International Communications in Heat and Mass Transfer 39 (2012) 745751

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International Communications in Heat and Mass Transfer

journal homepage: www.elsevier.com/locate/ichmt

Unsteady blood ow and mass transfer of a human left coronary artery bifurcation:
FSI vs. CFD
M. Malv a, b,, A. Garca a, J. Ohayon c, d, M.A. Martnez a, b
a
Aragn Institute of Engineering Research (I3A), Universidad de Zaragoza, C/Mara de Luna s/n, E-50018 Zaragoza, Spain
b
Centro de Investigacin Biomdica en Red en Bioingeniera Biomateriales y Nanomedicina (CIBER-BBN) C/Poeta Mariano Esquillor s/n, E-50018 Zaragoza, Spain
c
Laboratory TIMC/DyCTiM, UJF, CNRS UMR 5525, In3S, Grenoble, France
d
Engineering School Polytech Annecy-Chambry, University of Savoie, France

a r t i c l e i n f o a b s t r a c t

Available online 25 April 2012 In this study, a Fluid Solid Interaction analysis (FSI) of a computerized tomography (CT) scan reconstructed
left coronary artery was performed. The arterial wall was modeled as an isotropic hyperelastic material.
Keywords: The arterial wall shear stress (WSS) was computed in order to investigate a correlation between ow-
Coronary artery induced wall shear stress and geometry of the artery. An unsteady state FSI analysis with a commercial nite
FEM
element software was performed in order to evaluate the maximum and the minimum wall shear stress as a
Fluidsolid interaction
function of the ow regime and the arterial wall compliance in the left coronary. As boundary conditions,
CFD
Wall shear stress
physiological pressure waveforms were applied. Comparison of the computational results between the FSI
and rigid-wall models showed that the wall shear stress (WSS) distributions were substantially affected by
the arterial wall compliance. In particular, the minimum and maximum WSS values signicantly vary.
2012 Elsevier Ltd. All rights reserved.

1. Introduction
Cardiovascular diseases represent the most frequent cause of
death in modern civilization. In particular, these represent 49% of
death diseases in Europe and 38% in the United States [1]. The
common index for those pathologies, known as CVD (cardiovascular
disease) includes different kinds of cardiovascular diseases and it is
considered one of the most important references of world human
health [1]. CVD are divided into different classes: infarction (ischemic
or hemorrhagic), thrombosis, and aneurism [2]. A very important
class is the coronary disease, which is included in the category of
cardiovascular diseases with the index CAD (coronary artery disease).
In this class, the most important role is played by atherosclerotic
diseases caused by formation, developing, and rupture of atheroma-
tous plaques [2,3]. Studies on coronary arteries are normally focused
on hemodynamic aspects, neglecting the interaction between blood
ow and arterial walls, evaluating the WSS at the rigid walls and
connecting it with atheromatous pathologies [4,5]. Many works put
their attention only in particular regions of the coronary tree [6,7]
neglecting not only the vessel compliance but also the bifurcations,
considering only the main branch. Some other studies are focused
on coronary stenting technique [811]. Only recently, Torii et al.
[12] made a comparison between the WSS computed with rigid and
Communicated by W.J. Minkowycz.
Corresponding author at: Aragn Institute of Engineering Research (I3A),
Universidad de Zaragoza, C/Mara de Luna s/n, E-50018 Zaragoza, Spain
E-mail address: mmalve@unizar.es (M. Malv).
compliant wall for a stenotic RCA using physiological velocity and
pressure waveforms while Huo et al. [13,14] studied the effect of
the compliance on the WSS computation for a porcine RCA comparing
rigid wall and FSI simulations. Gijsen et al. [15] analyzed a left arterial
bifurcation showing the hemodynamics of a left main arterial bifurca-
tion of just one patient. Soulis et al. [16] studied a left arterial bifurca-
tion (LCA) of the main, the ascending, and the circumex arterial
branches but used a mean geometry. Finally, Goubergrits et al. [17]
performed a CFD simulation of a rigid wall based left arterial bifurca-
tion comparing the results with an in-silico experimental model. An
important feature of the coronary arteries, which is addressed in
limited CFD studies, is their predisposition to undergo large displace-
ments during the cardiac cycle [18]. Coronary arterial motion can be
described by overall vessel translation, stretching, bending and twist-
ing and to a lesser degree by radial expansion and axial torsion [19].
Although still debated in literature, arterial motion may alter the
uid mechanics in the coronaries as investigated in the following
works. Weydahl et al. [20] used a straight tube moving in the axial
direction where the axial movement function was obtained from
three-dimensional reconstruction of a biplane coronary angiogram.
Delno et al. [21] studied the inuence of local lateral vessel move-
ment on ow patterns in a straight compliant tube nding insigni-
cant transverse movement effect in the case of coronary arteries.
Furthermore, Waters and Pedley [22] studied the effects of uniform
time-dependent curvature on the ow eld and in a tube, driven by
an oscillatory pressure gradient with the same frequency as the
curvature variation. They found that WSS strongly depends on the
frequency of the curvature variation. Ramaswamy et al. [19]

