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MODELLING STENOSIS DEVELOPMENT IN
THE CAROTID ARTERY AT THE EARLY
STAGES OF STENOSIS DEVELOPMENT
A.C.Stamou1, J.M.Buick2
1 Faculty of Engineering and Computing, Coventry University
2 School of Engineering, Anglesea Building, Portsmouth
Objectives of the talk
Presentation outline
Description of the problem
Methodology
Lattice Boltzmann method
Stenosis growth model
Results
Conclusion
Presentation outline
 In the present work, the position of the development of a
stenosis in the carotid artery has been simulated based on
regions of stagnation in blood flow.
 The interest is focused on:
 the blood flow properties, computed here using the Lattice
Boltzmann Method,
 prediction of the initial growth of the stenosis, based on
regions of blood stagnation at the artery wall structure,
 variation of the haemodynamic properties with the growth of
the stenosis.
4
Carotid artery (ICA, ECA, CCA: External
Carotid Artery, Internal Carotid Artery,
Common Carotid Artery)
ICA
CCA
ECA
Regions prone
to stenosis
development
ATHEROSCLEROSIS AND SUSCEPTIBILITY
TO ATHEROSCLEROSIS
 Atherosclerosis, one of the major causes
of strokes. It is a disease which
 is likely caused by the lipoprotein
accumulation accompanied with
endothelial cell damage (1,2) on the wall
surface,
 manifests on areas of high curvature and
bifurcations.(1,2)
 These atherosclerotic-prone-sites are
often characterized by:
 low endothelial stress (3, 4)(endothelial
stress: the applied shear stress on the
walls because of the fluid movement),
 disturbed flow (2) (flow characterized by
high oscillations of the shear stress from
the predominant flow direction (5)),
 stagnant flow. (6)
LATTICE BOLTZMANN METHOD
 LBM equation-Kinematic behaviour
 𝑓 𝑥, 𝑡 is the particle distribution function
along the 𝑖 𝑡ℎ
direction
 Evolution equation
𝑓𝑖 𝑥 + 𝑒𝑖, 𝑡 + 1 = 𝑓𝑖 𝑥, 𝑡 + Ω𝑖 𝑥, 𝑡
where 𝑒𝑖 is the vector along link 𝑖,
 the collision operator is
Ω𝑖 𝑥, 𝑡 = −
1
𝜏
𝑓𝑖 𝑥, 𝑡 − 𝑓𝑖
𝑒𝑞
𝑥, 𝑡
and the equilibrium distribution function is
𝑓𝑖
𝑒𝑞
= 𝑤𝑖 𝜌 1 + 3𝑒𝑖 ⋅ 𝑢 +
9
2
𝑒𝑖 ⋅ 𝑢 2 −
3
2
𝑢2
where 𝑤𝑖 0 < 𝑤𝑖 < 1 is weight function and
the density and the velocity are given by:
𝜌 = 𝑓𝑖
8
𝑖=0 and 𝜌𝑢 = 𝑓𝑖 𝑒𝑖
8
𝑖=0
The D2Q9 lattice
STENOSIS GROWTH MODELLING
(CRITERIA)
 The velocity magnitude along the wall is considered of
significant effect on the simulation of the growth of the
stenosis.
 However, the maximum stagnation of the flow is
considered in our work as the criterion for the growth of
the stenosis, with stagnation index:
SI = N/T
 where T is the period of the cardiac pulse and N is the
number of time-steps in a period when 𝑢1, the local
velocity magnitude at the 1 grid length from the wall, is
less than 1% of the average 𝑢1 over the whole of the wall
during the previous period.
7
Arterial grid
CALCULATION OF THE
VELOCITY MAGNITUDE
 The simulation of the growth of the
stenosis is accomplished assuming
an extrapolation scheme that
supports the movement-boundary
mechanism.
 The velocity magnitude locally at the
1 grid space from the wall is worked
out, by:
𝑢1= 1 − 𝛿 *𝑢 𝑑 𝑝1
+ 𝛿 ∗ 𝑢 𝑑
 δ: distance of the first fluid node 𝑥 𝑓
 from the wall. 𝑢 𝑑𝑝1, 𝑢 𝑑, 𝑢1:velocities
 at 𝑥𝑓𝑓, 𝑥 𝑓 and one grid length (1 lu)
from the wall.
