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Effect of Blockage Area Variation on the Hemodynamic Characteristics in

Stenosed Artery using Numerical Techniques

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 International Conference on Mechanical, Industrial and Energy Engineering 2022
22-24 December, 2022, Khulna, BANGLADESH

ICMIEE22-042
Effect of Blockage Area Variation on the Hemodynamic Characteristics in Stenosed Artery using
Numerical Techniques
B. M. Arafat Rahman1,*, Ahmed Abrar Shayor2, Abdullah Al-Faruk 3
1
Department of Mechanical Engineering, Khulna University of Engineering & Technology, Khulna-9203, BANGLADESH
2
Department of Mechanical Engineering, Khulna University of Engineering & Technology, Khulna-9203, BANGLADESH
3
Department of Mechanical Engineering, Khulna University of Engineering & Technology, Khulna-9203, BANGLADESH

ABSTRACT
The investigation and in-depth study of vascular fluid dynamics play a critical role in the inquiry of how the progression
of atherosclerosis occurs, a large prominent disease in humans. Recent evolution in computational fluid dynamics (CFD) is
allowing contribution to monitoring flow in presence of stenosis without in-vivo techniques with sufficient accuracy and less
cost. Computer-based medical imaging techniques and mainly simulating complex flows would also help in developing
therapeutics and devices to detect the stenosis severity in advance using values of velocity, pressure, and other hemodynamics
parameters. In the present work two-dimensional artery models with single stenosis but with blockage percentages of 35%,
50%, 75%, 80%, 86%, and 95% respectively were taken for carrying out the analysis, a numerical simulation was hence
performed to assess the effect on physiological flows. The blood is stipulated to be incompressible, homogenous, and non-
Newtonian, while the artery is fixed and rigid. The continuity, momentum, and standard k-ω turbulence equations, as well as
the non-Newtonian Carreau model, will be used to describe the flow field in the mathematical model. Steady-state analysis
was carried out for the case since simple instantaneous analysis does not warrant a complex transient flow study. The velocity
profile, wall static pressure, wall shear stress, and turbulence intensity were measured in pre-stenotic, throat, and post-stenotic
regions. At the throat, the flow changes rapidly, causing an escalation in velocity and wall shear stress (WSS) deviating from
flow in the normal artery. In the post-stenotic region, the flow is quite turbulent, resulting in the creation of vortices. The
results indicated that the blockage caused the development of high velocity and along with the viscosity change causes high
WSS to develop on the wall. Because of the stenosis, the throat section has a significant pressure variation and flow becomes
turbulent due to crossing the critical Reynolds number. Also, it was found from the investigation that a 75 % blockage is
dangerous enough and 80% stenosis can be considered critical. This characterization of criticality was performed by studying
the turbulence intensity variable of the flowing biofluid (blood).

Keywords: CFD, Blood Flow, Stenosis, Blockage Area, Turbulence Intensity

1. Introduction combining fluid and solid solutions will aid in better

The inflammatory fibroproliferative response to grasping the trend of vascular disease [7]. Bathe et al.
numerous morphs of endothelial injury is classified as (1999), used ADINA Software was used to model
atherosclerosis, an arterial disease [1]. A fractional pulsatile and laminar flow through a flexible artery with
decrease in the artery cross-sectional area, known as stenosis. They looked at stenoses with an area reduction
stenosis, in atherosclerosis [2]. Atherosclerosis damages of 51 and 96 per cent and compared pressure drop and
arteries throughout the body. Atherosclerotic lesions are circumferential stress across the artery at different
most found in arterial sections with steep curvature or at instances. They also looked at how the Reynolds number
bifurcations and junctions, where they cause significant (Re) affects pressure descent [8]. Tang et al. (1999),
changes in flow structure [3]. Although the exact causes Using ADINA software, investigated flexible carotid
of this anomaly are still unknown, it has been established arteries with laminar flow involving symmetric stenosis.
that once modest stenosis develops, the ensuing flow Severe stenosis generates critical flow circumstances
disruption plays a critical part in the disease's including negative pressure gradient and high and low
advancement [4].In addition to traditional medical shear stress, which can lead to artery compression, plaque
methods for theorizing and assessing disease progression, rupture, platelet activation, and arterial thrombosis,
computational fluid dynamics is being used to investigate according to their findings [9]. Many experiments have
the role of hemodynamics in the regionalization, growth, been conducted to examine a steady turbulent flow [10]–
and advancement of atherosclerosis disease in the study [11]. Deshpande et al. (1980), used a Laser Doppler
of the reasons and amelioration of this disease. Some Anemometer (LDA) to study chaotic(turbulent) flow
researchers have concentrated on modelling the arterial through a stenosed tube with 75% reduction and Re
wall and examining the association between arterial wall ranging from 5000 to 15000 [12]. Ahmed et al. (1984),
stress and vascular wall disorders at the same time as used the LDA to determine the simplified time-
hemodynamic investigations [5], [6]. independent velocity field in the presence of symmetric
stenosis having stiff walls. At upstream of the stenosis,
Researchers have recently focused on biological systems
Re ranged from 500 to 2000, and stenoses of 25, 50, and
incorporating fluid-solid interactions in them,
75 per cent diameter decrease were investigated [11].
particularly cardiovascular systems. They anticipate that
Few experimental investigations for unstable turbulent

