Annals of Biomedical Engineering, Vol. 36, No. 11, November 2008 (
2008) pp.

1753–1763
DOI: 10.1007/s10439-008-9558-0

Hemodynamic Analysis of a Compliant Femoral Artery Bifurcation Model

using a Fluid Structure Interaction Framework
YOUNG-HO KIM,1 JONG-EUN KIM,1 YASUSHI ITO,1 ALAN M. SHIH,1 BRIGITTA BROTT,2
and ANDREAS ANAYIOTOS3,4
1
Department of Mechanical Engineering, University of Alabama at Birmingham, Birmingham, AL, USA; 2Division of
Cardiovascular Disease, University of Alabama at Birmingham, Birmingham, AL, USA; 3Department of Biomedical
Engineering, University of Alabama at Birmingham, 1075 13th Street South, Hoehn 368, Birmingham, AL 35294-4440, USA;
and 4Department of Mechanical and Materials Engineering, Cyprus University of Technology, Limassol 3036, Cyprus
(Received 25 May 2007; accepted 26 August 2008; published online 16 September 2008)

Abstract—The influence of wall motion on the hemodynamic INTRODUCTION

characteristics of the human femoral bifurcation and its
effects on the development of peripheral artery disease has
not been previously investigated. This study aimed in
investigating the hemodynamics of a compliant patient-
specific femoral artery bifurcation model by a fluid structure
interaction (FSI) scheme. The complex physiological geom-
etry of the femoral artery bifurcation was reproduced from
sequentially obtained transverse CT scan images. Velocity
waveforms derived from phase contrast MR images were
extracted and mapped to define boundary conditions. Equa-
tions governing blood flow and wall motion were solved
using an FSI framework that utilizes commercial codes:
FLUENT for computational fluid dynamics and ANSYS for
computational structural dynamics. The results showed that
wall compliance decreased flow velocities at the relatively
high curvature geometries including common and superficial
femoral artery (SFA), and it created strong recirculation in
the profunda femoris artery close to the bifurcation. In the
SFA region near the apex, time averaged wall shear stress
(TAWSS) differences up to 25% between compliant and rigid
models were observed. The compliant model also exhibited
lower TAWSS and oscillatory shear at the superior section of
the common femoral artery close to the bifurcation. The
presence of wall motion, however, created minor differences
in the general flow-field characteristics. We conclude that
wall motion does not have significant influence on the global
fluid dynamic characteristics of the femoral artery bifurca-
tion. Longer arterial segments need to be simulated to see the
effect of wall motion on tortuousity which was previously
cited as an important factor in the development of athero-
sclerosis at the femoral artery.
Keywords—Computational fluid dynamics, Fluid structure
interaction, Blood flow, Wall shear stress, CT image-based
model.
Address correspondence to Andreas Anayiotos, Department of
Biomedical Engineering, University of Alabama at Birmingham,
1075 13th Street South, Hoehn 368, Birmingham, AL 35294-4440,
USA. Electronic mail: aanayiot@eng.uab.edu
1753
Lower limb peripheral arterial disease (PAD) affects
approximately 8 million Americans.19 It is particularly
prevalent in elderly persons, affecting 12–20% those
over 65 years of age.38,43 Even in those who are
asymptomatic, it is associated with impaired function
and quality of life.34 Atherosclerosis is widely accepted
as the main causative factor in the development of
lower limb PAD. The atherosclerosis in PAD patients
is frequently observed on the site at the femoral artery
bifurcation at the division of the Common Femoral
Artery (CFA) into the Superficial Femoral Artery
(SFA) and the Profunda Femoris Artery (PFA).14,15
The PFA provides blood to the thigh muscle, while
the SFA provides blood to the lower limb and extends
to the popliteal artery. The lateral circumflex artery
(LCA), branches out from the PFA, the location of
which may vary in each patient. The development of
atherosclerotic plaque in the femoral artery restricts
blood supply to the lower extremities, leading to
ischemia and lower limb disability. The distensibility of
the arterial wall has usually been neglected in arterial
hemodynamic studies. Wall motion, however, may
influence the distribution of wall shear stress (WSS),
oscillatory shear index (OSI), wall shear stress tem-
poral gradient (WSSTG), curvature, and wall rough-
ness, which have previously been cited as having
an important role in the initiating mechanisms of
atherosclerosis.3,7,44–46,48,52
Experimental studies on arterial segments including
femoral artery bifurcations,7 femoral graft-artery
junctions,27 carotid artery bifurcations,6,30,36 and
arteriovenous anastomoses31 using idealized or sim-
plified arterial geometries have shown that hemody-
namic characteristics are influenced by anatomic
geometry, pulsatile flow, arterial curvature, arterial
0090-6964/08/1100-1753/0
2008 Biomedical Engineering Society
1754 KIM et al.

