Six Monthly Progress Report of Research Scholars

Period: (July) to (December), 2016

(DEPT. OF APPLIED MECHANICS)
1. Name

: SATYAJIT CHOUDHURY

2. Roll No

: AM15D401

3. Program

: (MS&PhD)

4. Specialization

: Fluid Mechanics

5. Category

: (Regular)

6. Guide(s)

: Dr. Prasad Patnaik BSV

Dr. Kameswararao A

7. Date of Joining

: 14-07-2015

8. Date of Registration

: 14-07-2015

9. Area of Research

: Hemodynamics and nutrients transport across arterial wall

10. Date of Comprehensive Examination : 11-07-2016

Details of Core Courses
S.No.
1

Course No.
AM5600

2
3
4
5
6

AM6100
ID6020
AM5530
AM5010
AM5630

7
8

AM5570
CH5100

Course Name
Computational Techniques in Applied
Mechanics
Biofluid Mechanics
Introduction to Research
Advanced Fluid Mechanics
Biomechanics
Foundation of Computational Fluid
Dynamics
Introduction to Turbulence
Multiphase Systems

Semester
Odd 2015

Grade
B

Odd 2015
Odd 2015
Odd 2015
Odd 2015
Even 2016

S
Pass
A
A
C

Even 2016
Odd 2016

A
B

Course Name
Turbulence Modeling

Semester
Odd 2016

Grade
B

Details of Elective Courses

S.No.
1

Course No.
AM5640

Date : 24-12-2016
IIT Madras, Chennai.

Signature of the Guide(s)

(Dr. Prasad Patnaik BSV)

Signature of the Scholar

(Dr. Kameswararao A)

(Satyajit Choudhury)

Problem Definition

Today cardiovascular diseases are the leading cause of death globally [1] and atherosclerosis is the root of
most of these diseases. Cholesterol is a lipid required by the cells for various biological processes and it is
carried by blood in the form of low density lipoprotein (LDL). LDL combines with the LDL receptors in
the cell membrane and the receptor-LDL-cholesterol complex enters the cell. However, if LDL-cholesterol
is not absorbed into the cells and remains in the blood, the excess LDL-cholesterol will move into the wall
of the arteries [2]. The fact that the presence of high blood cholesterol plays a role in the development of
atherosclerosis is well established. Atherosclerosis is a condition which results from the oxidation of lipids
in LDLs that is trapped in the extracellular matrix of the sub-endothelial space of the blood vessels [3].
It is followed by a series of complex bio-chemical processes which lead to the inflammation of the arterial
wall (shown in figure 1) thus constricting the lumen of the artery. In the due course of time the plaque
gets hardened with the deposition of calcium which at times raptues under the effect of wall shear stress.
Platelets migrate to the raptured area and form a thrombus in the arterial wall. When the thrombus breaks
away from its position it may occlude small arteries downstream which results in stroke or angina.
It has been observed that curved arteries, bifurcation and branching of arteries are the regions which
are more prone to atherosclerosis. The dynamics of blood flow in these specific regions are very different
from that of a usual straight blood vessel as shown in figure 2, 3 and 4 [2] . Hence, apart from the lipid
mechanism, the blood flow dynamics is also suspected to influence the initiation of the diseases. This idea
has resulted in number of hemodynamic theories of atherogenesis over time [2].
My research includes developing a multi-physics solver and apply it to study transport of blood, oxygen
and LDL through and across the layer of the arteries. Through this research insights will be gained into the
initiations and growth of atherosclerotic lesions

Figure 1: normal vs diseased arterial wall

(www.webmd.com/heart-disease/atherosclerosis19012)

Figure 2: Blood flow in curvature

( Chandran, Rittgers, Yoganathan., Biofluid Mech.)

Figure 4: Blood flow in branching

Figure 3: Blood flow in bifurcation
( Chandran, Rittgers, Yoganathan., Biofluid Mech.) ( Chandran, Rittgers, Yoganathan., Biofluid Mech.)
1

2
2.1

Work Done Before Review

Literature Review

In the literature, the study of nutrients transport across the arterial wall has been done using three basic
models of arteries. Most simple among them is the wall free model where the arterial wall is taken care by
the boundary condition of the fluid domain. Fazli et al., 2010 have used this model to study the effect of size
of LDL on the lumen surface concentration (LSC) [4]. They have also studied the effect of different blood
rheology and the pulsatile nature of blood flow on the LSC in a symmetrical 30-60% stenosed carotid artery
(shown in figure 7).
In the second model, the arterial wall is represented by single homogeneous layer. Moore et al., 1997
used this model to study the transport of oxygen in large arteries [5].
Last and the most realistic model is the multi-layered arterial model (shown in figure 5) where the study
is done by assigning realistic material properties to different layers of the artery. Kenjeres et al.,2013 used
a four layer arterial model to study LDL transport in anatomically realistic carotid bifurcation (shown in
figure 6) [6]. They found a strong correlation between the flow pattern and the uptake of LDL concentration
in the arterial wall. Their results show that many regions of low wall shear stress correspond to regions
of high LDL concentration along the lumenendothelium interface. Iasiello et al., 2016 used a multilayer
arterial model and studied LDL transport using four different blood rheological models and concluded that
the predictions made by Newtonian blood model are quite accurate in large and medium sized arteries [7].
A. Deyranlou et al., 2015 performed a numerical investigation on the influence of non-Newtonian fluid on
the LDL mass transfer in coronary carotid artery with mutilayer wall taking wall elasticity into account [8].

