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Patient-Specific Modeling of Blood Flow and

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Article in Annals of Biomedical Engineering · October 2010

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Annals of Biomedical Engineering, Vol. 38, No. 10, October 2010 ( 2010) pp. 3195–3209
DOI: 10.1007/s10439-010-0083-6

Patient-Specific Modeling of Blood Flow and Pressure in Human

Coronary Arteries
H. J. KIM,1 I. E. VIGNON-CLEMENTEL,2 J. S. COOGAN,3 C. A. FIGUEROA,3 K. E. JANSEN,1
and C. A. TAYLOR3,4
1
Aerospace Engineering Sciences, University of Colorado at Boulder, Boulder, CO 80309, USA; 2INRIA, Paris-Rocquencourt
BP 105, 78153 Le Chesnay Cedex, France; 3Department of Bioengineering, Stanford University, Stanford, CA 94305, USA; and
4
Department of Surgery, Stanford University, E350 Clark Center, 318 Campus Drive, Stanford, CA 94305, USA
(Received 29 September 2009; accepted 20 May 2010; published online 18 June 2010)

Associate Editor Peter E. McHugh oversaw the review of this article.

Abstract—Coronary flow is different from the flow in other
parts of the arterial system because it is influenced by the
contraction and relaxation of the heart. To model coronary
flow realistically, the compressive force of the heart acting on
the coronary vessels needs to be included. In this study, we
developed a method that predicts coronary flow and pressure
of three-dimensional epicardial coronary arteries by consid-
ering models of the heart and arterial system and the
interactions between the two models. For each coronary
outlet, a lumped parameter coronary vascular bed model was
assigned to represent the impedance of the downstream
coronary vascular networks absent in the computational
domain. The intramyocardial pressure was represented with
either the left or right ventricular pressure depending on the
location of the coronary arteries. The left and right ventric-
ular pressure were solved from the lumped parameter heart
models coupled to a closed loop system comprising a three-
dimensional model of the aorta, three-element Windkessel
models of the rest of the systemic circulation and the
pulmonary circulation, and lumped parameter models for the
left and right sides of the heart. The computed coronary flow
and pressure and the aortic flow and pressure waveforms
were realistic as compared to literature data.
Keywords—Blood flow, Coronary flow, Coronary pressure,
Coupled multidomain method.
INTRODUCTION
Computational simulations have been proven useful
in studying blood flow in the cardiovascular system24:
assessing hemodynamics of healthy and diseased blood
vessels,4,6 helping in the design and evaluation of vas-
cular medical devices,1,14 planning of vascular surgeries,
Address correspondence to C. A. Taylor, Department of Surgery,
Stanford University, E350 Clark Center, 318 Campus Drive,
Stanford, CA 94305, USA. Electronic mail: taylorca@stanford.edu
3195
and the prediction of the outcomes of interven-
tions.16,23 As the computing capacity and numerical
methods for simulation of blood flow advance, further
applications are anticipated.
However, computational simulations have been
rarely used to predict pulsatile flow and pressure fields
of three-dimensional coronary vascular beds, in part
because the flow rate and pressure in the coronary
vascular beds are highly related to the interactions
between the heart and the arterial system. Unlike flow
in other parts of the arterial system, coronary flow
decreases when the ventricles contract and increase the
intramyocardial pressure, which exerts an extravascu-
lar compressive force on the coronary vessels.17 Coro-
nary flow increases when the ventricles relax, thereby,
decreasing the intramyocardial pressure and extravas-
cular compressive force. Therefore, to model coronary
flow and pressure realistically, it is necessary to have a
model of the heart and a model of the arterial system
with consideration of the interactions between the two
models. Because of this complexity in modeling coro-
nary flow and pressure, most three-dimensional com-
putational studies have been conducted with only the
coronary arteries, ignoring the interactions between the
heart and the arterial system and prescribing, not pre-
dicting, coronary flow. Further, these studies have not
modeled realistic pressures and generally used traction-
free outlet boundary conditions whether the lateral
surfaces of the coronary arteries are considered as rigid
walls1,6 or compliant walls18,30 or the cardiac motions
due to the contraction and relaxation of the heart are
considered19,21 or not. Migliavacca and coworkers12,16
computed three-dimensional pulsatile coronary flow
and pressure in a single coronary artery, but this study
was performed with an idealized model and low mesh
0090-6964/10/1000-3195/0  2010 Biomedical Engineering Society
3196 KIM et al.

resolution. The analytic models used as boundary METHODS

conditions were coupled explicitly, necessitating either
subiterations within the same time step or a small time Three-Dimensional Finite Element Model of Blood
step size bounded by the stability of an explicit time Flow and Vessel Wall Dynamics
integration scheme. To predict physiologically realistic Blood flow in the large vessels of the cardiovascular
flow rate and pressure in the coronary arterial trees of a system can be approximated by the flow of a Newto-
patient, computational simulations should be robust nian fluid. Blood flow is modeled using the incom-
and stable enough to handle complex flow character- pressible Navier–Stokes equations, and the motion of
istics and the coupling with different scales of computer the vessel wall using the elastodynamics equations. In
models should be efficient and versatile.10 these equations, fluid–solid interface conditions, as
In previous studies, Vignon-Clementel et al.27,28 well as the initial and boundary conditions, are
developed boundary conditions for three-dimensional required to solve for the blood flow and the vessel wall
models of blood flow that can represent physiological dynamics of the fluid and solid domains, respectively.
conditions of each subject. For outlet boundaries of In this study, we used a fixed fluid mesh assuming
the arterial system excluding the coronary vascular small displacements of the vessel wall.5
beds, simple analytic models such as resistance, For a fluid domain X with its boundary C and a
impedance, and the three-element Windkessel model solid domain Xs with its boundary Csg ; the following
were assigned to model the arterial system absent in equations are solved for velocities ~ v; pressure p, and
the computational domain. This method is fully wall displacement ~ u .5,27
implicit and has proven to be versatile and robust. In a Given ~ f: X  ð0; TÞ ! R3 ; ~ fs : Xs  ð0; TÞ ! R3 ;
related study, we implemented a lumped parameter g: Cg  ð0; TÞ ! R ; ~
~ 3
g : Cg  ð0; TÞ ! R3 ; ~
s s
v0 : X ! R 3 ;
heart model as an inflow boundary condition of a s 3
u0 : X ! R ; and ~
~ s 3
u0;t : X ! R ; find ~ vð~ x; tÞ; and
x; tÞ; pð~
three-dimensional finite-element model of the aorta to uð~
~ xs ; tÞ for 8~x 2 X; 8~ xs 2 Xs ; and " t 2 (0, T), such
consider the interactions between the ventricle and the that the following conditions are satisfied:
arterial system.11 Again, a fully implicit method was
used to couple the heart model to the aortic model. We v;t þ q~
q~ v ¼ rp þ divðs Þ þ ~
v  r~ f
showed physiologically realistic flow and pressure 
fields for a subject-specific three-dimensional model of for ð~
x;tÞ 2 X  ð0;TÞ
the aorta with these boundary conditions.11 In addi- divð~vÞ ¼ 0 for ð~x;tÞ 2 X  ð0;TÞ
tion, constraints on the shape of the velocity profile at
the aortic inlet and select outlet boundaries were
s
q~ s ~s
x s ;tÞ 2 Xs  ð0; TÞ ð1Þ
u;tt ¼ r  r þ f for ð~

