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Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_3592_Библиотеки_им_академика_М_И_Перельмана

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μ
μ
Vascular and Intravascular Imaging Trends, Analysis, and Challenges, Volume 1
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Similarly, the radial (r) momentum equation is given as
vvv vvvρρ ρ ρ τ ττ
() ( ) 1( ) () 1( )
rzr rr zr rr
+
tzr
+
r
rrprzrrrr
2
θθθ
−=
+
+
.
(4.8)
Clearly, for axi-symmetric problems, two additional terms appear in the radial momentum equation. These terms are which is essentially an acceleration term (or convection term), and
2
on the left-hand side of equation (4.8),
vρθr/
r/
θθ
on the right­hand side of (4.8), which is a viscous force, arising from the tangential stresses due to the curvature effect.
The non-conservative form of the convective terms is as follows:
φφφ ρφφρρφ
ρ
⎢ ⎣

Non-conservative form of the convective terms
() 1( ) ( ) 1( ) ( )

Conservative form of the convective terms
+
v
+
t
+
rz
r
vv vvρφ ρ φ ρ φ
rz rz
+
() 1( ) ( )
=

Conservative form of the convective terms
v
⎥ ⎦
ztrr
+
() 1( )
=
φρ ρφ
rrvr
φ
⎢ ⎣
 
These terms are zero by virtue of the continuity equation
vvρφ ρ φ ρ φ
rz
+
− ∂
() ( ) ()
rz z
+
ρρ ρ
+
trrrz
+
v
z
r
+
rz
.
rv
r
r
v
ρ
φ
z
⎥ ⎦
trrrz tr
(4.9)
Therefore, the convective terms may be expressed either in terms of conservative or non-conservative forms and the former is preferred in the present formulation as it is best suited to nite volume formulations. For three-dimensional studies, corresponding three-dimensional forms of the equations are used.
4.3 Viscoelastic models of diseased blood
Most researchers have considered a Newtonian viscosity model for blood owing through blood vessels. Blood owing through a diseased blood vessel has certain characteristics which make the viscosity properties of the blood non-Newtonian [2].
4.3.1 Carreau model
The four-parameter non-Newtonian viscosity model proposed by Carreau [1] differs from other models primarily in the curvature of the curve near the transition points between the Newtonian plateaus and the power region as follows:
where λ = 3.131 is the time constant associated with the viscosity that changes with the shear rate, and n = 0.3568, a = 2.
= 0.056 Pa s
0
an a
(1)
μγ μ μ μ λγ∣∣ = + + ∣∣
() ( )[1 ( )] ,
∞∞
0
is the blood viscosity at a zero shear rate,
4-6
(4.10)
=∞0.0032 Pa s
,
μ
μ
5
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4.3.2 Power-law model
In [23], a viscosity model for blood is proposed, taking into account hematocrit and total protein minus albumin. It is known as the power-law model, also referred to as the best three variable model. It is represented by
τγγ=−k
n 1
(4.11)
and
1
n
U
*
μγ γ=
() .
k
1
n
l
In [6], Chien et al calculated normal blood sample parameters as k = 14.67 × 10
1
n
*
(4.12)
3
Pa s, and n = 0.7755. If n > 1, the uid is known as shear-thickening, while uid is shear-thinning if n < 1. The characteristic parameter for a power-law-model-based ow is Re
PL
.
As the power-law model does not have the capability of handling Newtonian regions of shear-thinning uids at very low and high shear rates, Cross [7] proposed a model which can be described as a shear rate dependent viscosity model:
μμ
where
= 0.0364 Pa s
0
∣∣ = +
μγ μ
()
()
⎡ ⎢
1
is the blood viscosity at a very low shear rate,
0
+
,
n
γ
γ
c
c
(4.13)
=−2.63 s
1
the reference shear rate and n = 1.45 is the model constant.
is
4.3.3 Quemada model
Further considering the viscosity of a concentrated disperse system, Quemada [20] proposed a model based on shear rate and hematocrits. The system of equations of shear stress and effective viscosity in tensorial form and dimensionless form are
⎛ ⎜
τμ
F
⎜ ⎝
1
kk
+
1 2
0
1/
γγ
+
γγ
c
2
/
c
φγ=−
⎟ ⎠
(4.14)
and
2
1
*
μγ μ
() 1
γ
c
where
F
are Quemada-model-based flow are Re
as 1060 kg m
6
10
*
=
c
1.2 10 Pa s
===
c
, the viscosity of plasma (the suspending medium), is
Ul/
3
3
and hematocrit is
1
kk1.88 s , 2.07 and 4.33.
, whereas the Newtonian viscosity of blood is considered as 2.02 ×
kg m−2s−1.
