stenosed.

The opposite occurs for dilatations but at much lower
›P magnitudes. For the narrowest sections (i.e. at the maximum
þ V
7r ¼ 2r7
V: ð7Þ
›t h1 and h2), the WSS and WPG values are significant.
However, for the widest sections (i.e. at the minimum h1 and
The Energy equation is formulated on the physical h2), these parameter values are not changing as significantly
principle that energy in the system has to be conserved. as in the narrowest sections. We note that the values of WSS
A general form of energy equation in the Eulerian frame and DP for normal (non-stenosed and non-dilated) arterial
can be written as segments, whereby h1 ¼ 0 and h2 ¼ 0, are 5.601 Pa and
425.806 Pa, respectively.
›E
r þ rðV
7ÞE ¼ 7
ðs
VÞ þ V
rb: ð8Þ
›t
3.2 Surface response graphs of WSS and WPG
The Momentum equation can be formulated based on
The effect of additional flow resistance can be further
the physical principle that momentum in the system has to
ascertained based on the velocity variation in an artery. For
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be conserved. A general form of momentum equation in

example, as the dilation increases, the vessel cross-sectional
the Eulerian frame can be written as
area enlarges and the flow velocity gradually decreases
›V while the pressure increases; for this case, the flow resistance
r þ rðV
7ÞV ¼ 7
s þ rb: ð9Þ will be minimal. However, the re-circulating motion of the
›t
fluid induces additional energy and pressure loss to flow,
causing extra flow resistance. In our study, due to the small
2.5.2 Solid domain arterial dilatation implemented, the flow separations are
The governing equation for the solid domain is formulated assumed to be negligible. As such, the flow resistance will
in the Lagrangian reference frame shown as follows: still show a decline when there is dilatation.
As depicted in Figure 5, the predicted average wall
›2 d G ›2 d G shear stress WSS and pressure drop DP (or flow resistance
rs hs þ a 0 d G 2 b ¼ PG ; ratio) surface response from CFD simulations illustrate a
›t 2 ›X 2
surface response trend that is identical with each other.
where a0 ¼ Ehs =r 2 ð1 2 y 2 Þ; b ¼ K T Bhs . Note that KT In particular, for the cases with dilation (i.e. where h1 and h2
denotes the Timoshenko shear correction factor and PG is are of negative value), the elastic artery has generated 3D
structural load on the interface G due to the external flow response results of WSS and DP values that are shown
forcing term from the fluid, dG is displacement at the to decline. However, this decline is not significant. The
interface, X is position in space and t is position in time. decline is also dissimilar in magnitude for the two WSS and
The solid domain is constructed in the ANSYS solver, DP cases. The minimum average wall shear stress ratio, l1
while the fluid domain is modelled in the CFX solver. The falls much below a value of one at 0.667, whereas the
in-between coupling is from the ‘setup’ of the two solvers. minimum flow resistance ratio l2 is very much closer to one
Once the simulation is run in the ‘solution’ window, it first at 0.987. With reference to this trend, dilatations can be
begins computing iterations for the solid domain by observed to have an influence on reducing WSS values with
initiating the ANSYS solver, and then progresses onto the respect to the normal and healthy artery, and may also have
fluid domain in the CFX solver. 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
3. Results
increase the WSS magnitude, which can be explained by the
3.1 Contour plots of WSS and WPG greater narrowing resulting from a larger extension of the
The study of flow of a viscous incompressible fluid through a stenosis. However, this does not affect DP since the pressure
compliant tube has many applications. One major appli- across the inlet and outlet is not dependent on the
cation is blood flow through human arteries. Understanding geometrical variation in between.
wave propagation in arterial walls, local haemodynamics, On the other hand, for those stenosis cases (i.e. where
temporal WSS and WPG are important in understanding the h1 and h2 are of positive value), both WSS and DP are
mechanisms leading to various complications in cardiovas- higher in values. The increment in these flow values with
cular function. Many clinical treatments can be studied in respect to the increasing stenosis is much more significant.