wall motion and arterial stenosis.1–3,6–8,16,22,26,27,31,32

Recent improvements in medical imaging techniques,
and three-dimensional geometric reconstruction of
arteries, allow computational fluid dynamic CFD
methods to investigate complex vascular flows through
patient-specific artery models.17,49,57
CFD studies, however, do not usually consider the
compliance of arterial wall due to the complexity of the
numerical modeling and the requirement for a fluid
structure interaction (FSI) environment to solve for the
coupled fluid/structure problem. The assumption of a
rigid wall in CFD analysis of arterial models may
underestimate the temporal and spatial magnitude
of slow moving zones.58 To assess the effect of wall
compliance on the near wall hemodynamic characteris-
tics of arteries such as WSS, OSI, and WSSTG, FSI
algorithms have been employed to take into account
the effect of arterial wall compliance in the fluid
dynamic analysis.10,13,29,33,56 Various arterial sites have
been analyzed by FSI such as the carotid arterial
bifurcation,54 an abdominal aortic aneurysm model,39 FIGURE 1. Structural (coarse) and fluid (fine) mesh of the
femoral artery bifurcation (A: Anterior, P: Posterior, L: Left, R:
and a stented aortic aneurysm model.28 Right views).
In this study, we aimed in assessing WSS, OSI, and
WSSTG in the femoral artery bifurcation by a newly
developed fluid structure interaction framework that
simultaneously computes both hemodynamic and used to create high-quality surface meshes. A tetra-
mechanical characteristics by taking into account the hedral mesh for CFD simulations was created by
interaction between blood flow and arterial wall subdividing non-simplicial elements in a hybrid mesh
motion. to estimate WSS precisely.20
The wall thickness of the CFA was set to 0.74 mm
by assuming a radius-to-thickness ratio of 4.122 using
the reconstructed geometry. This was adopted from a
MATERIAL AND METHODS previous reported study.48 The wall thickness could
not be obtained from the CT information due to the
Model Reconstruction and Mesh Generation
relatively large pixel size and low signal to noise ratio
A 6 cm-long biofidelic femoral bifurcation model (SNR) that did not allow clear distinction between
was reconstructed from CT data which provides a arterial wall and adjacent tissue structure. The same
better contrast of the arterial wall and lumen cross radius-to-thickness ratio was used to determine the
section than MR, but does not have the capability of thicknesses of the SFA, PFA and LCA. Figure 1
rendering the velocity measurements. A 992 CT scan illustrates structural and fluid meshes of the patient-
image set was obtained from a 55-year-old female specific femoral artery used in this study. A common
volunteer suffering from paraplegia. This dataset interface was defined at the inner wall of the femoral
ranges from the abdomen to the toes, using a GE artery. The finer mesh with 367,315 tetrahedra covers
LightSpeed Proscanner with 1.25 mm slice thickness the inside of the femoral artery and is used for flow
and 0.25 mm overlap. An informed written consent field analyses. There are 18,695 triangles on the com-
from the patient was received, and the protocol was mon interface. The coarse tetrahedral mesh repre-
approved by the local institutional review board. The senting the wall of the femoral artery is used for
60 slices of the images were used to reconstruct the structural analyses. It has 43,774 tetrahedra and 4761
femoral model. The image resolution was 512 9 512 triangles on the common interface.
pixels per slice, and each pixel represented a 0.79 9
0.79 mm2 area. Image segmentation and geometry
Fluid Structure Interaction Framework
extraction from the images were performed to obtain
the inner surface of the femoral artery. Two surface An in-house loosely coupled fluid structure inter-
triangulation methods, a direct advancing front action (FSI) framework was developed and employed
method and a modified decimation method,21 were for this study. This framework enables to select
 Hemodynamic Analysis of Femoral Artery Bifurcation
any well-proven CFD and computational structural
dynamic (CSD) codes. An accurate and efficient data
transfer between fluid and structure using interpolation
techniques is essential in space due to naturally
unmatched meshes between fluid and structure. The
framework consists of: a conservative point-wise
interpolation12 module for blood pressure transfer to
wall, a curvature-gradient index local fitting method24
for wall motion transfer to fluid domain, a semi-
torsional spring analogy55 for fluid volume mesh
movement, and a serial staggered method11 with sub-
cycling for synchronizing time levels between CFD and
CSD solvers. The entire FSI process is automatically
executed using Bash/Perl script files for data extrac-
tion, manipulation, file handling, and code execution.
The details of the FSI framework are described in the
literature.23 Two commercial codes, FLUENT for
CFD and ANSYS for CSD, were used in this study. In
order to take into account arterial dynamic wall mo-