F
2
0
QU
+
γγ
*
γγ
. The values of other parameters
+
kk
0
1/
φ = 0.4
The characteristic parameters for a
*
and
. The density of blood is considered
c
*
*
/
c
,
φ=−
*
c
(4.15)
4-7
b
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4.4 CFD modeling of blood flow in a diseased vessel
4.4.1 Laminar ow model
The laminar ow model of the internal ow regime in closed vessels can be modeled by the semi-implicit pressure linked equation (SIMPLE). It is a procedure for solving the governing equations of uid transport. The continuity equation can be discretized in this form of the laminar ow model by the following set of equations:
−+−+−=JA J A JA JA JA JA[][][]0
ee ww nn sn tt bb
(4.16)
or
N
faces
f
ff
=JA 0,
(4.17)
where uxes at the control volume faces are
ρρρρρρ======JuJ uJuJuJuJu(), (), (), (), (), (). (4.18)
eewwnnssttbb
To relate the face velocity,
vv
uww,,,,,
ewns t
, to the stored values of velocity at the cell centers, linear interpolation of cell-centered velocities to the faces will result in unphysical checker-boarding of pressure. To avoid checker-boarding, the face values of velocities are not averaged linearly, but using momentum-weighted averaging, as outlined in [21] using weighting factors based on the Using this procedure, the face ux for any face of the control volume,
coefcient.
a
P
, may be
f
written as
where
Jf
f
ff
++·−+∇·
vv
aa
Pc nc pc nc
ρ=
dp p r p p r(()) ()
f
+
,0 ,0 ,1 ,1
+
aa
Pc Pc
,0 ,1
c
c
0
=ˆ+−JJdp p(),
fff
00
()
c
1
cc01
c
11
(4.19)
(4.20)
ˆ
=
Jf
f
ff
With reference to gure 4.3,
the normal velocities, respectively, within the two cells on either side of the face
ˆ
The term
contains the inuence of velocities in these two adjacent cells andfis a
f
function of the average of the momentum equation. on either side of face
Figure 4.3. Control volume centroids of each control volume on either side of facef.
⎛ ⎜
vv
aa
Pc nc pc nc
ρ
f
+
,0 ,0 ,1 ,1
+
aa
Pc Pc
,0 ,1
p
C0
.
+∇−∇
dpr pr
(). ().]. (4.21)
[
fc c
and
are the pressures and
p
C1
4-8
⎞ ⎟
00 11
are coefcients for the cells
a
P
nC,0
and
nC,1
are
f
.
p
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Accordingly for the control volume, as shown in gure 4.3,
ww w
nn n
bb b
Now for a guessed pressure eld
*
JJdpp().
ee
=ˆ+−JJdp p
ee e
=ˆ+−JJdp p
=ˆ+−JJdp p
=ˆ+−JJdp p
sss
=ˆ+−JJdp p
tt t
=ˆ+−JJdp p
*
p
=
()
PE
()
WP
()
PN
()
SP
()
PT
().
BP
, the resulting east face flux from equation (4.22a)is
*
ˆ
+−
**
e
PE
a
(4.22 )
b
(4.22 )
c
(4.22 )
d
(4.22 )
e
(4.22 )
f
(4.22 )
(4.23)
This does not satisfy the volume continuity equation (4.15), so a correction
*
added to the face ux
Similarly, a pressure correction′pis added to the guessed pressure
corrected pressure
so that the corrected face uxebecomes
e
*
=+
JJ J.
e
ee
becomes
*
=+′
pp p.
p
The SIMPLE algorithm states that
Substituting
Similarly,
Jdp p().
e
in equation (4.22a) we obtain
e
*
=+′−
JJ dp p a( ). (4.27 )
e
e
=+′−
JJ dp p b() (4.27)
w
w
=+′−
JJ dp p c() (4.27)
n
n
=+′−
JJ dp p d() (4.27)
s
=+′−
JJ dp p e() (4.27)
t
t
=
*
*
*
s
*
e
PE
e
PE
w
WP
n
PN
s
SP
t
PT
(4.24)
*
so that the
(4.25)
(4.26)
is
e
*
=+′−
JJ dp p f( ). (4.27 )
b
b
b
BP
4-9
p
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Now putting the value of
**
JA dA p p JA dA p p
+
( ( )) ( ( ))
eee
e
*
JA dA p p JA dA p p
+
( ( )) ( ( ))
nnn
n
**
JA dA p p JA dA p p
+
( ( )) ( ( )) 0.