* Corresponding author. Tel.: +88-01721961399

E-mail addresses: [email protected]
flow due to the existence of stenosis exist due to the researched into the relationship between stenosis and
difficulty of conducting experiments.[12] aneurysm [23].Lorenzini et al. (2008), examined stenoses
with various geometric profiles such as trapezium, semi-
Ahmed et al. (1984), measured the pulsating flow field ellipse, and triangle in terms of non-Newtonian behavior.
hypothesizing, and implementing symmetric stenosis by [24]. Flow features in the proximal and distal end of
LDA. For testing, they used a sinusoidal inlet velocity stenosis have been studied in some of the prior
profile, 7.5 Womersley number, stenoses of 25, 50, and experimental and computational research studies,
75% blockage, and a mean Reynolds number of 600 [13]. including a full investigation of the rupture potential of
Transient or turbulent flow can occur even with a minor plaque. Aside from that, the flow patterns with increasing
percentage of stenosis, according to these experiments. severity have been widely researched for various
Results of the preceding experiments were employed to geometry along with different kinds of physiological
check numerical approaches for simulating turbulent models. In the current study, an attempt was carried out
flow in interior flows using the finite element program to demonstrate the substantial changes for several
FIDAP for example. Ghalichi et al. (1998), evaluated severities considering blood is homogeneous,
time dependent and turbulent flow. Their findings incompressible, and non-Newtonian. During a cardiac
revealed that when the flow becomes transitional or cycle, the shear rate in human arteries fluctuates from 1–
turbulent, the laminar flow model overstates the vortex 1200 s-1 [25]. As a result, blood behaves like non-
length [14]. Kader and Shenory et al. (2011), numerical Newtonian fluid at times during the cardiac cycle. To
simulation findings demonstrate that increasing the completely comprehend hemodynamics, necessary
degree of stenosis enhances the velocity and stenotic jet investigate into the non-Newtonian behavior of blood is
length. Their findings also show that the 3D stenotic CFD required.
model competently forecasts shifts in flow behavior with
increasing degree of the stenosis [15]. The flow is considered steady. For large arteries, the
steady flow assumption is reasonable since diastole,
Tu et al. (1996), performed a finite element numerical which lasts about two-thirds of the cardiac cycle, has a
analysis in an artery with a rigid wall, evaluating steady reasonably constant forward flow [26].
and unsteady blood flow through 25, 50, and 75%
stenosis [16]. Tu et al. (1996), used the Herschel–Bulkley 2. Model Description
model and evaluated the non-Newtonian (varying The model description including the geometry, mesh,
viscosity, physiological pulsatile blood flow through numerical studies are explained in detail as follows. It is
heavy stenosis. [16]. Razavi et al. (2011), conducted a to be mentioned that the modelling is being done for
comparison of other viscosity models as well as the systematic circulation of blood flow.
Newtonian model. They concluded that as the percentage
of stenosis grows, the flow downstream of stenosis gets 2.1. Geometry
more disrupted, and WSS formation at the throat region The form of the stenoses chosen for this study is
becomes more noticeable [17]. Ellahi et al. (201An 𝑟(𝑥)
= 0.5 − 𝐴[1 + cos⁡ 𝜋𝑥/𝐷], −𝐷 ⩽ 𝑥 ⩽ 𝐷
analytical investigation of a incompressible, pulsatile 𝐷
flow of micropolar non-Newtonian fluid was done in a with 𝑥 = 0 exactly at the middle of throat of stenosis and
stenosed artery. They discovered that when the stenosis 𝐷 is artery diameter. By considering D as reference
height grows, so does the flow impedance [18]. Karimi et length while making it dimensionless we get 1 non-
al. (2013), used a 3D model adopting axisymmetric dimensional form. Usually, the artery size is about 4 mm
stenosis conditions in common carotid artery to visualize [27]. The stenosed percentage is found from [1 −
the hemodynamical differences between 2D (𝑟/𝑅)2 ] , The throat and upstream arterial radius, are
axisymmetric and 3D models in pulsatile blood flow, represented by r and R respectively. To guarantee fully
employing Carreau with Modified Power-law models, developed upstream flow, a velocity profile was imposed
later Newtonian model as well. Discovery of asymmetric 8 diameters (D) before 𝑥 = 0 position. To allow for the
flow in the post stenosis zone, which can only be seen reconstruction of flow, the outlet boundary condition was
through 3D modelling was found [19]. Harloff et al. placed 20 diameters (D) downstream of the stenosis
(2013), used imaging in the 4D technique to study flow throat. Fig.1 shows the geometry for 75% stenosis. And
velocity within a stenosed artery [20]. Additionally, in Error! Reference source not found. shows the value of r a
recent years, certain researchers, such as Saleem et al. nd A for various percentages of stenosis.
(2014), have made significant contributions to the blood
flow modeling field in stenosed arteries [21].Tian et al.
(2013) computationally simulated non-Newtonian
models with pulsatile velocity across a stenosed artery
including varying degrees of severity and impact on the
WSS magnitudes, wall shear stress gradient (WSSG),
and other parameters on both walls, however the lower Fig.1 Geometry Description
wall had a much higher WSSG [22].Shupti et al. (2017)
worked with non-Newtonian fluid flow and moving wall,