detail only if a reliable model describing the response of However, the maximum ratio l1 rises to a value of 2.956,
arterial walls to the pulsatile blood flow is considered. whereas that of l2 is very much higher at 6.842. While
From Figures 3 and 4, it can be seen that both WSS and both the l1 and l2 surface plots of Figure 5 demonstrate
WPG properties are shown to demonstrate significant 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 plane, at different times in the ideal vessel with stenosis
ratio. It is possible that there can be some discrepancy in and dilatations. The blood flows from left to right as shown
the actual WSS and DP values in the event of stenosis due in the figure. The nature of blood flow through
to the additional flow resistance created by flow separation atherosclerotic arteries can assist our understanding of
at the downstream of the stenosis. Nonetheless, in general, the flow conditions within diseased arteries. For example,
existing theories agree reasonably well with the results higher velocity flow is observed at the site of stenosis, and
produced by the FSI framework. this can cause plaque rupture. Also, sudden pressure
release after stenosis can aggravate dilatations.
3.3 Velocity contour plots of stenosed artery flow
Based on flow visualisation in the diseased artery obtained 3.4 Summary of haemodynamic analysis
by numerical simulation of haemodynamic analysis, we In summary, as can be observed in Figures 3– 5, double
have plotted in Figure 6 velocity contours in the of X – Y 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 genesis and development of atherosclerosis, which thereby
investigating, and this is in contrast to the double motivates us to use them as exemplified parameters in our
dilatations case (based on h1 , 0 and h2 , 0). This parametric analysis framework.
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. 4. Discussion
Through qualitative visualisation that is coupled with the We have carried out CFD haemodynamic analysis of
quantitative analysis of WSS and DP, we can gain a clearer blood flow through atherosclerotic arteries. The resulting
insight into the haemodynamics of atherosclerotic arteries. generation of flow properties and parameters enables us to
Determination of these parameters can be helpful to understand the mechanisms of cardiovascular athero-
cardiologists because it is directly implicated in the 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 (Salzar et al. 1995; Thubrikar and Robicsek 1995; Delfino
with reference to the implications with atherosclerosis. 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
4.1 Implications in relevance with atherosclerosis stenotic part of the arteries experiences high WSS and
Research into the cause of atherosclerosis has been demonstrates to be more prone to plaque aggravation. This
performed for decades (Caro et al. 1971; Ku et al. 1985; has been consistent with the previous experimental studies.
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; 4.2 Elasticity of atherosclerotic arteries and its
Giddens et al. 1993; Lee and Chiu 1996; Kleinstreuer et al. implication in atherogenesis
2001), whereas high levels of this parameter tends to suppress Although there is no direct relationship between
it (Ku et al. 1985; Friedman et al. 1986; Giddens et al. 1993). deformation and atherogenesis, the presence and charac-
In addition to the low and oscillating WSS, the intramural terisation of high deformation regions at the throat of the
stress of the wall may also contribute to plaque growth at an artery has been investigated for inducing plaque rupture.
advance stage of the disease (Tang et al. 2008). Another Atherosclerotic plaque may be categorised into various
group believes that vessel wall thickening occurs in the event types, such as (i) atheromatous plaque that has an
of high shear stress (as reported by Wentzel et al. (2003) and artheroma or lipid pool covered with a fibrous cap, and (ii)
Joshi et al. (2004)). It is also believed that von Mises and a non-atheromatous plaque that consists of a connective
principal stress at the apex of the plaque can also be used to issue with admixed smooth muscle cells, and the calcified
characterise the initialisation and aggravation of its growth 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 resistance throughout the flow conditions. With the aid of
equations for a viscous incompressible fluid captures the 3D surface plots, strong support can be based on theory
experimentally measured viscoelastic properties of arterial relating to flow behaviour through a length of artery.