enforced using an augmented Lagrangian method to
where s ¼ lðr~ vÞ T Þ
v þ ðr~
resolve numerical instabilities that result from reverse 
and complex flow structures at boundaries.10 1
and rs ¼ C : ðr~ uÞT Þ
u þ ðr~
In this paper, we describe a method to calculate the   2
flow and pressure of three-dimensional coronary vas-
with the Dirichlet boundary conditions,
cular beds by considering the models of the left and
right sides of the heart, arterial system, and the inter-
vð~
~ x; tÞ ¼ ~ gð~x; tÞ for ð~ x; tÞ 2 Cg  ð0; TÞ
actions between them. For each coronary outlet, a ð2Þ
lumped parameter coronary vascular bed model was x s ; tÞ ¼ ~
uð~
~ g s ð~
x s ; tÞ for ð~
x s ; tÞ 2 Csg  ð0; TÞ
assigned to represent the impedance of downstream
the Neumann boundary conditions,
coronary vascular networks absent in the computa-
tional domain. We solved for coronary flow and ~
t~n ¼ ½p I þ s ~ ~ v; p; ~
n ¼ hð~ x 2 Ch
x; tÞ for ~ ð3Þ
 
pressure as well as aortic flow and pressure in patient-
specific models for rest and light and moderate exercise and the initial conditions,
conditions. Additionally, to demonstrate that these
methods can be utilized in clinical investigation, we ~vð~
x; 0Þ ¼ ~ v0 ð~
xÞ for ~ x2X
studied blood flow and pressure with different degrees uð~
~ s
x ; 0Þ ¼ ~ u0 ð~ s
x Þ for ~ x s 2 Xs ð4Þ
of stenosis. We created a stenosis in the left anterior x s ; 0Þ ¼ ~
u;t ð~
~ x s 2 Xs
x s Þ for ~
u0;t ð~
descending coronary artery by reducing the local
diameter of the geometric model by 40%, 50%, 60%, where the boundary C of the fluid domain is divided
and 75% and simulated a baseline (resting) condition into a Dirichlet boundary portion Cg and a Neumann
and a moderate exercise condition, where in the latter boundary portion Ch. Similarly, the boundary Cs of the
case we assumed that the downstream coronary vas- solid domain is divided into a Dirichlet boundary
cular beds were maximally dilated. portion Csg and a Neumann boundary portion Csh. They
 Patient-Specific Coronary Flow Modeling 3197

satisfy ðCh [ Cg Þ ¼ C; ðCsh [ Csg Þ ¼ Cs ; Ch \ Cg ¼ /; a model developed by Mantero et al.15 (Fig. 1). The
and Csh \ Csg ¼ /: coronary venous microcirculation compliance was
The density q and the dynamic viscosity l of the eliminated from the original model in order to simplify
fluid, and the density qs of the vessel walls are assumed the numerics. The coronary pressure and flow waveforms
to be constant. The external body force on the fluid retained realistic waveforms without the coronary
domain is represented by ~ f: Similarly, ~
fs is the external venous microcirculation compliance. The coronary vas-
body force on the solid domain, C is a fourth-order cular bed model consists of coronary arterial resistance

tensor of material constants, and rs is the vessel wall Ra, coronary arterial compliance Ca, coronary arterial

stress tensor. microcirculation resistance Ra-micro, myocardial compli-
To assign coronary outlet boundary conditions, the ance Cim, coronary venous microcirculation resistance
coupled multidomain method27 is utilized with a Rv-micro, coronary venous resistance Rv, and intramyo-
lumped parameter coronary vascular bed model. Simi- cardial pressure Pim(t). The modeling of the intramyo-
larly to the treatment of other outflow boundary con- cardial pressure is explained in the next subsection.
ditions, a lumped parameter model of coronary
 vascular
 For each coronary outlet surface Chcork we defined
~c the operators M and H as follows by replacing the
beds defines boundary operators M ¼ M ; M
m Chcor
coronary outlet pressure P(t) with the ordinary dif-
  ferential equation obtained from the lumped parame-
and H ¼ H ; H~c that represent the traction and ter coronary vascular bed model:
m Chcor   Z
flow at each coronary outlet surface Chcor . For the other M ð~ v;pÞ þ H ¼ R vðtÞ ~
~ ndC
boundaries, the same method is applied to assign an m m C Chcor
hcor k
impedance using a three-element Windkessel model.28 Z Z
k
!
t
The lateral surface of the fluid domain coincides with a þ ek1 ðtsÞ Z1 vðsÞ ~
~ ndCds I
0 Chcor 
membrane model of the vessel wall in the coupled k
!
momentum method for fluid–solid interaction.5 A sta- Z t Z
bilized semi-discrete finite element method25 is utilized þ ek2 ðtsÞ Z2 vðsÞ ~
~ n  s ~
ndCds ~ njChcor I ð5Þ
0 Chcor  k 
to solve for Eqs. (1)–(4) in this study.   k