tion, a time integration option in ANSYS was switched
on to include the inertial effect of the wall in the FSI
simulation.
MRI Velocity Mapping and Boundary Conditions
Phase contrast MRI data were acquired to measure
blood flow velocity at four different sections shown in
Fig. 2 (39.2 mm, 19.2 mm above branch and 11 mm,
21 mm below branch) by a GE MR scanner (1.5 T,
Signa). The scan parameters were 4 mm slice thickness,
40 ms TR, 6 ms TE, 32 cardiac phases, 20 FA,
113 9 150 cm FOV, and a 512 9 512 matrix. The
FIGURE 2. The four sections where the velocity profiles
were measured by MRI-PCA.
1755
encoding velocity was 150 cm/s corresponding to 180
phase shift. Only axial velocity was measured under the
assumption that in-plane velocity components are rel-
atively trivial. The image has 0.59 mm in-plane reso-
lution. To obtain velocity map from MRI during the
cardiac cycles, a region of interest was determined
manually around the vessel lumen detected age. The
phase angle value in each pixel was converted to
velocity by18:
V ¼ VENC
Uv =180 ; Uv ¼ ½180 ; 180  ð1Þ
where, VENC is encoding velocity, and Fv is the phase
angle obtained by phase image. The calculated velocity
then was mapped by an interpolation method based on
a radial basis function. The thin plate spline method9
was used for the interpolation. Time-dependent
velocity profiles were mapped through 32 cardiac
phases. Around 40 pixels for the SFA and PFA, and
20 pixels for the LCA were used to quantify the
velocity.
The mapped and interpolated flow rates used in
calculating velocity at the SFA, PFA and LCA outlets
were consistent with MRI data through the entire
cardiac cycle as shown in Fig. 3. These time-varying
mapped flow rate were used for three outlet boundary
conditions in FLUENT via user defined function
(UDF).
CFD analysis in rigid wall vessel simulations
may use only flow rate boundary conditions. However
in compliant wall vessel FSI simulations, a time-
dependent pressure profile, is necessary to apply forces
on the wall. The time dependent pressure profile at
Section 2 in Fig. 2 was used as the inlet boundary
condition. To calculate the pressure profile at Section 2,
FIGURE 3. Flow rate comparison between MRI-PCA calcu-
lated measurements and CFD simulated measurements at the
SFA, PFA and LCA outlets.
1756
FIGURE 4. Calculated pressure at Section 2 using the
Navier–Stokes equations for one dimensional flow in an
elastic tube with flow rates based on MRI-PCA.
two physiological flow rates at Sections 1 and 2 were
calculated based on the velocity profiles. The Navier–
Stokes equations for one dimensional flow in an elastic
tube can be reduced to5
Qi ðtÞ  Qo ðtÞ 3pr3 dPo ðtÞ
¼ ð2Þ
Dz 2hE dt
Po ðtÞ  Pi ðtÞ q dQi ðtÞ 8l
¼ 2 þ 4 Qi ðtÞ ð3Þ
Dz pr dt pr
where Qi and Qo are the flow rates at the Sections 1 and
2, respectively, Dz is the distance between Sections 1
and 2, Pi and Po are the pressure at the Sections 1 and
2, respectively, r is the inside radius of tube, h is the
wall thickness, q is the density of blood, l is dynamic
viscosity of blood and E is the elastic modulus set to
1.61e06 Pa.37 The pressure waveform estimated by
integrating Eq. (2) is illustrated in Fig. 4. This pressure
waveform was used as an inlet boundary condition at
the Section 2 by UDF in FLUENT. The mapped MRI
velocities at Section 4 (of the PFA, SFA, and LCA),
were used as the outlet boundary conditions.
Vessel Material Properties
The blood vessel was assumed as a homogenous,
hyperelastic, nonlinear, and nearly incompressible
material. Poisson’s ratio was set to 0.4999 to depict
incompressible material. The density of the vessel was
set to 1100 kg/m3. The in vivo material properties of
the CFA were identified through inverse finite element
(FE) analysis. An ideal cylinder FE model that surro-
gates the vessel from Section 1 to 2 in Fig. 2 was
generated. Mooney–Rivlin hyperelastic model35 was
used for the constitutive model of compliant arteries.
KIM et al.
TABLE 1. Modified coefficients of five-coefficient Mooney-
Rivlin model for patient-specific arterial properties.
Parameters C10 C01 C20 C11 C02
Values (kPa) 4.10 2.75 590.42 857.18 0
The strain energy potential W is expressed by five
parameters Cij ‘s in incompressible Mooney–Rivlin
model:
X
2
W¼ Cij ðI1  3Þi ðI2  3Þj i; j ¼ 0; 1; 2 ð4Þ
iþj¼1
where I1 and I2 are strain invariants. In this study, the
five parameters in Eq. (4) were based on the results of
in vitro tensile test from literature.41 The value of C10,
however, was modified to consider in vitro property of
the PAD patients, in which the blood vessel is pre-
pressurized at the diastolic phase. For this, the pres-
sure difference between systolic and diastolic phase
from Eq. (2) was applied to the ideal cylinder. The
value of C10 was determined until the diameter change
reached to the 6.2% diameter change of the CFA for
the PAD patient at a systolic phase.50 The five
parameters used in Mooney–Rivlin model are shown
in Table 1.
Time Averaged WSS, OSI, and WSSTG
Time averaged wall shear stress (TAWSS) was
measured by calculating temporal mean of WSS during
an entire cardiac cycle. OSI was obtained using the
form26:
RT