ICMIEE22-042- 2
Table 1 r and A for various percentages of stenosis value is higher than 1. But in boundary layer we need
skewed layers of mesh as they are more stretched but
Stenosed r A with less height. The skewness for most of the elements
Percentage close to 0 and (maximum 0.85). So, the Skewness
35% 0.4031 0.0485 property is very good along with the orthogonal qualities
50% 0.354 0.073 are also very satisfactory as most of the element has
75% 0.25 0.125 orthogonal quality value as 1.
86% 0.187 0.1565 2.2. Blood Properties
95% 0.1118 0.19425 The fluid (blood) is considered homogeneous,
2.1 Mesh Generation incompressible, and non-Newtonian. The mass density of
In this step, the geometrical model is discretized blood is considered as 1060 Kgm-3. The flow is
into various infinitesimally small volumes. Number of considered as steady. For Non-Newtonian fluid,
elements and nodes created for each geometry are shown according to Pierre Carreau's suggested Carreau model-
in Table 2.
𝜇 = 𝜇∞ + (𝜇0 − 𝜇∞ )[1 + (𝛾𝑐 𝛾˙)2 ]𝑛−1/2 (1)
Table 2 The number of nodes and elements generated in
each geometry Where 𝜇∞ = 0.0035 Pa a.s, 𝜇0 = 0.056 Pa. 𝑠, 𝛾𝑐 =
Model Name Nodes Elements 3.313 s, 𝛾˙ is the instantaneous shear rate, and n=0.356