þ s jChcor  Aek1 t  Bek2 t I

 k 
Z t Z t 
The Lumped Parameter Model of Downstream k1 ðtsÞ k2 ðtsÞ
Coronary Vascular Beds  e  Y1 Pim ðsÞds  e  Y2 Pim ðsÞds I
0 0 
h i
The lumped parameter model of coronary vascular M~c ð~
v;pÞ þ H ~c ¼~vjChcor
Chcor k
beds coupled to each coronary outlet surface is based on k

C D EF A: Inlet - coupled to lumped parameter heart model

B
G
RLA-V L LA-V RLV-art L LV-art
ELA ELV (t)

ELA RLA-V LLA-V RLV-art LLV-art

A V
B-H: Outlets - coupled to A -Inlet
2.1
a three-element Windkessel
Elastance function
(mmHg/cm3)

i A model
ELV ( t) k c b Rp Rd
V
j e C
h gd f 0
V 0 Time (s) 0.952

H a-k: Coronary outlets - coupled to lumped

Rpd Rpp LRV-art RRV-art LRA-V RRA-V ERA parameter coronary vascular model
Ra Ra-micro
- Rv-mi
v cro

Cim
Ca Rv
Cp ERV (t ) Pim

V V V

FIGURE 1. Problem specification of the inlet, upper branch vessels, the descending thoracic aorta, and coronary outlets for
simulations of blood flow in a normal thoracic aorta model with coronary outlets. Note that all the outlets of the three-dimensional
computational model feed back in the lumped model at (V).
3198 KIM et al.

where P(t) and Q(t) are the pressure and flow at the The velocity and pressure fields in the three-dimensional
coronary outlet surface and I is an identity tensor. The domain and its boundaries were solved implicitly.