0735-1933/$ see front matter 2012 Elsevier Ltd. All rights reserved.
doi:10.1016/j.icheatmasstransfer.2012.04.009
746 M. Malv et al. / International Communications in Heat and Mass Transfer 39 (2012) 745751
reconstructed a segment of the left anterior descending (LAD) coro-
nary artery without any bifurcating branches using a coupled angio-
graphic and intravascular ultrasound (IVUS) data at ten different
phases of the cardiac cycle. Comparing their results of steady ow
analysis, pulsatile ow analysis and pulsatile ow with imposed arte-
rial motion, they found that arterial motion substantially affects the
uid dynamics in LAD. More recently, Prosi et al [23] studied the ef-
fect of arterial motion at bifurcating vessels by studying a realistic
model of the LAD and its rst diagonal branch, while Pivkin et al.
[24] investigated a coronary bifurcation model lying on a sphere of
varying radius that represented an idealized heart surface. They
showed that the ow rate ratio between the side branch and the
main branch in the vicinity of the bifurcation is signicantly
inuenced by the combined unsteady phenomena of ow and vary-
ing geometry. Finally Theodorakakos et al. [25] investigated the effect
of the myocardial motion on pulsating blood ow distribution on a
stenotic LAD branch coronary artery. They found an important inu-
ence of pulsatile ow on the overall coronary uid dynamics but no
signicant differences in WSS spatial distribution between stationary
and moving coronary artery. In particular, their predictions indicate
that myocardial motion had only a minor effect on ow distribution
within the arterial tree relative to the effect of the blood pressure
pulse. Fluid solid interaction approach (FSI) has been applied to car-
diovascular problems such as abdominal/thoracic aortas [26]
including aortic aneurysm [27], carotid artery bifurcations [28,29], ce-
rebral aneurysm [3032], and coronary artery [33,34] among others.
Other approaches have been used by Zeng et al. [35] investigating
the effect of the wall compliance based on time-dependent medical
images and Berthier et al. [36] constructing CFD models based on
RCA angiograms. They studied the ow differences caused by assum-
ing different vessel cross-sectional shapes and sizes. Moreover Ding
et al. [37] used medical imaging technique to study the arterial mo-
tion without considering the compliance itself. In a previous study
[38] we analyzed the coronary wall stiffness of 8 patients trying to
nd correlation with the atheromatous plaque locations, neglecting
the contribution of the blood ow. The aim of this work is to evaluate
how the wall compliance can affect the blood ow pattern and the
WSS in a human LCA using comparing FSI and CFD analysis.
2. Materials and methods
2.1. Vascular reconstruction and numerical grid generation
The 3D coronary artery model of a 60-year-old healthy patient
was made with the help of computer imaging techniques. The
patient-specic geometry was reconstructed using computed tomog-
raphy (CT) scans at one time point of the cardiac cycle. The cross-
sectional lumen area was assumed to be circular and to avoid poten-