2D Stenosed 122206 120700 2.3 Governing Equations

Artery
Continuity Equation:
Edge sizing and Face meshing has been done for this 𝜕𝜌
+
1 𝜕(𝑟𝜌𝑢𝑟 )
+
1 𝜕(𝜌𝑢𝜃 )
+
𝜕(𝜌𝑢𝑧 )
=0 (2)
geometry. For edge sizing geometry has been divided 𝜕𝑡 𝑟 𝜕𝑟 𝑟 𝜕𝜃 𝜕𝑧
into 3 sections with the longest section being pre-stenotic Since the problem is assumed to be steady-state &
and shortest the stenotic region. In pre stenotic section 𝜕𝜌
incompressible, so time-dependent parameter ( ) & 𝜌
the number of divisions has been taken 360. At the 𝜕𝑡
stenotic throat the number of divisions has been taken dropped from the equation & get,
160(finest to capture better flow physics as flow reach 1 𝜕(𝑟𝑢𝑟) 1 𝜕(𝑢𝜃 ) 𝜕(𝑢𝑧 )
+ + =0 (3)
transitional stage). The post stenotic region the number 𝑟 𝜕𝑟 𝑟 𝜕𝜃 𝜕𝑧
of divisions has been taken 900(also finer to capture more Navier's Stock equation. It mostly deals with fluid
flow physics as flow becomes turbulent. And at inlet and velocity and pressure parameters. We can calculate the
outlet the number of divisions has been taken 85 with a flow characteristics by utilizing various boundary
biasing factor 15 for reducing element size at near wall conditions. Incompressible and incompressible flows,
for better results. The mesh behavior has been taken as both the momentum and Bernoulli's equations are applied.
Hard. For Face Meshing elements type has been taken as They are mostly intended for streamlined computations.
quadrilaterals as can be perceived from Fig.2. The total of forces operating on a fluid body element to
its accelerating rate of change of momentum is depicted
by the momentum equation.
In cylindrical coordinates, (r, ⁡𝜃⁡ , z) the Navier-stokes
incompressible fluid’s equation of motion, with a
constant dynamic viscosity 𝜇⁡and density⁡𝜌 are:
Fig.2 Meshing of the geometry
2
𝐷𝑢𝑟 𝑢𝜃 𝜕𝑝 𝑢𝑟 2 𝜕𝑢𝜃
𝜌[ −⁡ ]=− +𝑓𝑟 +𝜇⁡ [∇2 𝑢𝑟 − ⁡ −⁡ 2⁡ ] (4)
𝐷𝑡 𝑟 𝜕𝑟 𝑟2 𝑟 𝜕𝜃

𝐷𝑢𝜃 𝑢𝜃 𝑢𝑟 1 𝜕𝑝 𝑢𝜃
𝜌[ + ]=− + 𝑓𝜃 +𝜇⁡ [∇2 𝑢𝜃 − ⁡ +
𝐷𝑡 𝑟 𝑟 𝜕𝜃 𝑟2
2 𝜕𝑢𝑟
⁡⁡⁡⁡⁡⁡⁡⁡⁡⁡⁡⁡⁡⁡⁡⁡⁡⁡⁡⁡⁡⁡⁡⁡⁡⁡⁡⁡⁡⁡⁡⁡⁡⁡⁡⁡⁡⁡⁡⁡⁡⁡⁡⁡⁡⁡⁡⁡⁡⁡⁡⁡⁡⁡⁡⁡⁡⁡⁡⁡⁡⁡⁡⁡⁡⁡⁡⁡⁡⁡⁡⁡⁡⁡⁡⁡⁡⁡⁡⁡⁡⁡⁡ 2 ⁡ ]⁡(5)
𝑟 𝜕𝜃
𝐷𝑢𝑧 𝜕𝑝
𝜌 = −⁡ + 𝑓𝑧 + 𝜇⁡∇2 𝑢𝑧 (6)
𝐷𝑡 𝜕𝑧

Where 𝑢𝑟 , 𝑢𝜃 , 𝑢𝑧 are the velocities in the r, 𝜃⁡, z

cylindrical coordinate directions, p is the pressure,𝑓𝑟 , 𝑓⁡𝜃
are the body force components in the r, 𝜃 , z directions
Fig.3 Aspect Ratio of the Mesh Elements 𝐷
and the operators ⁡&⁡∇2 are
𝐷𝑡
The Aspect Ratio, Skewness and Orthogonal Quality of 𝐷 𝜕 𝜕 𝑢𝜃 𝜕 𝜕
= + 𝑢𝑟 + + 𝑢𝑧 (7)
mesh has been monitored closely for analyze the Mesh 𝐷𝑡 𝜕𝑡 𝜕𝑟 𝑟 𝜕𝜃 𝜕𝑧
quality. As from Fig.3 We can see that most of the areas
𝜕2 1 𝜕 1 𝜕2 𝜕2
the aspect ratio is equal to 1. In the boundary layer its 𝛻2 = +⁡ + ⁡ + (8)
𝜕𝑟 2 𝑟 𝜕𝑟 𝑟 2 𝜕𝜃 2 𝜕𝑧 2