coefficients k1, k2, A, B, R, Z1, Y1, Z2, and Y2 are
defined using the lumped parameter model of down- Computation of the Intramyocardial Pressure
stream coronary vascular beds as follows:
qffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffi Depending on the location of the coronary vascular
p1 þ p21  4p0 p2 beds, the coronary beds experience different intramy-
k1 ¼ ocardial pressure Pim. Coronary flow in the left coro-
2p2
qffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffi nary vascular beds is decreased significantly in systole
p1  p21  4p0 p2 because the left ventricle operates in a high pressure
k2 ¼ range. However, the right coronary flow does not
2p2
" decrease in systole because the right ventricle operates
1 dQ in a lower pressure range than the left ventricle.17 Even
A ¼ qffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffi ðq2 k1 þ q1 ÞQð0Þ þ q2 ð0Þ
p21  4p0 p2 dt the maximum right ventricular pressure is one-fifth of
  # the average aortic pressure.17 To accommodate the
dP change in the intramyorcardial pressure depending on
þ b1 Pim ð0Þ þ p2 k2 Pð0Þ  ð0Þ
dt the location of the coronary vascular beds, we imple-
" mented a closed loop system and computed the left and
1 dQ right ventricular pressure. Previously, we had devel-
B ¼ qffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffi ðq2 k2 þ q1 ÞQð0Þ þ q2 ð0Þ
p21  4p0 p2 dt oped a boundary condition coupling a lumped
  # parameter model representing the left side of the heart
dP to the inlet of the thoracic aorta to compute the left
þ b1 Pim ð0Þ þ p2 k1 Pð0Þ  ð0Þ
dt ventricular pressure.11 In this study, another lumped
q2 parameter right heart model was coupled to the pul-
R¼ monary circulation to compute the right ventricular
p2
pressure. Depending on the location of the coronary
q2 k21 þ q1 k1 þ q0 outlet boundaries, we used the left ventricular pressure
Z1 ¼ qffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffi
p21  4p0 p2 to represent the intramyocardial pressure of the left
coronary arteries and the right ventricular pressure to
b1 k1 þ b0
Y1 ¼ qffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffi represent the intramyocardial pressure of the right
p21  4p0 p2 coronary arteries. The closed loop system implemented
in these simulations is plotted in Fig. 1.
q2 k22 þ q1 k2 þ q0
Z2 ¼ qffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffi
p21  4p0 p2 Choice of the Parameter Values for the Coronary Model
b1 k2 þ b0
Y2 ¼ qffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffi The flow distribution to each primary branch of the
p21  4p0 p2 coronary arteries was calculated on the basis of mor-
phology data and data from the literature.31 We
with the following coefficients: assumed that the mean coronary flow is 4.0% of the
p0 ¼ 1 cardiac output.17 For each coronary outlet surface,
coronary venous resistance was calculated on the basis
p1 ¼ Ra-micro Ca þ ðRv þ Rv-micro ÞðCa þ Cim Þ
of the mean flow and assigned venous pressure
p2 ¼ Ca Cim Ra-micro ðRv þ Rv-micro Þ according to literature data.17 We then computed
q0 ¼ Ra þ Ra-micro þ Rv þ Rv-micro coronary arterial resistance and coronary arterial
q1 ¼ Ra Ca ðRa-micro þ Rv þ Rv-micro Þ microcirculation resistance on the basis of mean flow,
mean arterial pressure, and the coronary impedance
þ Cim ðRa þ Ra-micro ÞðRv þ Rv-micro Þ
spectrum using literature data.3,26 The capacitance
q2 ¼ Ca Cim Ra Ra-micro ðRv þ Rv-micro Þ values were adjusted to give physiologically realistic
b0 ¼ 0 coronary flow and pressure waveforms using literature
b1 ¼ Cim ðRv þ Rv-micro Þ data.3
During simulated exercise, the mean flow to the
Using these operators defined above, we couple the coronary vascular bed was increased to maintain the
flow and pressure at each coronary outlet surface mean flow at 4.0% of the cardiac output. However, we
between the upstream three-dimensional finite element set a threshold value below which the resistance cannot
model and the downstream lumped parameter model. decrease. The coronary parameter values for each
 Patient-Specific Coronary Flow Modeling
coronary outlet surface were modified by decreasing
the total resistances and increasing the capacitances
and the ratio of the coronary arterial resistance to the
total coronary resistance based on literature data.3
The parameter values of the lumped parameter
heart model and three-element Windkessel models
were determined to match subject-specific cardiac
output and pulse pressure.11
Exercise Simulations
In this study, we simulated two different levels of
exercise conditions. First, for the simulation with
normal coronary arteries, we simulated rest and light
exercise conditions. The light exercise condition is
similar to a brisk walk. We doubled the cardiac output
and heart rate, and the coronary flow was doubled to
meet the increased metabolic demands accordingly.
However, the downstream coronary vascular networks
were not dilated maximally. Second, for the simula-
tions with different degrees of stenosis, we simulated
moderate exercise to approximate maximal dilation of
downstream coronary vascular networks. This way, we
can study how different degrees of stenosis reduce the
coronary flow reserve affecting the coronary flow and
pressure waveforms. To simulate moderate exercise,
we tripled the cardiac output and heart rate and the
mean coronary flow was increased by 350%.
Simulation Details
Blood was approximated as incompressible New-
tonian fluid with a density of 1.06 g/cm3 and a
dynamic viscosity of 0.04 dynes/cm2 s for all the
simulations. The blood vessel walls were modeled with
a linearly elastic material. Poisson’s ratio was 0.5 with
a wall density of 1.0 g/cm3 and a uniform wall thick-
ness of 0.1 cm. The inlet and the outlet rings were fixed
in space and time.5 The mesh generated was aniso-
tropic with local refinement on exterior surfaces and
coronary vascular beds with five semi-structured layers
within the boundary layer.20 The solutions were run
until the relative pressure fields at the inlet and outlets
did not change more than 1.0% compared to those in
the solutions at the same phase in the previous cardiac
cycle.
We constructed the geometrical model used in these
simulations from cardiac-gated computer tomography
data of a 36-year-old healthy male subject. The model
started from the root of the aorta, ended above the
diaphragm, and included major coronary arteries (left
anterior descending, left circumflex, and right coronary
arteries) and major branches of them and main upper
branch vessels (right subclavian, left subclavian, right
vertebral, left vertebral, right carotid, and left carotid
3199
arteries). For the inlet, we coupled the lumped
parameter heart model.11 For the coronary outlets, we
assigned lumped parameter coronary vascular mod-
els.15 For the upper branch vessels and the descending
thoracic aorta, we assigned three-element Windkessel
models (Fig. 1). The flow distribution used to evaluate
the resistance/impedance of each coronary, upper
branch, and descending thoracic aortic outlet was set
based on literature data.29 Boundary conditions were
adjusted to match both the flow distribution and the
measured brachial artery pulse pressure.13,22 Addi-
tionally, we adjusted the Young’s modulus of the
blood vessel walls to match the measured wall defor-
mations of the aorta on the basis of the cardiac-gated
computer tomography data. In this study, we modeled
the wall deformability with the uniform Young’s
modulus of 6.26 9 106 dynes/cm2. We also found
tethering areas using this patient’s cardiac-gated com-
puter tomography data and fixed those areas in space
and time in the computer model. For the coronary
vessels, we identified thin strips approximating the
intersection between the coronary arteries and epicar-
dial surface of the heart and fixed the surface of the
coronary arteries along the strips.
To demonstrate that these methods can be utilized
in clinical investigation, we studied blood flow and
pressure with different degrees of stenosis. We created
a stenosis in the left anterior descending coronary
artery by reducing the local diameter of the geometric
model by 40%, 50%, 60%, and 75% and simulated a
rest condition and a moderate exercise condition,
where in the latter case we assumed that the down-
stream coronary vascular beds were maximally dilated.
RESULTS
Simulations of Coronary Flow and Pressure of a Normal
Thoracic Aortic Model with Epicardial Coronary
Arteries at Rest and During Light Exercise
In these simulations, we studied coronary flow and
pressure of normal coronary arteries for rest and light
exercise conditions. Solutions were obtained using a
1,768,953 element (339,664 node) finite element mesh
with a time step size of 0.25 ms to simulate a resting
condition and 0.125 ms to simulate a light exercise
condition. The shape of the velocity profiles of the inlet
and of the outlets of the upper branch vessels, and the
descending thoracic aorta was constrained to an axi-
symmetric shape with a profile order of nine.10
To simulate light exercise, the resistance value of the
descending thoracic aorta was decreased in order to
increase flow to the lower extremities. The cardiac
cycle was shortened to simulate increased heart rate
until the systolic pressure of the thoracic aorta
3200 KIM et al.

increased by 20% compared to the resting state.2 The
boundary conditions of the upper branch vessels were
unchanged. The parameter values of the closed loop
system are shown in Table 1, and the parameter values
of the Windkessel models are shown in Table 2. The
contractility of this subject was not changed for the
light exercise simulation. Table 3 shows the parameter
values of the lumped parameter coronary vascular
models assigned to each coronary outlet for rest and
light exercise conditions.
Figure 2 shows computed pressure and flow wave-
forms of the inlet and the outlets for rest and light
exercise conditions of the normal thoracic aorta. The
pressure–volume loops of the left and right ventricles
for both conditions are also shown. The cardiac cycle
decreased from 1.0 to 0.5 s, the cardiac output
increased from 5 to 10.3 L/min, and systolic blood
pressure increased from 124 to 149 mmHg. However,
the stroke volume increased little from 83 to 86 cc
signifying the increase in the cardiac output was mainly
due to the shortening of the cardiac cycle, not due to
the increase of the stroke volume.
Figure 2 also shows that the upper branch vessels
experience retrograde flow in diastole. Retrograde flow
to the upper branch vessels is severe in the light exer-
cise condition, even though the same boundary con-
ditions were assigned to the upper branch vessels,
likely due to the increased flow demand of the
descending thoracic aorta. Figure 2 also shows the
pressure waveforms of the upper branch vessels and
the descending thoracic aorta. The pressure waveform
of the descending thoracic aorta decays faster during
exercise than in the resting condition.
In Fig. 3, coronary flow and pressure waveforms of
the left anterior descending, left circumflex, and right
coronary arteries are plotted for rest and exercise

TABLE 1. Parameter values of the closed loop system at rest (R), during light exercise (E1), and during moderate exercise (E2)
for the simulations of thoracic aorta with coronary arteries.