ttt
t
JJJJJ,,,,,
ewnstb
PE
PN
PT
−+′−
−+′−
in the continuity equation (4.15),
eww
w
+
sss
s
bbb
b
SP
BP
WP
Rearranging equation (4.13) we can write the equation as follows:
P
P
=
E
E
+
W
W
+
N
N
+
S
S
+
+
T
B
T
B
where
= + + +++a dAdA dAdAdAdA
Peewwnnssttbb
=adA
Eee
=adA
Www
=adA
nnn
=adA
sss
=adA
Ttt
=adA
Bbb
⎤ ⎦
+
=
+ap ap a p ap ap ap ap b,
+
(4.28)
(4.29)
a(4.30 )
b(4.30 )
c(4.30 )
d(4.30 )
e(4.30 )
f(4.30 )
g(4.30 )
Δ
** ** **
bJAJA JAJA JAJA f f
e
e
n
n
t
t
w
w
s
s
b
00
ρρ=++−−−+
().
b
PP PP
V
Δ
t
h
(4.30 )
Equation (4.29) represents the discretized continuity equation as an equation for
pressure correction
. From equation (4.29) we obtain the pressure correction
p
and putting the value of′pin equation (4.26) we obtain the correct pressure eld which satises the continuity equation (4.27). Then putting this pressure eld in the momentum equation (4.29), we obtain the correct velocity.
The proles at a particular blockage show similar trends of distribution. The agreement between the power-law model and cross model is remarkable, except for the type II prole at 56% obstruction where the cross model shows a atter distribution with relatively high magnitude. It can be observed again from the plots that the post-stenotic zone for higher blockage endures a long zone of oscillatory shear stress although the magnitude is relatively less. It is well understood that the ow structure of a stenosed vessel is dominated by vortical structures and the post­stenotic recirculation region [19].
Figure 4.4 shows a contour plot of the time averaged velocity stream function for the type 1 inlet velocity prole at different degrees of stenosis, considering the power­law viscosity model. The comparison is performed at two different Reynolds numbers in gure 4.4, denoted as Re I and Re II. At low Reynolds numbers,
4-10
p
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Figure 4.4. Contour view of velocity proles of blood owing through mild stenosed vessel at various time steps.
recirculation bubbles propagate away from the region of stenosis with time, producing a lower severity of stenosis (at 25%).
The numerical study of aneurysm was performed using two rheological models, namely the power-law model and Quemada model, to represent the diseased state of blood in a developing ow condition in a straight blood vessel with severe aneurysm of 250% of the mean diameter of the vessel [5]. The results for such a situation of fusiform aneurysms has not been not widely covered. Investigations were performed within the range 690 Re 2760. The responses of two different non-Newtonian viscosity models (namely power-law and Quemada) to different shear rate param­eters near the boundaries are compared. Stream lines in the duct of the geometry are shown in gure 4.4, which reects the development of vortices, considering the power-law model as the viscosity model for blood. As the resolution of the ow increases, the vortex size becomes amplied, signifying the serious affects of the aneurysm on the ow of blood.
A transient nature of ow development occurs in ducts with certain geometry. Such a phenomenon occurs due to the development of a vortex, initiating with offset damping, as depicted in gure 4.5.
4.5 Evaluation of the shear index on the vascular wall
The uid-mechanical parameters, such as shear stress, vortical structures, pressure proles and velocity distribution, can be evaluated from the time-dependent primitive variable data. Two important parameters need special mention in this context as they have relevance to the health of arterial tissue, namely the time­averaged wall shear stress (TAWSS) and the oscillator shear index (OSI) as described by [22]. TAWSS can be simply integrated and averaged over a time cycle. Wall shear stress is determined as
u
x
r
wall
×+′
4-11
μ=−
2
RzWSS (1 ( ) ).
(4.31)
1
η
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Figure 4.5. Stream line at different time steps at Re I (for the power-law model).
u
Downstream from the stenosis,
′=Rz() 0
The axial component of the velocity u
Rz
Let
x
u
x
2
QR
π
/
M
0
Rz,() ,
()
η===
R
0
, therefore,
is already calculated by equation (4.31).
x
r
be the non-dimensional variables. The
Rz
()
WSS
x
μ=−
r
wall
.
boundary conditions are the following:
The velocity is zero at the wall: There is symmetry in relation to the z-axis of the tube:
⁎⁎
3
uu
xx
0, and 0 for 0
3
η
η
Let the axial velocity along the z-axis be
Finally, the ow rate is conserved:
The coefcients A
⁎⁎
,0, 4
===+ ==−
awa a w
012
xx x
of equation (4.16) can also be written as
i
0, for
x
.
η===
⁎⁎
==
QQQ Rz ud/2()
6
Q
,0, 3
aaw
2
(())
Rz
.