j~
s jdt
R 0T ð5Þ
0 j~ sx jdt
where T is the time for a cardiac cycle, ~ sx is the
instantaneous WSS vector and ~ s
is the WSS compo-
nent acting in the direction opposite to the temporal
mean WSS vector. The WSSTG is defined as a maxi-
mum among the gradients of WSS in two consecutive
time steps during the cycle.54
RESULTS
Wall Displacement
Time-varying lumen diameters of the CFA and SFA
are measured at Sections 2 and 3 as shown in Fig. 2,
respectively. The maximum anterior-to-posterior
lumen diameters of CFA and SFA at peak systole are
6.35 and 4.67 mm, respectively. This corresponds to
5.7% and 3.7% expansion of the lumen diameter at
 Hemodynamic Analysis of Femoral Artery Bifurcation
FIGURE 5. Time-dependent lumen diameter changes: (a)
CFA at Sections 2; (b) SFA at Sections 3.
peak systole as shown in Fig. 5. The increase of ante-
rior-to-posterior lumen diameters of CFA and SFA is
larger than that of right-to-left ones.
Flow Pattern Comparison
The validity of the CFD and FSI models in com-
parison to the raw MRI data in the model, are dem-
onstrated in the time histories of Figs. 6a and 6b,
where good agreement is seen. The hemodynamic
characteristics of the compliant model through the FSI
analysis are compared to those of the rigid wall model
using CFD analysis. Figures 7a and 7b show the
instantaneous streamlines during the deceleration
phase of the cycle at phases 0.23/0.78 s and 0.54/0.78 s,
respectively. More recirculation in the PFA section
close to the bifurcation in the compliant model is
1757
FIGURE 6. Time-dependent velocity at Section 3: (a) Near
right wall; (b) Near posterior wall.
observed. The recirculation is more accentuated later
in diastole for phase 0.54/0.78 s. The velocity contours
in Fig. 8 show that wall compliance decreases flow
velocities at the posterior CFA at Section 2 and the
anterior SFA at Section 3 where the radius of curva-
ture is relatively high.
Wall Shear Stress
Comparison of the instantaneous peak systolic WSS
distributions between the compliant and rigid cases is
shown in Fig. 9. A maximum difference between the
two models is shown at the left anterior view close to
the branch of PFA. The plots demonstrating the dif-
ference in TAWSS, WSSTG, and OSI between the two
cases are illustrated in Figs. 10–12, respectively. As
seen in Fig. 9, high WSS is shown at the branch of
PFA and bifurcation. Low WSS regions appear
around the outer wall of the posterior view upstream
of the bifurcation and on anterior to left aspect close to
1758
FIGURE 7. Comparison of streamlines between rigid and compliant arteries: (a) at time 0.2926/0.78 s; (b) at time 0.5368/0.78 s.
the branch of PFA where the geometry has a mild
curvature along the distal direction. In these regions,
the TAWSS for the compliant model appears to be
only 10% lower than the rigid model, and there are
some patchy regions that illustrate OSI differences up
to 25%. In contrast, the WSSTG difference contour
plots in Figs. 11a and 11b show the highest (25%)
difference on the posterior right side of the SFA near
the bifurcation along the distal direction.
DISCUSSION
Correct modeling of fluid dynamics and the char-
acterization of the near wall phenomena is important
in understanding the initializing mechanisms and the
development of atherosclerotic plaque as well as pre-
dicting changes that may occur with treatments such as
stent placement or surgical repair. Our results indicate
KIM et al.
that there are significant differences up to 25% in wall
shear stress temporal gradient (WSSTG) between a
rigid and a compliant model of the femoral artery. The
10–25% difference regions (Fig. 11) cover a wide
extent in the superficial femoral artery near the bifur-
cation. There is also a significant region of differences
from 5 to 20% at a region of the common femoral
artery near the bifurcation (Fig. 11). Our results also
show that there are some regions of differences in
oscillatory shear index (OSI) that reach up to 25% at
the common femoral artery close to the bifurcation.
There has not been a previous study on the com-
pliance of the femoral bifurcation, however, Younis
and colleagues54 used an FSI technique to study an
image based model of the carotid bifurcation. They
reported minor differences in TAWSS differences
between the rigid and compliant models. They found,
however, significant differences in the WSSTG and
OSI between the two models except at the apex. In our
 Hemodynamic Analysis of Femoral Artery Bifurcation 1759