R E1 E2 R E1 E2

RLA-V (dynes s/cm5) 5 5 5 RRA-V (dynes s/cm5) 5 5 5

LLA-V (dynes s2/cm5) 5 5 5 LRA-V (dynes s2/cm5) 1 1 1
RLV-art(dynes s/cm5) 10 10 10 RRV-art (dynes s/cm5) 10 10 10
LLV-art (dynes s2/cm5) 0.69 0.69 0.69 LRV-art (dynes s2/cm5) 0.55 0.55 0.55
ELV,max (mmHg/cc) 2.0 2.0 2.2 ERV,max (mmHg/cc) 0.5 0.5 0.5
VLV, 0 (cc) 0 0 0 VRV, 0 (cc) 0 0 0
VLA, 0 (cc) 260 260 260 VRA, 0 (cc) 260 260 260
ELA (mmHg/cc) 270 350 360 ERA (mmHg/cc) 60 80 80
tmax (s) 0.33 0.25 0.15 Cardiac cycle (s) 1.0 0.5 0.3
Rpp (dynes s/cm5) 16 16 2 Cp (cm5/dynes) 0.022 0.022 0.02
Rpd (dynes s/cm5) 144 144 38

TABLE 2. Parameter values of the three-element Windkessel models at rest (R), during light exercise (E1), and during moderate
exercise (E2) for the simulations of thoracic aorta with coronary arteries.

B-R B-El B-E2 C-R C-El C-E2 D-R D-El D-E2

Rp (103 dynes s/cm5) 1.49 1.49 0.20 1.41 1.41 0.19 10.7 10.7 1.44
C (1026cm5/dynes) 235 235 31.8 248 248 33.5 32.9 32.9 4.45
Rd (103 s/cm5) 15.1 15.1 20.0 14.3 14.3 19.0 108 108 143

E-R E-El E-E2 F-R F-El F-E2 G-R G-El G-E2

Rp (103dynes s/cm5) 1.75 1.75 0.24 7.96 7.96 1.08 1.80 1.08 0.24
C (1026 cm5/dynes) 201 201 27.1 44.0 44.0 5.95 195 195 26.3
Rd (103 dynes s/cm5) 17.6 17.6 23.4 80.5 80.5 107 18.2 18.2 24.1

H-R H-El H-E2

3 5
Rp (10 dynes s/cm ) 0.227 0.225 0.08
C (1026 cm5/dynes) 1540 1600 1200
Rd (103 dynes s/cm5) 2.29 0.676 0.45

B denotes right subclavian artery, C denotes right carotid artery, D denotes right vertebral artery, E denotes left carotid artery, F denotes left
vertebral artery, G denotes left subclavian artery, and H denotes descending thoracic aorta. Note that the parameter values of the upper
branch vessels are the same for the light exercise and resting conditions and change for the moderate exercise condition.
 Patient-Specific Coronary Flow Modeling 3201

TABLE 3. Parameter values of the lumped parameter models of the coronary vascular beds at rest (R), during light exercise (E1),
and during moderate exercise (E2) for the simulations of thoracic aorta with coronary arteries.

Ra Ra-micro Rv + Rv-micro Ca cim

R E1 E2 R E1 E2 R E1 E2 R E1 E2 R E1 E2

a: LAD1 183 177 76 299 56 24 94 44 18 0.34 0.75 0.75 2.89 6.88 6.88
b: LAD2 131 126 52 214 40 16 67 32 13 0.48 1.02 1.02 4.04 9.34 9.34
c: LAD3 123 91 51 148 39 16 65 31 12 0.49 1.07 1.07 4.16 9.74 9.74
d: LAD4 75 55 31 90 24 10 40 19 7 0.80 1.74 1.74 6.82 15.9 15.9
e: LCX1 49 47 20 80 15 6.2 25 12 5 1.28 2.79 2.79 10.8 25.4 25.4
f: LCX2 160 154 65 261 49 20 82 39 15 0.39 0.85 0.85 3.31 7.78 7.78
g: LCX3 216 208 87 353 66 27 111 53 21 0.29 0.63 0.63 2.45 5.74 5.74
h: LCX4 170 164 68 277 52 21 87 41 16 0.37 0.80 0.80 3.12 7.29 7.29
i: RCA1 168 163 71 274 51 22 86 40 16 0.37 0.83 0.83 3.15 7.60 7.60
j: RCA2 236 229 98 385 72 31 121 56 23 0.26 0.59 0.59 2.24 5.38 5.38
k: RCA3 266 257 110 435 81 35 136 64 25 0.23 0.52 0.52 1.99 4.72 4.72
c*: LAD3 100 51 146 16 65 12 0.49 1.07 4.16 9.74
c**: LAD3 89 51 146 16 65 12 0.49 1.07 4.16 9.74
c***: LAD3 80 51 98 16 65 12 0.49 1.07 4.16 9.74
c****: LAD3 57 51 93 16 65 12 0.49 1.07 4.16 9.74
d*: LAD4 65 31 89 10 40 7 0.80 1.74 6.82 15.9
d**: LAD4 54 31 89 10 40 7 0.80 1.74 6.82 15.9
d***: LAD4 48 31 58 10 40 7 0.80 1.74 6.82 15.9
d****: LAD4 35 31 57 10 40 7 0.80 1.74 6.82 15.9

c* denotes LAD3 with 40% diameter reduction, c** denotes LAD3 with 50% diameter reduction, c*** denotes LAD3 with 60% diameter
reduction, and c**** denotes LAD3 with 75% diameter reduction. Similarly, d* denotes LAD4 with 40% diameter reduction, d** denotes LAD4
with 50% diameter reduction, d*** denotes LAD4 with 60% diameter reduction, and d**** denotes LAD4 with 75% diameter reduction. Note
that the unit of the resistance values are in 103 dynes s/cm5 and the unit of the capacitance values are in 1026 cm5/dynes.