Figure 5: Multiple layers in artery

S. Kenjeres and A. de Loor., J.Royal Society,
Interface, 2013

Figure 6: Realistic carotid bifurcation

S. Kenjeres and A. de Loor., J.Royal Society,
Interface, 2013

Figure 7: Stenosis geometry used by Fazli et al., 2010

Figure 8: input velovity used by Fazli etal., 2010

2.2

Six courses were completed before review

2

Work Done during Review

3.1

The variation of LDL concentration along the wall of an idealized artery

has been studied.

Figure 9: schematic diagram of the artery

3.1.1

Assumptions

Artery is assumed to be a rigid cylindrical tube.

Walls of the artery is assumed completely impermeable to LDL.
A constant radial (filtration) velocity is assumed at the arterial wall.
Blood flow is assumed Newtonian,laminar and steady with a fully developed parabolic inlet condition.
3.1.2

Values of the parameters

R = 3.5 mm
3.1.3

L = 154 mm

U0 = 0.119 ms1

Vw = 4 108 ms1

C0 = 1

Governing Equations

Navier-Stokes Equation
V
P
+ (V )V =
+ 2 V
t

(1)

where = kinematic viscosity = 3.2857 106 m2 s1

Scalar(LDL)Transport Equation
C
+ (V )C = D2 C
t

(2)

where D = dif f usion coef f icient

3.1.4

Boundary Condition

Inlet



r
2
Vx = 2U0 1
R

Vr = 0

C = C0

wall
Vx = 0
outlet

Vr = Vw
V
=0
n

C
= CVw
n

C
=0
n

(3)

(4)

(5)

3.1.5

Methodology

Since the domain is axis-symmetric and the flow is laminar (Re = 250), computation is simplified only by
soving the axial and radial direction momentum (N-S) equations.The transport equation has been solved
separately after a converged steady state velocity profile has been achieved, as the flow is steady and LDL is
assumed a passive scalar.Same mesh is used for the discretization of both N-S equation and Scalar Transport
equation. The mesh is made finer near the wall and the wall to properly resolve the concentration and
the velocity profile. SIMPLE algorithm has been employed in open-source CFD software to solve the N-S
equation. The concentration variation achieved has been validated against the work of Fazli et al., [4].
3.1.6

Validation

The variation of LDL concentration along the arterial wall in the axial direction is plotted for three different
values of diffusion coefficient: 5 1012 m2 s1 , 10 1012 m2 s1 , 2 1011 m2 s1 . The simulation for
D = 5 1012 has been carried out in grids of two different resolutions 80 600 and 90 700 (shown in fig
10) to make sure that the results are grid independent. Rest of the simulation is carried on 90 700 grid.
As we can see from the graphs, concentration increases, first rapidly and then slowly as we move along
the wall in the axial direction. As the magnitutde of diffusion coefficient increases, LDL concentration on
the wall decreases. Thus, we have lowest LDL concentration for D = 2 1011 (shown in fig 13). As we can
see from the figures below, obtained plots are quite close to the plots from Fazli et al.,[4]

Figure 10: Grid Independence Test

Figure 12: Concentration variation along the

wall in axial direction for D = 10 1012

Figure 11: Concentration variation along the

wall in axial direction for D = 5 1012

Figure 13: Concentration variation along the

wall in axial direction for D = 2 1011

3.2

Two courses completed during review

3.3

Was TA to the course AM2540

References
[1] http://www.who.int/mediacentre/factsheets/fs310/en/, 2014.
[2] A. P. Yoganathan K. B. Chandran, S. E. Rittgers. Biofluid Mechanics- THE HUMAN CIRCULATION.
CRC Press, Taylor and Francis Group, second edition, 2012.
[3] A. M. Fogelman J. S. Frank L. L. Demer P. A. Edwards A. D. Watson J.A. Berliner, M. Navab and A. J.
Lusis. Atherosclerosis: Basic Mechanisms. Circulation, 1995.
[4] M. R. Sadeghi S. Fazli, E. Shirani. Numerical simulation of LDL mass transfer in a common carotid
artery under pulsatile flows. Journal of Biomechanics, 2010.
[5] J. A. Moore and C. R. Ethier. Oxygen mass transfer calculations in large arteries. Journal of Biomechanical Engineering, 1997.
[6] S. Kenjeres and A. de Loor. Modelling and simulation of low-density lipoprotein transport through
multilayered wall of an anatomically realistic carotid artery bifurcation. Journal of the Royal society,
Interface, 2013.
[7] A. Andreozzi N. Bianco M. Iasiello, K. Vafai. Analysis of non-Newtonian effects on Low-Density Lipoprotein accumulation in an artery. Journal of Biomechanics, 2016.
[8] M .R. Sadeghi A. Deyranlou, H. Niazmand. Low-density lipoprotein accumulation within a carotid
artery with multilayer elastic porous wall: fluid- structure interaction and non-newtonian considerations.
Journal of Biomechanics, 2015.

Future Plans

In this research I will be developing a multi-physics solver in OpenFOAM, that can simulate steady and
pulsatile flow of blood, oxygen and nutrients. The blood flow and LDL mass transfer across the several layers
of the arterial wall will be simulated. The developed solver will be applied to study hemodynamics,O2 and
LDL concentrations in both healthy as well as pathological arteries. To begin with, idealised arteries with
and without pathology such as stenosis and aneurysms will be considered. Further into the research, subject
specific geometries will be analysed. The solver will be thoroughly validated with existing data from the
literature. As the time permits, the elasticity of the walls will also be considered leading to fluid-structure
interaction of the blood flow with the lumen walls.

Visible Research Output

Nil

Any Other Information

Nil