FIGURE 8. Comparison of velocity between rigid and compliant arteries at peak pressure loads: (a) Rigid CFA at Section 2;
(b) Compliant CFA at Section 2; (c) Rigid SFA at Section 3; Compliant SFA at Section 3.

study, the wall compliance created minor TAWSS
differences at most locations, but up to 25% differ-
ences in WSSTG and OSI at some locations. We had
observed 20% reduction in instantaneous WSS for the
compliant model around the branch at peak systole
which is somewhat lower than in what is reported in
previous studies.2,40 However, this can be explained by
the lower distensibility of the muscular femoral arter-
ies which was modeled as opposed to greater disten-
sibility of large elastic arteries such as aortic and
carotid.25,42,53
It has been widely accepted that WSS and related
parameters such as WSSTG and OSI are important
factors in the development of atherosclerosis on the
femoral artery,22,46,47,51 and the carotid artery.1,2,16,26
Ku and colleagues26 reported low OSI in addition
to low WSS enhanced the development of plaques.
Bao and colleagues4 showed that WSSTG leads to
enhanced endothelial proliferation.
Our data show that compliance increases the regions
of high OSI and WSSTG making thus specific regions
of the femoral artery bifurcation more prone to the
development of disease. However, in addition to OSI
and WSSTG, curvature, wall roughness and wall
motion have also been indicated to have a role in the
initializing mechanisms of atherosclerosis at the fem-
oral artery bifurcation.7,44–46,52 The current study
could not assess the effects of wall motion in changes
in roughness, or curvature.
Earlier experimental studies have also revealed that
the inherent tortuousity of the femoral artery increases
the rate of atherosclerosis and that the inner curvature
walls are more prone to atherosclerotic plaques than
the outer curvature walls.45,46 These studies also sug-
gested that the curvature of the SFA is more of a risk
factor for atherosclerosis than the presence and loca-
tion of branches. Wood and colleagues52 showed a
strong correlation between tortuousity and flow dis-
turbance in computational reconstructed SFA’s. They
suggested that the regions of low time averaged WSS
might be high-risk regions of atherogenesis and pro-
gression of atheroma. A limitation of this present study
is that the arterial segment simulated had significant
curvature but no tortuousity. Longer sections of
this artery may be able to incorporate the effect of
tortuousity and need to be simulated in the future to
1760 KIM et al.

FIGURE 9. Instantaneous WSS contours of rigid and compliant artery and difference contour between them at peak systole and at
different angles: (a) WSS of rigid artery at right; (b) WSS of rigid artery at left; (c) WSS of compliant artery at right; (d) WSS of
compliant artery at left; (e) WSS difference at right; (f) WSS difference at left.

evaluate the effect of wall compliance on tortuousity
WSSTG and OSI.
CONCLUSIONS
Using an in house FSI system, the flow character-
istics and WSS field of a compliant femoral artery
bifurcation model was studied in comparison to a rigid
model. Minor differences were found in TAWSS and
differences of 25% in WSSTG were observed at the
bifurcation on the side of the SFA. The general
velocity field was essentially insensitive to wall motion.
We conclude that wall compliance at the femoral
artery bifurcation does not significantly change
parameters previously reported as important in the
development of arterial disease but longer arterial
segments need to be simulated to see the effect of wall
motion on tortuousity.
 Hemodynamic Analysis of Femoral Artery Bifurcation 1761

FIGURE 10. TAWSS difference contour between them at different angles: (a) TAWSS difference at right; (b) TAWSS difference at
left.

FIGURE 11. WSSTG difference contour between them at different angles: (a) WSSTG difference at right; (b) WSSTG difference at
left.