η==
⁎⁎
xx
34
for
=
w
M
= 0
1
2
0
.
.
η
x
6
Q
(())
Rz
2
4-12
(4.32)
1
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⁎⁎
uw w
xx x x
4
⎜ ⎝
6
Q
2
(())
Rz
2
ηη∴=+− + + −
⎟ ⎠
3
w
⎜ ⎝
6
Q
2
(())
Rz
4
. (4.33)
⎟ ⎠
Here, the polynomial degree is limited to four. Since the ow rate is known as a function of time, the determination of the A determination of the velocity along the z-axis, i.e. by the experimental values. Finally, as
Rz()
coefcients is equivalent to the
i
The values of
.
x
downstream from the stenosis, wall
=
w
x
are given
shear stress can now be obtained:
u
x
=−
η
Qw12 4 .
x
(4.34)
Wall shear-stress plots for vessels with 25% and 50% blockages are calculated using the above equation, and are presented later in this section.
Wall shear stress based descriptors are also used as markers for calculating various states of the endothelial wall of the vessel. Gradient-based descriptors and harmonic-based descriptors are calculated in this chapter. The WSS spatial gradient (WSSG) is a marker of endothelial cell tension. It is calculated from WSS gradient tensor components parallel and perpendicular to the TAWSS vector (m and n, respectively) [ 8]:
T
1
=
⎛ ⎜
0
2
ττ
wm wn
,
+
2
,
dtWSSG
.
Tmn
(4.35)
Figure 4.6 shows the comparative behavior of WSSG in a diseased vessel under the in uence of variations in ow rates.
The maximum absolute rate of change in WSS magnitude over the cardiac cycle is also known as the temporal gradient of WSS (WSST), and it is calculated as follows:
WSST max . (4.36)
⎜ ⎝
t
τ=∂
w
⎟ ⎠
Table 4.1 shows transient evaluations of WSST in diseased and healthy arteries at Reynolds numbers Re I, Re II and Re III.
Figure 4.6. Graphical representation of WSSG distribution in diseased blood vessel at different Re.
4-13
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Table 4.1. Transient form of WSST in both diseased and healthy vessels.
Healthy vessel Diseased vessel
Viscosity model Flow rate
Power-law Re I 0.0147 0.0147
Re II 0.0127 0.0187 Re III 0.0094 0.0085
Quemada Re III 0.0122 0.0101
WSST WSST
The behavior of WSST is not similar to that of WSSG for the Quemada model. Here, the Quemada model shows better responses to WSST, but it also depends on ow rate. It is observed that WSST decreases with increased ow rate in a healthy vessel. However, an oscillatory behavior of WSST is found in diseased vessels with increased ow rate.
Figure 4.7 shows a comparative behavior of WSST in a healthy vessel under the inuence of variations in ow rates. WSST in the axial direction (x-direction) is found to be more pronounced than WSST in the radial direction (y-direction) at Re I and Re II. However, with a further increase in ow rate to Re II, an oscillatory behavior of WSST is observed in both the x- and y-directions. With a further increase in ow rate to Re III, it is observed that WSST in the radial direction is greater than that in the axial direction.
The harmonic component of WSS waveforms can be a possible metric of disturbed ow. This statement is supported by results revealing that endothelial cells sense and respond to the frequency of the WSS proles. The time varying WSS magnitude at each node can be Fourier decomposed, and the dominant harmonic (DH) is dened as the harmonic with the highest amplitude [12]. DH is calculated as
Table 4.2 shows transient evaluations of DH in diseased and healthy arteries at Reynolds numbers Re I, Re II and Re III. It can be seen that the value of DH increases with increased ow rate in the diseased vessel, whereas it behaves in oscillatory manner in the healthy vessel. However, DH also shows better responses to the ow when considering the rheological properties of the uid as in the Quemada model.
4.5.1 Oscillatory shear index
The OSI can be dened as
where τ
is the time-mean wall shear stress, also known as time-averaged wall
mean
shear stress (TAWSS), and τ and they are formulated using
ww w00
1
1 , (4.38)
=−OSI
2
is the time-mean magnitude of the wall shear stress,
mag
τω π=≡=Fnw F TDH max( ( )), FFT( ), 2 / . (4.37)
τ
mean
τ
mag
4-14
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Figure 4.7. Graphical representation of WSST distribution in a healthy blood vessel at (a) Re I, (b) Re II and (c) Re III.
Table 4.2. DH in both diseased and healthy vessels.
Viscosity model Flow rate
Power-law Re I 30.6964 30.6964
Quemada Re III 24.0394 84.4652
Healthy vessel Diseased vessel DH DH
Re II 5.5557 70.6169 Re III 13.2493 82.7616
4-15