ICMIEE22-042- 3
The following two equations determine the turbulent turbulence kinetic energy and specific dissipation rate.
kinetic energy and specific dissipation rate of the For the convergence of the simulations residuals absolute
conventional k-ω model respectively: criteria had been taken as 1e-6.
∂ ∂ ∂ ∂k Hemodynamic characteristics of the fluid must be set
(𝜌k) + (𝜌kui ) = (Γk ) + Gk − Yk + Sk (9) before the non-Newtonian Carreau model can be
∂t ∂xi ∂xj ∂xi
∂ ∂ ∂ ∂𝜔
activated in ANSYS Fluent to create non-Newtonian
⁡ (𝜌𝜔) + (𝜌𝜔ui ) = (Γ𝜔 ) + G𝜔 − Y𝜔 + S𝜔 (10) fluid.
∂t ∂xi ∂xj ∂xj

3.4 Model Validation

These equations, Gk illustrates how mean velocity It was compared to the study of Ghalichi et al. (1998)
gradients cause turbulence to produce kinetic energy. G𝜔 [22] to validate the model. Wall shear stress as a function
of Reynolds number at the stenotic neck Saad and
represents the generation of ω. Γk and represents the
Giddens (1983) [21] provided the original data for all the
effective diffusivity of k and ω, respectively. Yk and experimental measurements.
represent the dissipation of k and ω due to turbulence. Sk 0.6
and are user-defined source terms. The impact on the
overall structure of the flow field is controlled by a low Present Work
Reynolds number correction factor, which is given as: 0.4

τ/ρv2
𝛼0∗ +Ret ⁡/Rk
𝛼 ∗ = 𝛼∞
∗
( ) (11) Ghalichi et al. (1998)
1+Ret ⁡/Rk
0.2
ρk β ∗ Experimental Data,
Where, 𝑅𝑒𝑡 = , R k =6, 𝛼0∗ = 𝑖 , β𝑖 = 0.072, 𝛼∞ =1, Saad and Giddens
μω 3
Closure Coefficient for the Transitional k- ω Model 0 (1983)
∗ ∗
are:- 𝛼∞ =1, α∞ =0.52, 𝛽∞ = 0.09, 𝛽i = 0.072, R k = 6, 0 500 1000 1500 2000
Re
and R𝛽 = 8
Fig.5 Model Validation
The three main characteristics that describe blood flow
via an artery are mass conservation, momentum Fig.5 shows there is a deviation of present work from
conservation, and transfer of turbulence. The fluid Ghalichi’s work. For Re 500 the error is about 7.92%. For
(blood) is homogeneous, incompressible, and non- Re 1000 the error is about 2.67%, For Re 1500 the error
Newtonian. The mass density of blood is considered as is about 3.86% and for the Re 2000 the error is about
1060 Kgm-3. The flow is considered as steady. The 9.09%. There is a huge deviation with the experimental
Standard k-ω model will be used for turbulence modeling. values of Saad and Giddens, but the trend of plot is
identical.
• 2D
• Non-Newtonian, Incompressible & steady flow
4.0 Result and Discussion
• Rigid wall Fig.6 shows that centerline static pressure distribution
• Reynolds number range 400 to 1500 for various mesh sizes. The number of elements and
• 35%, 50%, 75%, 86% & 95% stenosis region nodes for various mesh sizes are given in Table 3.
will be considered Table 3 Number of elements and nodes for various Mesh
• Mesh Name Elements Number Nodes Number
3. Numerical Modelling
By designating the inlet flow as "velocity inlet" at the Mesh 0 27993 27060
preset esteem and the output flow as "pressure outlet," Mesh 1 71500 72666
boundary conditions are established. A healthy person
has a systolic pressure of about 120 mmHg and a diastolic Mesh 2 94650 95988
pressure of about 80 mmHg. As a result, 100 mmHg was Mesh 3 120700 122206
chosen (about 13332 Pascal) as the static gauge pressure
at the outlet by averaging the two phases' pressures. Mesh 4 149910 151584
The wall-designated boundary line was subjected to a 102
stationary and no-slip condition Fig.4 shows the 102 Mesh 0
Pressure(mmHg)

boundary conditions. Mesh 1

101
Mesh 2
101 Mesh 3

100 Mesh 4
Fig.4 Boundary Condition of the geometry
100
The solution method for this simulation is that solving the -10 0 10 20 30
equations coupled algorithm had been used as pressure x/D
velocity coupling. And for spatial discretization second Fig.6 Centerline Pressure difference (number of elements)
order algorithm had been used for pressure, momentum,