FIGURE 12. OSI difference contour between them at different angles: (a) OSI difference at right; (b) OSI difference at left.
1762 KIM et al.
ACKNOWLEDGMENT
The authors would like to thank Mr. Corey Shum in
the Enabling Technology Laboratory, University of
Alabama at Birmingham for extracting geometry data
from the CT scan.
REFERENCES
1
Anayiotos, A., S. Jones, D. P. Giddens, S. Glagov, and C.
K. Zarins. Shear stress at a compliant model of the human
carotid bifurcation. J. Biomech. Eng. 116(1):98–106, 1994.
doi:10.1115/1.2895710.
2
Anayiotos, A., P. D. Pedroso, E. C. Elefhteriou,
R. Venugopalan, and W. Holman. Effect of a flow-
streamlining implant at the distal anastomosis of a coro-
nary artery bypass graft. Ann. Biomed. 30(7):917–926,
2002. doi:10.1114/1.1500407.
3
Back, L. H., M. R. Back, E. Y. Kwack, and D. W.
Crawford. Flow measurements in a human femoral artery
model with reverse lumen curvature. J. Biomech. Eng.
110(4):300–309, 1988.
4
Bao, X., C. Lu, and J. A. Frangos. Temporal gradient in
shear but not steady shear stress induces PDGF-A and
MCP-1 expression in endothelial cells: role of NO, NF
kappa B, and egr-1. Arterioscler. Thromb. Vasc. Biol.
19(4):996–1003, 1999.
5
Flow in large blood vessels, Fluid Dynamics in Biology,
Contemporary Math. Series, edited by A. Y. Cheer and C. P.
Van Dam, Amer. Math. Soc. Providence, 1992, pp. 479–518.
6
Botnar, R., G. Rappitsch, M. B. Scheidegger, D. Liepsch,
K. Perktold, and P. Boesiger. Hemodynamics in the car-
otid artery bifurcation: a comparison between numerical
simulations and in vitro MRI measurements. J. Biomech.
33(2):137–144, 2000. doi:10.1016/S0021-9290(99)00164-5.
7
Cho, Y. I., L. H. Back, and D. W. Crawford. Pressure
difference-flow rate variation in a femoral artery branch
casting of man for steady flow. J. Biomech. Eng.
105(3):258–262, 1983.
8
Cho, Y. I., L. H. Back, and D. W. Crawford. Experimental
investigation of branch flow ratio, angle, and Reynolds
number effects on the pressure and flow fields in arterial
branch models. J. Biomech. Eng. 107(3):257–267, 1985.
9
Duchon, J. Splines minimizing rotation-invariant semi-
norms in Sobolev spaces. Constructive Theory of Func-
tions of Several Variables. Lect. Notes Math. 571:85–100,
1977.
10
Duncan, D. D., C. B. Bargercon, S. E. Borchart, O. J.
Deters, S. A. Gearhart, F. F. Mark, and M. H. Friedman.
The effect of compliance on wall shear in casts of a human
aortic bifurcation. J. Biomech. Eng. 112(2):183–188, 1990.
doi:10.1115/1.2891170.
11
Farhat, C., and M. Lesoinne. Two efficient staggered
algorithms for the serial and parallel solution of three-
dimensional nonlinear transient aeroelastic problems.
Comput. Meth. 182:499–515, 2000.
12
Farhat, C., M. Lesoinne, and P. LeTallec. Load and mo-
tion transfer algorithms for fluid/structure interaction
problems with non-matching discrete interfaces: momen-
tum and energy conservation, optimal discretization and
application to aeroelasticity. Comput. Meth. 157:95–114,
1998.
13
Friedman, M. H., G. M. Hutchins, C. B. Bargeron, O. J.
Deters, and F. F. Mark. Correlation between intimal
thickness and fluid shear in human arteries. Atherosclerosis
39(3):425–436, 1981. doi:10.1016/0021-9150(81)90027-7.
14
Futterman, L. G., and L. Lemberg. Peripheral arterial
disease is only the tip of the atherosclerotic ‘‘Iceberg’’. Am.
J. Crit. Care. 11(4):390–394, 2002.
15
Garasic, J. M., and M. A. Creager. Percutaneous inter-
ventions for lower-extremity peripheral atherosclerotic
disease. Rev. Cardiovasc. Med. 2(3):120–125, 2001.
16
Gijsen, F. J. H., D. E. M. Palmen, M. H. E. van der Beek, F.
N. van de Vosse, M. E. H. van Dongen, and J. D. Janssen.
Analysis of the axial flow field in stenosed carotid artery
bifurcation models-LDA experiments. J. Biomech.
29(11):1483–1489, 1996. doi:10.1016/0021-9290(96)84544-1.
17
Giordana, S., S. J. Sherwin, J. Peiro, D. J. Doorly, J. S.
Crane, K. E. Lee, N. J. W. Cheshire, and C. G. Caro. Local
and global geometric influence on steady flow in distal
anastomoses of peripheral bypass grafts. J. Biomech. Eng.
127(7):1087–098, 2005. doi:10.1115/1.2073507.
18
Higgins, C. B., and A. Roos. MRI and CT of the
Cardiovascular System, 2nd edn. Lippincott Williams &
Wilkins, 2005.
19
Hirsch, A. T., M. H. Criqui, D. T. Jacobson, J. G.
Regensteiner, M. A. Creager, J. W. Olin, S. H. Krook, D.
B. Hunninghake, A. J. Comerota, M. E. Walsh, M. M.