walls in the modelled arterial length. Using estimates To study the coupling between the motion of the vessel
based on an energy inequality, coupled with the wall and pulsatile blood flow, a detailed description of
asymptotic analysis and homogenisation theory, it is the vessel wall biomechanical properties may lead to a
possible to derive an effective, closed FSI model and a fast mathematical and numerical problem whose complexity is
numerical solver whose solutions capture the viscoelastic beyond today’s computational capabilities. The nonlinear-
properties of major arteries. The reduced effective model ity of the underlying FSI is so severe that even a simplified
reveals several interesting features of the coupled FSI description of the vessel wall mechanics assuming
problem. homogeneous linearly elastic behaviour leads to compli-
It is also of interest from the evidence of the 3D surface cated numerical algorithms with challenging stability and
plots that elastic boundary conditions seemed to have a convergence properties. To devise a mathematical model
higher resistance to that of the rigid boundary conditions. that will lead to a problem that is agreeable to numerical
This result is because energy is taken to deform the blood methods producing computational solutions in a reason-
vessel, hence there is a loss of momentum and more able period (time frame), various simplifications need to
resistance is added due to the loss of momentum and in the be introduced. They can be based on simplifying model
direction of flow. With comparisons between transient and assumptions, capturing only the most important physics of
steady state flows, the transient flow conditions seemed to the problem or on the simplifications utilising special
have a higher resistance, which corresponds to a higher problem features, such as special geometry, symmetry and
flow resistance ratio to that of steady state flow conditions. periodicity.
This is also due to the scenario in which the energy in the Devising an accurate model for the mechanical
pulse generated by the pump (heart) begins to lose the behaviour of arterial walls is more complicated. Arterial
momentum throughout the length of artery due to friction walls are anisotropic and heterogeneous and composed of
from the arterial walls. A consistent flow through the layers with different biomechanical characteristics.
length of the artery will seem to experience mush less A variety of different models has been suggested in the
 10 J. Wu et al.

literature to model the mechanical behaviour of arteries. Chaichana T, Sun Z, Jewkes J. 2013a. Hemodynamic impacts of
They range from the detailed description of each of the left coronary stenosis: a patient-specific analysis. Acta
Bioeng Biomech. 15(3):107– 112.
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Chaichana T, Sun Z, Jewkes J. 2013b. Hemodynamic impacts of
response of the vessel wall assuming homogeneous, various types of stenosis in the left coronary artery
linearly elastic behaviour. bifurcation: a patient-specific analysis. Phys Med.
29(5):447– 452.
Delfino A, Stergiopulos N, Moore JE, Meister JJ. 1997. Residual
5. Conclusion strain effects on the stress field in a thick wall finite element
model of the human carotid bifurcation. J Biomech.
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In this study, the numerical simulations of variational Glagov S, Zarins CK, Giddens DP, Ku DN. 1989. Mechanical
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determine the unsteady flow behaviour throughout the Newtonian blood flow in human right coronary arteries:
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using 3D surface plots of the average WSS and pressure Joshi AK, Leask RL, Myers JG, Ojha M, Butany J, Ethier CR.
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Conflict of interest statement Kleinstreuer C, Hyun S, Buchanan JRJ, Longest PW, Archie JPJ,
We confirm that all authors of this manuscript have no Truskey GA. 2001. Hemodynamic parameters and early
intimal thickening in branching blood vessels. Crit Rev
conflicts of interest to declare. Biomed Eng. 29(1):1 – 64.
Kompatsiaris I, Tzovaras D, Koutkias V, Strintzis MG. 2000.
Deformable boundary detection of stents in angiographic
Funding images. IEEE Trans Med Imaging. 19(6):652– 662.
Ku DN, Giddens DP, Zarins CK, Glagov S. 1985. Pulsatile flow
This work is supported by the National Natural Science and atherosclerosis in the human carotid bifurcation. Positive
Foundation of China [grant number 61272328]. correlation between plaque location and low oscillating shear
stress. Arterioscler Thromb Vasc Biol. 5(3):293 – 302.
Lee D, Chiu JJ. 1996. Intimal thickening under shear in a carotid
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