ICMIEE22-042- 4
 86% and 95% the turbulence intensity is high (>5%) in
The centerline static pressure distribution plot is deviated the post stenotic region.
a bit for Mesh 0. But for the rest of the mesh sizes (Mesh 125 Stat Press

Wall Static Pressure (mmHg)

1-Mesh 4) the pressure distribution is identical. It 120 35%
suggests that the solution is grid-independent after Mesh Stat Press
115 50%
1 and onwards. And the simulation is carried out by
110 Stat Press
setting the mesh elements 120700 and nodes 122206 75%
which is Mesh 3 because of the smaller changes in 105
Stat Press
Pressure values compared to Mesh 4(almost no change at 100 80%
all) than Mesh 2. The main aim being accurate results. 95 Stat Press
90 86%

85
-10 0 10 20 30
x/D
Fig.9 Wall static pressure for various stenosed
percentages 35%, 50%, 75%, 80%, 86% and 95%

Fig.9 shows that wall static pressure at inlet is maximum

Fig.7 Static Pressure distribution contour for various and minimum at the outlet for all five geometries.
stenosis (a) 35% (b) 50% (c) 75% (d) 80% (e) 86% and Though the outlet pressure is same in all the
(f) 95% models but there shows a significant change in inlet
Fig.7 demonstrates that the static pressure distribution is pressure. Higher the stenosed percentage the higher the
largest at the intake and least at the outflow. For the 95% inlet pressure is. The outlet pressure for all geometries is
stenosis, the pressure differential is extremely large 100 mmHg which is average pressure of systole and
(16000 Pa to 13000 Pa). Additionally, except for the area diastole. But the inlet pressure of 95% stenosed artery is
close to the stenosis, the fluctuation in pressure with about 120 mmHg. So, there is a heavy fluctuation of
respect to the length of the artery is linear. Pressure pressure at the stenotic region which leads to fatal
fluctuations near to the stenosis are deadly, given that the condition. In 35% and 50% the pressure fluctuation in
value of it is very high for 95% stenosis. In 35% stenosis stenotic region is mild. In the 85% stenosed artery this
a very little fluctuation of pressure is perceived in the fluctuation isn’t that much but still considerable. In 75%
artery, not fatal. In case of 50% the fluctuation increased stenosed artery the fluctuation is 7 mmHg (1000 Pa). This
but not that high. Fluctuation became much higher after is not so severe but growing from here can lead towards
75% which is technically bad for health. After that at 86% danger. In 95% artery some fluctuation is visible at post
and 95% the fluctuations became more than 1000 Pa stenotic region. That’s because of heavy turbulence and
worsening the condition. large vortex generation.
36.0% 3.2
Turbulence Intensity

32.0% Turb Intensity 35%

Turb Intensity 50% 2.8
28.0% Vel 35%
Velocity (ms^-1)

24.0% Turb Intensity 75% 2.4 Vel 50%

20.0% Turb Intensity 80% 2.0 Vel 75%
16.0% Turb Intensity 86% Vel 80%
Turb Intensity 95% 1.6
12.0% Vel 86%
8.0% 1.2
Vel 95%
4.0% 0.8
0.0% 0.4
-10 0 10 20 30 0.0
x/D
-10 0 10 20 30
x/D
Fig.8 Turbulence Intensity for various stenosis (a) 35% Fig.10 Velocity Profile for various stenosed percentages
(b) 50% (c) 75% (d) 80% (e) 86% and (f) 95% 35%, 50%, 75%, 80%, 86% and 95%
Fig. 10 shows that velocity fluctuation due to various
Fig.8 shows that the turbulence intensity inside the artery obstruction geometries. The inlet velocity is same for all
for various blockage geometries. Since the ratio of the the models which is steady. The outlet velocity is almost
standard deviation of the fluctuating velocity to the mean same for all the models. There is a big increase in velocity
velocity determines the severity of the turbulence. It in stenotic region for 95% stenosis. For 86% stenosis
evaluates how severe turbulence cases are. In 35% and there is also a significant increase in velocity at stenosis.
50% stenosed artery the turbulence is very less in the post But for the other three models the velocity increase isn’t
stenotic region. As the stenosis increases the turbulence that much significant. That’s because of the pressure drop
intensity in the post stenotic region is also increasing. It in the stenotic region. Cause pressure and velocity have
is also seen that the turbulence intensity occurs mostly proportional relation. The static pressure fluctuation is
where the streamline doesn’t pass through (separation more at stenosed area. So, velocity also fluctuated
region). In higher stenosed blockage artery 75%, 80%, reversely. The velocity fluctuation at post stenotic region