McDermott, and W. R. Hiatt. Peripheral arterial disease
detection, awareness, and treatment in primary care.
JAMA 286(11):1317–1324, 2001. doi:10.1001/jama.286.11.
1317.
20
Ito, Y., A. M. Shih, B. K. Soni, and K. Nakahashi.
Multiple marching direction approach to generate high
quality hybrid meshes. AIAA J. 45(1):162–167, 2007.
doi:10.2514/1.23260.
21
Ito, Y., P. C. Shum, A. M. Shih, B. K. Soni, and K. Na-
kahashi. Robust generation of high-quality unstructured
meshes on realistic biomedical geometry. Int. J. Numer.
Meth. Eng. 65(6):943–973, 2006. doi:10.1002/nme.1482.
22
Jones, C. J. H., M. J. Lever, Y. Ogasawara, K. H. Parker,
K. Tsujioka, O. Hiramatsu, K. Mito, C. G. Caro, and F.
Kajiya. Blood velocity distributions within intact canine
arterial bifurcations. Am. J. P. 262:H1592–H1599, 1992.
23
Kim, Y. H. Development of efficient algorithms for fluid-
structure interaction framework and its applications. Ph.D.
Dissertation, University of Alabama at Birmingham, 2006.
24
Kim, Y. H., and J. E. Kim. New hybrid interpolation
method for motion transfer in fluid structure interactions.
J. Aircraft 43(2):567–569, 2006. doi:10.2514/1.15097.
25
Kornet, L., A. P. Hoeks, J. Lambregts, and R. S. Reneman.
Mean wall shear stress in the femoral arterial bifurcation is
low and independent of age at rest. J. Vasc. Res. 37(2):
112–122, 2000. doi:10.1159/000025722.
26
Ku, D. N., D. P. Giddens, C. K. Zarins, and S. Glagov.
Pulsatile flow and atherosclerosis in the human carotid
bifurcation. Arteriosclerosis 5(3):293–302, 1985.
27
Lei, M., C. Kleinstreuer, and J. P. Archie. Geometric
design improvements for femoral graft-artery junctions
mitigating restenosis. J. Biomech. 29(12):1605–1614, 1996.
28
Li, Z., and C. Kleinstreuer. Fluid-structure interaction
effects on sac-blood pressure and wall stress in a stented
aneurysm. J. Biomech. Eng. 127(4):662–671, 2005.
doi:10.1115/1.1934040.
29
Liepsch, D., and S. Moravec. Pulsatile flow of non-
newtonian fluid in distensible models of human arteries.
Biorheology 21(4):571–586, 1984.
 Hemodynamic Analysis of Femoral Artery Bifurcation
30
LoGerfo, F. W., M. D. Nowak, W. C. Quist, H. M.
Crawshaw, and B. K. Bharadvaj. Flow studies in a model
carotid bifurcation. Arteriosclerosis 1(4):235–241, 1981.
31
Loth, F., N. Arslan, P. F. Fischer, C. D. Bertram, S. E. Lee,
T. J. Royston, R. H. Song, W. E. Shaalan, and H. S.
Bassiouny. Transitional flow at the venous anastomosis of an
arteriovenous graft: Potential relationship with activation of
the ERK1/2 mechanotransduction pathway. J. Biomech.
Eng. 125(1):49–61, 2003. doi:10.1115/1.1537737.
32
Mark, F. F., C. B. Bergeron, O. J. Deters, and M. H.
Friedman. Variations in geometry and shear rate distribu-
tions in casts of human aortic bifurcations. J. Biomech.
22(6–7):577–582, 1989. doi:10.1016/0021-9290(89)90009-2.
33
Maurits, N. M., G. E. Loots, and A. E. P. Veldman. The
influence of vessel wall elasticity and peripheral resistance
on the carotid artery flow wave form: a CFD model com-
pared to in vivo ultrasound measurements. J. Biomech.
40(2):427–436, 2007. doi:10.1016/j.jbiomech.2005.12.008.
34
McDermott, M. M., K. Liu, P. Greenland, J. M. Guralnik,
M. H. Criqui, C. Chan, W. H. Pearce, J. R. Schneider, L.
Ferrucci, L. Celic, L. M. Taylor, E. Vonesh, G. J. Martin,
and E. Clark. Functional decline in peripheral arterial
disease: associations with the ankle brachial index and leg
symptoms. JAMA 292(4):453–461, 2004. doi:10.1001/jama.
292.4.453.
35
Mooney, M. A theory of large elastic deformation. J. Appl.
Physiol. 11:582–592, 1940. doi:10.1063/1.1712836.
36
Motomiya, M., and T. Karino. Flow patterns in the human
carotid artery bifurcation. Stroke 15(1):50–56, 1984.
37
Mozersky, D. J., D. S. Sumner, D. E. Hokanson, and D. E.
Strandness, Jr. Transeutaneous measurement of the elastic
properties of the human femoral artery. Circulation
46(5):948–955, 1972.
38
Ostchega, Y., R. Paulose-Ram, C. F. Dillon, Q. Gu, and
J. P. Hughes. Prevalence of peripheral arterial disease and
risk factors in persons aged 60 and older: data from the
national health and nutrition examination survey 1999–
2004. J. Am. Geriatr. Soc. 55(4):583–589, 2007. doi:10.1111/
j.1532-5415.2007.01123.x.
39
Papaharilaou, Y., J. A. Ekaterinaris, E. Manousaki, and
A. N. Katsamouris. A decoupled fluid structure approach
for estimating wall stress in abdominal aortic aneurysms.
J. Biomech. 40(2):367–377, 2007. doi:10.1016/j.jbiomech.