conditions. For the left anterior descending and cir-
cumflex coronary arteries, coronary flow is high in
diastole and low in systole because the intramyocardial
pressure approximated by the left ventricular pressure
is elevated in systole. On the contrary, the right coro-
nary artery has high flow in systole and low flow in
diastole because the intramyocardial pressure caused
by the right ventricular pressure operates in a low
pressure range. By coupling the lumped parameter
heart models and the lumped parameter coronary
vascular models to a three-dimensional finite element
model of the aorta, we were able to obtain realistic
coronary flow and pressure waveforms17 because we
considered the effects of the contraction and relaxation
of the left and right ventricles. The coronary pressure
waveforms are similar to the aortic pressure waveform
unlike the coronary flow waveforms, which are
dependent on the location of the myocardium the
coronary arteries feed. During light exercise, the cor-
onary flow doubled to meet the demands of the heart.
For the resting condition, the mean coronary flow to
the left anterior descending coronary artery was 1.3 cc/s,
the mean flow to the left circumflex coronary artery
was 1.5 cc/s, and the mean flow to the right coronary
artery was 0.6 cc/s, to yield a total coronary flow of
3.4 cc/s. During light exercise, the coronary flow
doubled achieving a mean flow of 2.8 cc/s to the left
anterior descending coronary artery, 3.1 cc/s to the left
circumflex coronary artery, and 1.1 cc/s to the right
coronary artery, and a total coronary flow of 7.0 cc/s.
Wall shear stress of the coronary arteries for the
resting condition and the light exercise condition are
also plotted for peak-systole, peak left coronary flow,
and late diastole in Fig. 4. For the light exercise con-
dition, the wall shear stress increased as higher volume
of flow traveled to the coronary arteries from the left
ventricle. The left coronary arteries experience higher
wall shear stress fields in late systole and late diastole
whereas the right coronary arteries experience higher
wall shear stress fields in systole due to the asynchrony
of the maximum flow in the left and right coronary
arteries.
Simulations of Coronary Flow and Pressure
with Different Degrees of Stenosis at the Left
Anterior Descending Coronary Artery
In these simulations, we studied how the degree of a
stenosis in the left anterior descending coronary artery
affects coronary flow and pressure. For the normal
case with no stenosis in the left anterior descending
coronary artery, solutions were obtained using a
1,768,953 element and a 339,664 node mesh with a time
step size of 0.25 ms to simulate a resting condition and
0.1 ms to simulate a moderate exercise condition. The
shape of the velocity profiles at the inlet and at the
3202 KIM et al.

D-Left vertebral Pressure-volume loops E-Right carotid

138 150 138
Left ventricle (rest)
Pressure (mmHg)

Pressure (mmHg)

Pressure (mmHg)
Right ventricle (rest)
Left ventricle (exercise)
Right ventricle (exercise)

68 0 68
0 1 0 150 0 1
Time (s) Volume (cc) Time (s)
D-Left vertebral E-Right carotid
7.5 Rest 39
Flow rate (cc/s)

Flow rate (cc/s)

Exercise
C D E F
B
G
0 1
-1.5 -7 0 1
Time (s) Time (s)

C-Left carotid G-Right subclavian

138 138
Pressure (mmHg)

Pressure (mmHg)
68 68
0 1 0 1
Time (s) Time (s)
C-Left carotid
A G-Right subclavian
31 37
Flow rate (cc/s)

Flow rate (cc/s)

0 1 0 1
-6 -7
Time (s) Time (s)
H
B-Left subclavian A-Aortic inlet H-Descending thoracic aorta
138 138 138
Rest
Pressure (mmHg)

Pressure (mmHg)

Pressure (mmHg)

Exercise

68 68 68
0 1 0 1 0 1
Time (s) Time (s) Time (s)
B-Left subclavian A-Aortic inlet H-Descending thoracic aorta
30 580 400
Rest
Flow rate (cc/s)

Flow rate (cc/s)

Flow rate (cc/s)

Exercise

-5 0 1 -20 -40
0 1 0 1
Time (s) Time (s) Time (s)

FIGURE 2. Pressure–volume loops of the left and right ventricles and flow and pressure waveforms of the descending thoracic
aorta and upper branch vessels for resting and light exercise cases with normal coronary anatomy.
 Patient-Specific Coronary Flow Modeling
Pressure
a-d: Left anterior descending coronary
Pressure (mmHg) 138
68
0 Time (s)
e-h: Left circumflex coronary
138
Pressure (mmHg)
68
0 1
Time (s)
i-k: Right coronary
138
Pressure (mmHg)
68
0 1
Time (s)
FIGURE 3. Flow and pressure waveforms of coronary arteries at rest and during light exercise case.
outlets of the upper branch vessels and the descending
thoracic aorta were constrained to an axisymmetric
shape with a profile order of nine.10 For a stenosis case
with 40% diameter reduction in the left anterior
descending coronary artery, solutions were obtained
using a 1,813,097 element and a 350,123 node mesh
with the same time step size as in the normal case. For
a stenosis case with 50% diameter reduction in the left
anterior descending coronary artery, solutions were
obtained using a 2,576,721 element and a 475,723 node
mesh with the same time step size as in the normal case.
For a stenosis case with 60% diameter reduction in the
left anterior descending coronary artery, solutions
were obtained using a 3,146,766 element and a 575,122
node mesh with the same time step size as in the nor-
mal case. Finally, for a stenosis case with 75% diam-
eter reduction in the left anterior descending coronary
artery, solutions were obtained using a 3,836,663 ele-
ment and a 722,518 node mesh with the same time step
size as in the normal case. The increase in the mesh size
was due to the additional refinements in the area of
stenosis.
For resting conditions, we decreased the resistance
of the coronary model downstream of the stenosed
3203
Rest Flow
a-d: Left anterior descending coronary
Exercise 4.5
Flow rate (cc/s)
0
1 0 Time (s) 1
e-h: Left circumflex coronary
5
Flow rate (cc/s)
a
i 0
0 1
Time (s)
k c b Right coronary
2
Flow rate (cc/s)
f e
h gd
0
0 1
Time (s)
artery until we obtained the same mean flow to these
outlets as with the normal case. We recorded the
pressure loss through these stenosed regions in
Table 4. To dilate the downstream coronary vascular
networks to maximum, we simulated moderate exer-
cise by decreasing the resistance value of the descend-
ing thoracic aorta and shortened the cardiac cycle to
increase cardiac output threefold compared to the
resting state. In the exercise simulations, we assumed
that the downstream coronary vasculatures were
maximally dilated and assigned the same boundary
conditions with the normal case to all the stenosis
cases. The flow difference downstream of the stenosed
artery was recorded in Table 4. Table 3 shows the
parameter values of the lumped parameter coronary
vascular models assigned to each coronary outlet for
rest and moderate exercise conditions for the normal
case and all the stenosis cases.
At rest, the downstream coronary boundary condi-
tions were modified until the same mean flow was
achieved through the stenosed artery. However, as the
same mean flow traveled through the stenosed artery, a
pressure loss occurred due to the viscous loss through
the stenosis and complex flow structures distal to the
3204 KIM et al.