ICMIEE22-042- 5
is seen for 95% and 86% stenosis as well. At post stenotic Fig.14 shows that the wall shear stresses the pre stenotic
region for higher blockage geometries velocity trend throat dramatically increased up to 50 Pa which can
moves erratically from centerline for a certain period. damage the artery wall and cause rapture in the pre
280 stenotic region.
240 Wall Shear
Wall Shear Stress (Pa)

200 Stress 35%

Wall Shear
160 Stress 50%
Wall Shear
120 Stress 75%
Wall Shear
80 Stress 86%
40 Wall Shear
Stress 95%
0
-10 0 10 20 30
x/D
Fig.11 Wall Shear Stress for various stenosed Fig.14 Wall Shear Stress for 80% stenosis artery
percentages 35%, 50%, 75%, 80%, 86% and 95%

Fig.11 shows that variation of wall shear stress. Since the

severity of stenosis increases, the WSS also increase, and
the maximum variation is dominated by 95%. The pre
stenotic region has a modest increase in shear stress while
increasing dramatically in the proximal stenotic area.
Whereas it reduces further in the distal stenotic and post
stenotic region. This reduction in shear stress boosts the
production of reactive oxygen species, which in turn
boosts LDL oxidation in the intima. The result obtained
Fig.15 Turbulence Intensity for 80% stenosis artery
from 35% and 50% stenosis agrees well with the clinical
observation and the result for 75% isn’t considered much
Fig.15 shows that the turbulence intensity at the post
severe but still injurious to health. The critical stenosis
stenotic region rise above 5% which exceeds medium
can be considered as 80% based on the above findings.
turbulence limit is very abnormal for blood flow through
Given that it is lethal for 80% of arteries, the pressure
an artery. It can cause troubles to a human being.
variation near to the stenosis is highly significant. as
shown in Fig.12 The fluctuation of pressure is about
5.Conclusion
14000 Pa to 13000 Pa. This high pressure in the pre
In this work, a Carreau model of blood flow through a
stenosis region can very well damage the artery wall in
stenosed artery was validated (assuming fluid to be non-
pre stenosis area.
Newtonian) and simulated through varying blockages-
35%, 50%, 75%, 80%, 86% and 95%.
i. It is seen that blood flow switches from laminar
to turbulent at post stenotic region.
ii. The turbulence intensity increases with the
stenosis percentage and as severity increases the
velocity and shearing stress increase in the
stenosed area. The most stress being imposed in
the stenosed area.
Fig.12 Static Pressure Distribution for 80% stenosed iii. Turbulence intensity goes past medium
artery turbulence limits for 80% stenosis and more
than that. From velocity values 75 % blockage
is inconvenient to health and 80% stenosis can
be considered critical Anything higher would
cause serious trouble decreasing blood supply
(95% - fatal).
Thus, a closer inspection of the critical stenosis
percentage shows how the various parameters indicate
the change and measuring those can help predict the
condition of cardiovascular systems. The investigation
Fig.13 Turbulence Intensity Contour for 80% stenosis answers the main question of interest here that from
In Fig.13 shows that the turbulence intensity at the post above 75% condition warrants surgery and below might
stenotic region is high enough to cause trouble. For this in some cases allow therapeutics only.
turbulence vortex length is also increased which is Some extensions to the work need to be considered for
abnormal for blood flow through an artery. further analysis. The fluid-structure interactions (FSI)

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NOMENCLATURE

WSS Wall Shear Stress

k Turbulent Kinetic Energy
ω Specific Dissipation Rate
D Diameter of Artery
2D Two Dimensional
Re Reynolds Number
x Axial location of the flow field
ρ Density of Blood
τ Shearing Stress
γ Shear Rate
r Stenosed Throat Radius

ICMIEE22-042- 8

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