tial computational singularities induced by a nonuniform surface
reconstruction, a b-spline surface was performed using the commer-
cial software SolidWorks (Dessault, SolidWorks Corp., France). As
shown in Fig. 1, the arterial tree considered in this study included
the left main coronary artery (LM) and its principle branches: the
left descending artery (LAD) and the left circumex artery (LCx).
The actual data, including the intraluminal vessel wall, were imported
into the commercial software FEMAP (Siemens PLM Software, Plano,
TX, USA). Then, the initial rough geometry was smoothed and the
computational uid mesh was built. The uid tetrahedral mesh was
generated starting from the internal shell that represents the numer-
ical uid solid interface domain. The nal mesh was imported into the
software package ADINA R&D Inc (Watertown, MA, USA) where the
FSI and rigid wall simulations were performed. As usual, in order to
establish the adequate element size for the computations, a sensitiv-
ity study was conducted. Different grids were evaluated to better
compute the WSS. Special attention was given to the near-wall re-
nement where the tetrahedral elements were converted to prisms
LM
LCx
~~
LAD
~
Fig. 1. LCA reconstructed from CT scans. LCA main diameters are: DLM 0.005 mm,
DLCx 0.00325 mm and DLAD 0.00375 mm.
[39] (see Fig. 2 (a)). Four different meshes of 100,000, 200,000,
400,000 and 800,000 elements respectively were tested. For reason
of computational time, the comparison was performed only through
rigid wall simulations. Velocity proles and WSS were computed at
several time points during the cardiac cycle with the four grids in
order to get a relation between discretization error and element
size, and hence, an estimation of the required element size; the com-
putational grids used in this study possessed nally 400,000 elements
(see Fig. 2 (a)). Moreover, to facilitate the uid dynamic model,
5-diameter inlet and 15-diameter outlet extensions were added
[40]. For the solid grid, since no data were available from real images,
a constant thickness of 0.6 mm [41] was given to the arterial wall. A
full hexahedral mesh of 30,000 elements was created using the
meshing tool of the commercial software ABAQUS Inc. The computa-
tional uid and solid grids are represented in Fig. 2.
2.2. The intravascular blood ow
As reported in previous works on human coronary arteries
[12,15,40], the blood rheology was assumed as Newtonian. In partic-
ular, according to literature, the blood density was taken as
1050 kg/m 3 and a blood viscosity of 0.003528 Pa was considered
[40,42,43]. Since the Reynolds number based on the average arterial
diameter was Re = 150, the blood ow was assumed laminar and in-
compressible under unsteady ow conditions.
2.3. Material wall properties
The arterial wall was modeled as a hyperelastic incompressible
isotropic and homogeneous material. In this study, the viscoelasticity,
the active behavior of muscle bers of the artery, and the intrinsic an-
isotropy, due to the preferencial directions of collagen and muscle -
bers, were not considered. The arterial bifurcation was then
characterized by the following strain energy function W:



W D1 exp D2 I 1 3 1 U J ; 1
where I 1 is the rst invariant of the deviatoric right CauchyGreen
tensor C J 2=3 FT F, J = det(F) is the Jacobian, F is the standard defor-
mation gradient, U is the volumetric energy function and D1, D2 are
material constants. In particular we considered D1 = 3.71 Pa and
D2 = 140.2. This strain energy function was initially proposed by
Demiray et al. [44], and, most recently, used by Delno [45] for carot-
id artery. Even knowing that the vascular tissue has a clearly
 M. Malv et al. / International Communications in Heat and Mass Transfer 39 (2012) 745751
LM
LAD
LCx
a) fluid grid
Fig. 2. LCA computational mesh: uid (a) and solid (b) grid with close-up view on the inlet.
anisotropic behavior and it is also layer-specic, for this preliminary
FSI study, we considered a homogeneous and isotropic function as a
rst approximation. The function parameters were tted using the
experimental tests of human coronary arteries obtained by Carmines
et al. [46]. For further explanations see Rodriguez et al. [47].
2.4. Physiological boundary conditions
As usual for FSI analyses, mixed velocitypressure condition are
required in order to correctly compute ow features and structural
stresses, strains and displacements. In this work we used velocity
and pressure waveforms measured by Davies et al. [48] with
intracoronary wires in the left anterior descending, and circumex ar-
teries. These curves were applied in the commercial software to the
already mentioned branch extensions in order to perform the simula-
tions. Both FSI and the CFD simulations were performed using the
same boundary conditions in order to correctly postprocess the com-
parison. No-slip wall boundary condition was imposed at the internal
surface of the arterial wall, which for the FSI simulation represented
also the uidstructure interface. Finally, at the extensions extremi-
ties of the solid model, no axial or transaxial motion was permitted.
This constraint, though non-physiological, as the inlet and outlets
should be allowed to deform radially to correctly simulate tethering
of the artery, is commonly assumed in nite element studies of coro-
naries [12,30] and aneurysms [31,39].
3. Results
The lumen wall displacements were analyzed rst. The maximum
displacement (3.1 mm) is reached in the LAD branch at peak pressure
(time, t = 0.44 s). This displacement is affected by the boundary con-
ditions applied to the solid model as reported in other works which
implied the same constraint condition [12,30]. The LCA displacement
observed in vivo is of course larger than what we computed, as the
myocardial motion was neglected in this work. However, it is not
clear how much the model restriction affects our solution, since
more realistic boundary conditions and the inclusion of the men-
tioned cardiac wall motion could deeply increase the wall displace-
ment. Diameter variations during a cardiac cycle are 0.055 mm,
0.037 mm, and 0.049 mm on LM, LCx, and LAD respectively. By nor-
malizing the changes with their corresponding diameter, we obtained
1.06%, 0.85%, and 0.98% respectively. Our results agree with those
747
b) solid grid
obtained in other works [12] showing that the arterial wall compli-
ance remains small during the cardiac cycle. Moreover, the diameter
variations are near to those reported by Schaar et al. [49] using
ultrasound-based intravascular palpography (12%) but smaller
than those reported by Qiu et al. [50] for an elastic coronary artery
model, where a maximal diameter variation of 5% was imposed to
the curved compliant tube. In Fig. 3 the logarithmic circumferential
strain distribution is shown at selected time points during the cardiac
cycle. The maximal strain, located in a small region of the bifurcation,
at the beginning of the LCx branch, is of about 16% at time t = 0.4 s.
On the contrary, the maximal strain during systole is of about 15%,
slightly less than that of diastole. The values we found are higher
than what were found by Ding et al. [37] using biplanar angiogram.
However, it has to be noted that the values we found take into
account the circumferential strain starting from the zero-pressure
conguration, which, before reaching time, t = 0 s of the cardiac
cycle, gives the major contribution. The computed maximal strain
without this contribution is less than 2% which again agrees with
Schaar et al. [49].
Since it is well established that WSS plays a central role in athero-
genesis for vessel hemodynamics, we made a comparison between
the rigid wall and FSI to examine the effect of the wall compliance
on this parameter and assess the importance of FSI simulation in cor-
onary hemodynamics in a similar way to that of Torii et al. [12] for the
right coronary artery (RCA). We rst show the correlation between
the WSS and the velocity eld at the arterial wall which is similar
for both rigid and FSI computations. Concentrating our attention on
the bifurcation (see Fig. 4), we can identify ve different areas. The
blood ow near the bifurcation separates from the arterial wall (re-
gion 1) causing a high WSS region and generating a recirculation
area that causes a low WSS region at the proximal section of the bifur-
cation, inside both the LCx (region 2) and LAD branches (region 5).
Two regions characterized by a high WSS value are found in the distal
section of the bifurcation caused by the blood ow impacting against
the arterial wall at the entrance of the LCx (region 3) and LAD bra-
nches (region 4). This correlation between WSS distribution and the
velocity eld near the bifurcation matches well with other results in
previous works by Soulis et al. [16] and Joshi et al. [40] among others.
The strong correlation between low WSS and localization of athero-
matous plaques in arterial bifurcation is well known in previous liter-
atures [4,5,51]. The overall WSS distribution is in accordance with the
localization of atherosclerotic lesions in this area, as documented in
748 M. Malv et al. / International Communications in Heat and Mass Transfer 39 (2012) 745751