8
APPLYING THE MOVING
BOUNDARY MECHANISM
 Picking out the point satisfying the mechanical
criterion (stagnation)
 Applying the illustrated boundary-movement
scheme at the first fluid node from the wall
 Comparing the 𝛿 and 𝑙 (the distance the
boundary moves, here set to 0.5)
 𝛿 ≦ 𝑙 ∶ the selected fluid node 𝑥𝑓 turns to
wall (case a)
 𝛿 > 𝑙: the selected fluid node 𝑥𝑓 remains a
fluid node (case b)
 Working out the new 𝛿′
 𝛿′
= 𝑙 − 𝛿 (case a)
 𝛿′
= 𝛿 − 𝑙 (case b)
 Set up the new boundary as shown
Movement-boundary mechanism
RESULTS ANALYSIS
The presentation of the results is structured as follows:
 Stenosis development in layers
Effect of stenosis growth on the blood flow along
the wall
Flow profiles
10
STENOSIS DEVELOPMENT
 The stenosis is formed in layers
built up on the outer walls of the
ECA and ICA.
 The stenosis layers are built up
consecutively on either the same
arterial wall or on the opposite
wall.
 The growth occurs on the ECA
below the bifurcation.
 In the ICA the stenosis occurs
from slightly below the bifurcation
and extends significantly in to the
ICA.
Stenosis growth in layers with Ts, the number of
grid sites, originally in the blood flow region,
which have been enclosed by the growth of the
stenosis.
11
CHANGE IN THE WALL VELOCITY
WITH STENOSIS GROWTH
B)A)
The growth of the stenosis influences mainly
the flow at the stenosed regions.
A) Velocity magnitude along the ECA
B) Velocity variation with the growth of
the stenosis as a function of TS
12
FLOW PROFILES
(UNSTENOSED ARTERY)
 Velocity Magnitude  Shear Stress
Over ½ cardiac pulse
At the peak-pressure-time over the full cardiac pulse
STENOSIS-GROWTH
PROGRESSION
14
FLOW PROFILES
(FULLY STENOSED ARTERY)
 Velocity Magnitude  Shear Stress
Over ½ cardiac pulse
Conclusions
The position of the stenosis has been simulated
here based on regions of flow stagnation.
The stenosis is formed on the outer wall of both
the ICA and the ECA in the region where vortex
motion develops in the healthy artery.
The growth of the stenosis influences mainly the
flow close to the stenosed wall.
An increased velocity was observed in both the
ICA and the ECA with the growth of the stenosis.
Future research
 Simulation of the progression of the stenosis in a number
of other arteries which are similarly susceptible to this
disease, in particular the human aorta
 Comparison of haemodynamics between stenosed and
stented arteries
 Simulation of the non-Newtonian blood considering
alternative models to the Carreau-Yasuda
 Development of a 3D model to enable the secondary flows
in the artery to be assessed and their effect on stenosis
development
References
1. C.G. Caro. Atherioscler Thromb Vasc Biol. 29: 18-161, 2009.
2. X. He, D.N. Ku. Journal of Biomechanical Engineering. 118: 74-82,
1996.
3. Y.S. Chatzizisis, M. Yoman, A.U. Coskun, R. Beigel, B.V. Stone, C.
Meynard et al. Circulation. 117: 993-1002, 2008.
4. J. Knight, U. Olgac, S.C. Saur, D. Poulikakos, W. Marshall, P.C. Cattin
et al. Atherosclerosis. 211: 445-450, 2010.
5. D.N. Ku, D.P. Giddens, C.K. Zarins and S.Glagov. Atherioscler Thromb
Vasc Biol. 5: 293-302, 1985.
6. C.V. Soulis, O. P. Lampri, D.K. Fytanidis and G.D. Giannoglou.
Biomedical Engineering, 2011 10th International Workshop on 5-7
Oct. 2011 1-4.