2005.12.013.
40
Perktold, K., and G. Rappitsch. Computer-simulation of
local blood-flow and vessel mechanics in a compliant car-
otid-artery bifurcation model. J. Biomech. 28(7):845–856,
1995. doi:10.1016/0021-9290(95)95273-8.
41
Prendergast, P. J., C. Lally, S. Daly, A. J. Reid, T. C. Lee,
D. Quinn, and F. Dolan. Analysis of prolapse in cardio-
vascular stents: a constitutive equation for vascular tissue
and finite element modeling. J. Biomech. Eng. 125(5):692–
699, 2003. doi:10.1115/1.1613674.
42
Rhee, K., and S. M. Lee. Effects of radial wall motion and
flow waveform on the wall shear rate distribution in the
divergent Vascular Graft. Ann. Biomed. 26(6):955–964,
1998. doi:10.1114/1.31.
43
Sanctis, J. T. D. Percutaneous interventions for lower
extremity peripheral vascular disease. Am. Fam. Physician
64(12):1965–1972, 2001.
44
Smedby, O. Do plaques grow upstream or downstream: an
angiographic study in the femoral artery. Arterioscler.
Thromb. Vasc. Biol. 17(5):912–918, 1997.
45
Smedby, O., and L. Bergstrand. Tortuosity and athero-
sclerosis in the femoral artery: what is cause and what is
1763
effect? Ann. Biomed. 24(4):474–480, 1996. doi:10.1007/
BF02648109.
46
Smedby, O., J. Johansson, J. Molgaard, A. G. Olsson, G.
Walldius, and U. Erikson. Predilection of atherosclerosis
for the inner curvature in the femoral artery. A digitized
angiography study. Arterioscler. Thromb. Vasc. Biol.
15(7):912–917, 1995.
47
Smedby, O., S. Nilsson, and L. Bergstrand. Development
of femoral atherosclerosis in relation to flow disturbance.
J. Biomech. 29(4):543–547, 1996. doi:10.1016/0021-9290
(95)00070-4.
48
Smilde, T. J., F.W. van den Berkmortel, G. H. Boers, H.
Wollersheim, T. de Boo, H. van Langen, and A. F.
Stalenhoef. Carotid and femoral artery wall thickness and
stiffness in patients at risk for cardiovascular disease, with
special emphasis on hyperhomocysteinemia. Arterioscler.
Thromb. Vasc. Biol. 18(12):1958–1963, 1998.
49
Steinman, D. A. Image-based computational fluid dynam-
ics modeling in realistic arterial geometries. Ann. Biomed.
30(4):483–497, 2002. doi:10.1114/1.1467679.
50
Tai, N. R., A. Giudiceandrea, H. J. Salacinski, A. M.
Seifalian, and G. Hamilton. In vivo femoropopliteal arte-
rial wall compliance in subjects with and without lower
limb vascular disease. J. Vasc. Surg. 30(5):936–945, 1999.
doi:10.1016/S0741-5214(99)70020-0.
51
Wensing, P. J., L. Meiss, W. P. Mali, and B. Hillen. Early
atherosclerotic lesions spiraling through the femoral artery.
Arterioscler. Thromb. Vasc. Biol. 18(10):1554–1558, 1998.
52
Wood, N. B., S. Z. Zhao, A. Zambanini, M. Jackson, W.
Gedroyc, S. A. Thom, A. D. Hughes, and X. Y. Xu.
Curvature and tortuosity of the superficial femoral artery: a
possible risk factor for peripheral arterial disease. J. Appl.
Physiol. 101(5):1412–1418, 2006. doi:10.1152/japplphy-
siol.00051.2006.
53
Wu, S. P., S. Ringgaard, S. Oyre, M. S. Hansen, S. Rasmus,
and E. M. Pedersen. Wall shear rates differ between the
normal carotid, femoral, and brachial arteries: an in vivo
MRI study. J. Magn. Reson. Imaging 19(2):188–193, 2004.
doi:10.1002/jmri.10441.
54
Younis, H. F., M. R. Kaazempur-Mofrad, R. C. Chan, A. G.
Isasi, D. P. Hinton, A. H. Chau, L. A. Kim, and R. D. Kamm.
Hemodynamics and wall mechanics in human carotid bifur-
cation and its consequences for atherogenesis: investigation of
inter-individual variation. Biomech. Model. Mechanobiol.
3:17–32, 2004. doi:10.1007/s10237-004-0046-7.
55
Zeng, D., and R. Ethier. A semi-torsional spring analogy
model for updating unstructured meshes in 3D moving
domains. Finite. Elem. Anal. Des. 41(11–12):1118–1139,
2005.
56
Zhang, W., C. Herrera, S. N. Atluri, and G. S. Kassab. Effect
of surrounding tissue on vessel fluid and solid mechanics.
J. Biomech. Eng. 126(6):760–769, 2004. doi:10.1115/
1.1824128.
57
Zhao, S. Z., P. Papathanasopoulou, Q. Long, I. Marshall,
and X. Y. Xu. Comparative study of magnetic resonance
imaging and image-based computational fluid dynamics for
quantification of pulsatile flow in a carotid bifurcation
phantom. Ann. Biomed. 31(2):962–971, 2003. doi:10.1114/
1.1590664.
58
Zhao, S. Z., X. Y. Xu, A. D. Hughes, S. A. Thom, A. V.
Stanton, B. Ariff, and Q. Long. Blood flow and vessel
mechanics in a physiologically realistic model of a human
carotid arterial bifurcation. J. Biomech. 33(8):975–984,
2000. doi:10.1016/S0021-9290(00)00043-9.