Inlet flow rate (cc/s)

580 a
Rest
A Exercise

b c B C
-20
0 Time (s) 1

Rest A B C

Exercise a b c

Wall shear stress (dynes/cm2 )

0 7.5 15 22.5 30

FIGURE 4. Wall shear stress of coronary arteries for peak systole, peak left coronary flow rate, and mid-diastole at rest and during
light exercise.

TABLE 4. Mean left anterior descending coronary artery flow stenosed region as shown in Table 4. During exercise,
and pressure at rest and during moderate exercise for the the same coronary boundary conditions were assigned
simulations of coronary flow and pressure with different
degrees of stenosis in the left anterior descending coronary to the coronary outlets. A noticeable pressure loss and
artery. flow rate decrease occurred in the case of the stenosis
with 75% diameter reduction.
Mean coronary Mean pressure
flow (cc/s) (mmHg)
The boundary conditions of the upper branch ves-
sels were changed to obtain the same mean flow rate as
Mean coronary flow and pressure at rest in the resting state. The parameter values of the closed
Normal 1.1 94 loop system is shown in Table 1 and the parameter
40% Diameter reduction 1.1 93
50% Diameter reduction 1.1 92
values of the Windkessel models are shown in Table 2.
60% Diameter reduction 1.1 86 The contractility of this subject was increased 10% for
75% Diameter reduction 1.1 78 this moderate exercise simulation.2
Mean coronary flow and pressure at moderate exercise Figure 5 depicts flow and pressure waveforms of the
Normal 3.7 85 left anterior descending coronary artery for rest and
40% Diameter reduction 3.4 77
50% Diameter reduction 3.2 73
moderate exercise conditions. Note that we plotted
60% Diameter reduction 3.0 67 the flow and pressure waveforms of the 50% and
75% Diameter reduction 1.8 36 75% diameter reduction cases only. We see that the
 Patient-Specific Coronary Flow Modeling 3205

Normal 50% diameter reduction 75% diameter reduction

Left anterior descending coronary flow at rest Left anterior descending coronary pressure at rest
3 130
Normal

Pressure (mmHg)
50% diameter reduction
Flow rate (cc/s)

75% diameter reduction

Normal
50% diameter reduction
75% diameter reduction
0 60
0 1 0 1
Time (s) Time (s)
Left anterior descending coronary flow at exercise Left anterior descending coronary pressure at exercise
11 130
Normal Normal

Pressure (mmHg)
50% diameter reduction
Flow rate (cc/s)

50% diameter reduction

75% diameter reduction 75% diameter reduction

0 0
0 0.3 0 0.3
Time (s) Time (s)

FIGURE 5. Effect of stenosis on coronary artery flow and pressure at rest and during moderate exercise. The pressure was
computed downstream of the stenosis. Note that only 50% and 75% diameter reduction cases are plotted.

Left anterior descending coronary to the stenosed regions and they propagate longer for
5
more severe stenosis. Note that we selected 50% and
4 75% diameter reduction cases only.
Flow rate (cc/s)

2
1
0
0 20
Diameter reduction (%)
Rest Exercise
FIGURE 6. Mean flow rate of the left anterior descending
coronary artery vs. degree of stenosis for rest and moderate
exercise.
coronary flow tripled and the pressure pulse also
became larger for the exercise condition. The pressure
loss increased as more flow traveled through the ste-
nosed regions in the cases of 50% and 75% diameter
reduction.
Figure 6 shows the mean flow in the stenosed artery
in both resting and moderate exercise conditions. We
also plotted the experimental results of Gould et al. for
comparison.7 Figure 7 shows volume rendered velocity
magnitudes of the coronary arteries during moderate
exercise. Complex flow structures are observed distal
DISCUSSION
We have successfully developed and implemented a
40 60 80 100 coronary boundary condition that couples a lumped
parameter coronary vascular model to each coronary
Rest (Gould et al) Hyperemia (Gould et al)
outlet of a three-dimensional finite element model of the
aorta and epicardial coronary arteries. We also used an
inflow boundary condition coupling a lumped parame-
ter heart model and a closed loop model to represent the
intramyocardial pressure by considering the interac-
tions between the heart and arterial system. Fluid–
structure interaction simulations were performed to
better represent flow and pressure waveforms. Addi-
tionally, we were able to obtain robust and stable solu-
tions by constraining the shape of the velocity profiles of
the boundaries that experienced retrograde flow.
Using the lumped parameter coronary vascular
model along with the inflow boundary condition that
couples the lumped parameter heart model and the
closed loop system, we studied how changes in car-
diac and arterial properties affect coronary flow and
3206 KIM et al.