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MODELLING STENOSIS DEVELOPMENT IN THE CAROTID ARTERY AT THE EARLY STAGES OF STENOSIS DEVELOPMENT (3)

  • 1. MODELLING STENOSIS DEVELOPMENT IN THE CAROTID ARTERY AT THE EARLY STAGES OF STENOSIS DEVELOPMENT A.C.Stamou1, J.M.Buick2 1 Faculty of Engineering and Computing, Coventry University 2 School of Engineering, Anglesea Building, Portsmouth
  • 2. Objectives of the talk Presentation outline Description of the problem Methodology Lattice Boltzmann method Stenosis growth model Results Conclusion
  • 3. Presentation outline  In the present work, the position of the development of a stenosis in the carotid artery has been simulated based on regions of stagnation in blood flow.  The interest is focused on:  the blood flow properties, computed here using the Lattice Boltzmann Method,  prediction of the initial growth of the stenosis, based on regions of blood stagnation at the artery wall structure,  variation of the haemodynamic properties with the growth of the stenosis.
  • 4. 4 Carotid artery (ICA, ECA, CCA: External Carotid Artery, Internal Carotid Artery, Common Carotid Artery) ICA CCA ECA Regions prone to stenosis development ATHEROSCLEROSIS AND SUSCEPTIBILITY TO ATHEROSCLEROSIS  Atherosclerosis, one of the major causes of strokes. It is a disease which  is likely caused by the lipoprotein accumulation accompanied with endothelial cell damage (1,2) on the wall surface,  manifests on areas of high curvature and bifurcations.(1,2)  These atherosclerotic-prone-sites are often characterized by:  low endothelial stress (3, 4)(endothelial stress: the applied shear stress on the walls because of the fluid movement),  disturbed flow (2) (flow characterized by high oscillations of the shear stress from the predominant flow direction (5)),  stagnant flow. (6)
  • 5. LATTICE BOLTZMANN METHOD  LBM equation-Kinematic behaviour  𝑓 𝑥, 𝑡 is the particle distribution function along the 𝑖 𝑡ℎ direction  Evolution equation 𝑓𝑖 𝑥 + 𝑒𝑖, 𝑡 + 1 = 𝑓𝑖 𝑥, 𝑡 + Ω𝑖 𝑥, 𝑡 where 𝑒𝑖 is the vector along link 𝑖,  the collision operator is Ω𝑖 𝑥, 𝑡 = − 1 𝜏 𝑓𝑖 𝑥, 𝑡 − 𝑓𝑖 𝑒𝑞 𝑥, 𝑡 and the equilibrium distribution function is 𝑓𝑖 𝑒𝑞 = 𝑤𝑖 𝜌 1 + 3𝑒𝑖 ⋅ 𝑢 + 9 2 𝑒𝑖 ⋅ 𝑢 2 − 3 2 𝑢2 where 𝑤𝑖 0 < 𝑤𝑖 < 1 is weight function and the density and the velocity are given by: 𝜌 = 𝑓𝑖 8 𝑖=0 and 𝜌𝑢 = 𝑓𝑖 𝑒𝑖 8 𝑖=0 The D2Q9 lattice
  • 6. STENOSIS GROWTH MODELLING (CRITERIA)  The velocity magnitude along the wall is considered of significant effect on the simulation of the growth of the stenosis.  However, the maximum stagnation of the flow is considered in our work as the criterion for the growth of the stenosis, with stagnation index: SI = N/T  where T is the period of the cardiac pulse and N is the number of time-steps in a period when 𝑢1, the local velocity magnitude at the 1 grid length from the wall, is less than 1% of the average 𝑢1 over the whole of the wall during the previous period.
  • 7. 7 Arterial grid CALCULATION OF THE VELOCITY MAGNITUDE  The simulation of the growth of the stenosis is accomplished assuming an extrapolation scheme that supports the movement-boundary mechanism.  The velocity magnitude locally at the 1 grid space from the wall is worked out, by: 𝑢1= 1 − 𝛿 *𝑢 𝑑 𝑝1 + 𝛿 ∗ 𝑢 𝑑  δ: distance of the first fluid node 𝑥 𝑓  from the wall. 𝑢 𝑑𝑝1, 𝑢 𝑑, 𝑢1:velocities  at 𝑥𝑓𝑓, 𝑥 𝑓 and one grid length (1 lu) from the wall.
  • 8. 8 APPLYING THE MOVING BOUNDARY MECHANISM  Picking out the point satisfying the mechanical criterion (stagnation)  Applying the illustrated boundary-movement scheme at the first fluid node from the wall  Comparing the 𝛿 and 𝑙 (the distance the boundary moves, here set to 0.5)  𝛿 ≦ 𝑙 ∶ the selected fluid node 𝑥𝑓 turns to wall (case a)  𝛿 > 𝑙: the selected fluid node 𝑥𝑓 remains a fluid node (case b)  Working out the new 𝛿′  𝛿′ = 𝑙 − 𝛿 (case a)  𝛿′ = 𝛿 − 𝑙 (case b)  Set up the new boundary as shown Movement-boundary mechanism
  • 9. RESULTS ANALYSIS The presentation of the results is structured as follows:  Stenosis development in layers Effect of stenosis growth on the blood flow along the wall Flow profiles
  • 10. 10 STENOSIS DEVELOPMENT  The stenosis is formed in layers built up on the outer walls of the ECA and ICA.  The stenosis layers are built up consecutively on either the same arterial wall or on the opposite wall.  The growth occurs on the ECA below the bifurcation.  In the ICA the stenosis occurs from slightly below the bifurcation and extends significantly in to the ICA. Stenosis growth in layers with Ts, the number of grid sites, originally in the blood flow region, which have been enclosed by the growth of the stenosis.
  • 11. 11 CHANGE IN THE WALL VELOCITY WITH STENOSIS GROWTH B)A) The growth of the stenosis influences mainly the flow at the stenosed regions. A) Velocity magnitude along the ECA B) Velocity variation with the growth of the stenosis as a function of TS
  • 12. 12 FLOW PROFILES (UNSTENOSED ARTERY)  Velocity Magnitude  Shear Stress Over ½ cardiac pulse
  • 13. At the peak-pressure-time over the full cardiac pulse STENOSIS-GROWTH PROGRESSION
  • 14. 14 FLOW PROFILES (FULLY STENOSED ARTERY)  Velocity Magnitude  Shear Stress Over ½ cardiac pulse
  • 15. Conclusions The position of the stenosis has been simulated here based on regions of flow stagnation. The stenosis is formed on the outer wall of both the ICA and the ECA in the region where vortex motion develops in the healthy artery. The growth of the stenosis influences mainly the flow close to the stenosed wall. An increased velocity was observed in both the ICA and the ECA with the growth of the stenosis.
  • 16. Future research  Simulation of the progression of the stenosis in a number of other arteries which are similarly susceptible to this disease, in particular the human aorta  Comparison of haemodynamics between stenosed and stented arteries  Simulation of the non-Newtonian blood considering alternative models to the Carreau-Yasuda  Development of a 3D model to enable the secondary flows in the artery to be assessed and their effect on stenosis development
  • 17. References 1. C.G. Caro. Atherioscler Thromb Vasc Biol. 29: 18-161, 2009. 2. X. He, D.N. Ku. Journal of Biomechanical Engineering. 118: 74-82, 1996. 3. Y.S. Chatzizisis, M. Yoman, A.U. Coskun, R. Beigel, B.V. Stone, C. Meynard et al. Circulation. 117: 993-1002, 2008. 4. J. Knight, U. Olgac, S.C. Saur, D. Poulikakos, W. Marshall, P.C. Cattin et al. Atherosclerosis. 211: 445-450, 2010. 5. D.N. Ku, D.P. Giddens, C.K. Zarins and S.Glagov. Atherioscler Thromb Vasc Biol. 5: 293-302, 1985. 6. C.V. Soulis, O. P. Lampri, D.K. Fytanidis and G.D. Giannoglou. Biomedical Engineering, 2011 10th International Workshop on 5-7 Oct. 2011 1-4.