Inflow waveform
1000
Velocity magnitude (cm/s)
Flow rate (cc/s)
A 0 15 30 45 60

B
-50
0 0.3
Time (s) A B

Normal

50% diameter
reduction

75% diameter
reduction

FIGURE 7. Volume rendered velocity magnitudes of coronary arteries with different degrees of stenosis during moderate exer-
cise. Note that only 50% and 75% diameter reduction cases are plotted.

pressure. We examined how coronary flow and pres-
sure change for resting and light exercise conditions for
normal coronary anatomy. We then created stenoses in
the left anterior descending coronary artery to inves-
tigate how the coronary flow and pressure change for
different degrees of stenoses at rest and moderate
exercise condition when the downstream coronary
vascular beds are maximally dilated.
For the simulations at rest and during light exercise,
the computed coronary flow and pressure waveforms
 Patient-Specific Coronary Flow Modeling
were realistic and the asynchrony of the left and right
coronary arteries were represented as we approximated
the intramyocardial pressure with the left and right
ventricular pressure depending on the location of the
coronary arteries. For the simulations with different
degrees of stenosis in the left anterior descending cor-
onary artery at rest and moderate exercise, the reduc-
tion in the coronary flow was more apparent for the
moderate exercise case because more energy loss
occurs as more coronary flow travels through the ste-
nosed region. We also demonstrated a greater pressure
loss across the stenosed region as the degree of stenosis
increases. Especially, the pressure loss did not increase
linearly resulting from the energy dissipated due to the
viscous loss and the turbulence in the stenosed region.
Figure 6 showed that the relationship between the
mean coronary flow and the degree of stenosis is
comparable to results obtained from experimental
techniques.7 Gould et al.7 created temporary stenosis
in the left circumflex artery of canines and injected
Hypaque to simulate hyperemic conditions in canine
coronary arteries. They observed that the mean flow
did not decrease up to 85% diameter reduction at
rest and 30–45% diameter reduction at hyperemia.
Although our study focused on different physiologic
conditions of moderate exercise rather than hyperemia,
our results with resting and moderate exercise condi-
tions yield similar behaviors because in both maximal
hyperemia and simulated moderate exercise condi-
tions, we assume that the downstream coronary vas-
cular beds are maximally dilated to receive more flow
from the aorta. We also observed that the flow
remained the same up to 75% diameter reduction case
at rest. In Gould et al.’s plot, the mean flow at rest
slightly increased for mild stenosis cases but in our
study, we aimed to have the same mean flow for mild
stenosis cases, thus, we maintained the same mean flow
at rest up to 75% diameter reduction case. The slope
during moderate exercise is comparable to the slope in
hyperemia although there is a difference in the mag-
nitude of the mean flow. In Gould et al.’s paper, the
mean flow at hyperemic state increased 409% com-
pared to the baseline value whereas in our study, we
designed that the mean flow increased 350% at mod-
erate exercise compared to the baseline value.
Our method has three primary limitations. First, we
did not consider the motion of the heart during the
cardiac cycle. We fixed the coronary arteries to the
epicardial surface of the heart and fixed the surface in
space and time. In reality, the heart moves significantly
to contract and relax during the cardiac cycle. This
movement is large and cannot be modeled using the
coupled momentum method,5 which is a linearized
approach using a fixed fluid mesh. A different
approach, such as an arbitrary Lagrangian–Eulerian
3207
formulation, would be needed to represent the move-
ment of the heart over the cardiac cycle. However,
previous studies showed that the effects due to the
movement of the heart were secondary and did not
affect the pressure and flow fields as much as the
geometry and the boundary conditions.18,19,21,30
Second, we assumed that the left coronary arteries
transport blood to the left ventricle and the right cor-
onary arteries transport blood to the right ventricle. In
reality, however, the coronary vascular networks
experience nonuniform intramyocardial pressure
depending on the location of the coronary networks.
To consider nonuniform intramyocardial pressure, a
three-dimensional nonuniform model of the heart as
well as the mapping of the coronary arteries to the
location of the myocardium that the arteries perfuse
should be considered. For example, a three-dimen-
sional model of cardiac ventricular mechanics can be
used to compute nonuniform intramyocardial pressure
acting on the coronary vascular beds.8,9
Third, we assumed a uniform Young’s modulus for
the whole computational model although we know
that the vessel wall properties vary spatially. To con-
sider nonuniform vessel wall properties, noninvasive
methods of estimating wall thickness and elastic (vis-
coelastic) wall properties should be developed. In this
study, rather than considering nonuniform wall prop-
erties, we adjusted the vessel wall properties so that the
wall deformation of the descending thoracic aorta fit
the experimental data reasonably well.
CONCLUSIONS
A coronary boundary condition that couples a
lumped parameter coronary vascular model to each
coronary outlet of a three-dimensional finite element
model of the aorta and epicardial coronary arteries is
developed. An inflow boundary condition coupling a
lumped parameter heart model and a closed loop
model is implemented to represent the intramyocar-
dial pressure by considering the interactions between
the heart and arterial system. We considered fluid–
structure interaction to better represent flow and
pressure waveforms. Using the lumped parameter
coronary vascular model along with the inflow
boundary condition that couples the lumped param-
eter heart model and the closed loop system, we can
predict coronary flow and pressure realistically using
anatomic data obtained from medical imaging tech-
niques and study how changes in cardiac and arterial
properties affect coronary flow and pressure and vice
versa. Further, we can utilize these methods to
investigate different vascular interventions of cardio-
vascular disease.
3208 KIM et al.

ACKNOWLEDGMENTS boundaries for three-dimensional finite element simulations

of blood flow. Comput. Methods Appl. Mech. Eng. 198(45–
Hyun Jin Kim was supported by a Stanford Grad- 46):3551–3566, 2009.
11
uate Fellowship. This material is based upon work Kim, H. J., I. E. Vignon-Clementel, C. A. Figueroa, J. F.
supported by the National Science Foundation under LaDisa, K. E. Jansen, J. A. Feinstein, and C. A. Taylor. On
coupling a lumped parameter heart model and a three-
Grant No. 0205741. The authors gratefully acknowl-
dimensional finite element aorta model. Ann. Biomed. Eng.
edge the assistance of Dr. Nathan M. Wilson for 37(11):2153–2169, 2009.
assistance with software development. The authors 12
Lagana, K., R. Balossino, F. Migliavacca, G. Pennati,
gratefully acknowledge Dr. Farzin Shakib for the use E. L. Bove, M. R. de Leval, and G. Dubini. Multiscale
of his linear algebra package AcuSolveTM (http://www. modeling of the cardiovascular system: application to the
study of pulmonary and coronary perfusions in the uni-
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ventricular circulation. J. Biomech. 38(5):1129–41, 2005.
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