t = 0.42 s

t = 0.57 s

a) Epicardiumfacing side b) Pericardiumfacing side

Fig. 3. Logarithmic circumferential strain of the coronary artery at peak systole (0.57 s) and diastole (0.42 s).

ref [52] and ref [53]. In particular, the low WSS distribution is in ac-
cordance with plaque localization [54,55]. In Fig. 5 is shown a com-
parison between the temporal maximal and minimal shear stress
(in the regions 1 and 2 of Fig. 4), respectively, for rigid wall and FSI
simulation. As expected, both curves show the same trend as the
inlet velocity condition, but no negligible differences may be found
in the WSS values. While the highest value of maximum WSS is reg-
istered for the CFD computation, the highest value of the minimum
was found for the FSI analysis. At the beginning of the systole we
can observe that while the WSS maxima almost overlap (from
t = 0.01 s to t = 0.1 s, Fig. 5 (a)), the minima already shows a gap of
7.5% at time t = 0.1 s. In the systolic phase, the difference between
both WSS maxima is more pronounced with a peak difference of
10% at t = 0.38 s, while before reaching the diastole both curves
completely overlap (see Fig. 5 (a)). In this case, the maximum WSS
value is registered for the rigid wall computation. For the minimum
WSS on the contrary, at t = 0.1 s the difference between the two cur-
ves is even more pronounced reaching a value of about 60% between
both peaks (see Fig. 5 (b)). In this case highest value is registered for
the CFD-analysis. At the beginning of the diastolic phase (time point
t = 0.43 s of the cardiac cycle), the trend observed during the systole
inverts. A bigger gap of about 10% is reached at time t = 0.6 s on the
maximum WSS, but in this case, the CFD computation shows the
highest value. For the minimum WSS the gap at the time point
t = 0.6 s is close to 50%. Finally, during diastole, the gap between the
curves of maximum WSS disappears almost linearly till a complete
overlapping at the end of the cardiac cycle (see Fig. 5 (a)), while the
gap between the minima WSS remains constant (see Fig. 5 (b), from
time t = 0.7 s to t = 0.8 s). The reason of those discrepancies is not to-
tally clear, although the compliance of the arterial walls dilates the
vessel and the WSS could be consequently altered as observed in
other works [12,35]. This ndings are in agreement with previous
studies on human RCA [12] but differ from the results obtained by
Huo et al. [13,14] for a porcine RCA. While the WSS comparison
showed by Torii et al [12] conrms our results, the WSS discrepancies
between rigid wall and FSI simulation computed in ref. [13] are in fact
smaller. The reason for that can be found in the different type of
boundary conditions used in both works. In fact, while we used

0.455

0.245

0.035

7.8

1 4 4.2

2 3
0.6

Fig. 4. Velocity eld (in [m/s]) generating the WSS (in [Pa]) at the arterial wall (FSI simulation, t = 06 s.
 M. Malv et al. / International Communications in Heat and Mass Transfer 39 (2012) 745751 749

a) b) x 103
10 16
Rigid wall Rigid wall
FSI 14 FSI
8
12
Max WSS [Pa]

Min WSS [Pa]

6 10

8
4
6
2
4

0 2
0 0.2 0.4 0.6 0.8 1 0 0.2 0.4 0.6 0.8 1
time [s] time [s]

Fig. 5. Comparison of the temporal variation of the maximum (a) and minimum (b) WSS for FSI and rigid wall simulations (zones 1 and 2 in Fig. 4).

physiological velocity and pressure waveforms, Huo et al. [13] im-
posed ow-velocity conditions at the inlet and at all outlets of his
model. This may affect not only the WSS computation but also the
computed wall compliance, since no pressure conditions are given.
Since low and oscillatory WSS plays an important role in atherogene-
sis, the WSS related to hemodynamic parameters needs to be exam-
ined. In particular, as in other studies [12,30], the time-averaged
WSS (TAWSS) was considered. This parameter was compared be-
tween the FSI and rigid-wall models to assess the importance of FSI
in determining coronary hemodynamics. The TAWSS is dened as:
T FSI approach especially regarding the WSS. These results may be
1
TAWSS j jdt
T0 W
where W is the WSS vector and T is the period of the cardiac cycle. As
shown in Fig. 6, the TAWSS is high at the bifurcation (areas 1, 3 and 4
of Fig. 4) due to the ow divider which causes high velocity gradient
near the wall. Dilatation of the vessel due to the pulsating ow in-
duced a reduction of the blood velocity causing consequently lower
WSS values (3.7 Pa for FSI and 3.9 Pa for rigid wall). The low TAWSS
distribution is more extended for FSI model with respect to the rigid
wall model (cf. Fig. 6 and Fig. 4, regions 2 and 5). Finally, the minima
TAWSS at the bifurcation are almost identical for both models
(0.0103 Pa for FSI and 0.0105 Pa for rigid wall).
4. Discussion
The presented simulations show discrepancies between CFD and
2 strongly affected by the neglected cardiac-induced vessel motion.
Coronaries are in fact embedded in the myocardium and the heart
beating basically drives not only their uid dynamics (the ow is di-
astolic) [56] but also their wall displacements [57]. However, this ef-
fect is still on study and debated in literature [20,2225,58,59].
The work of Prosi et al. [23] shows the importance to impose

FSI
LM
LM
LAD

LCx
LCx
LAD 3
LAD

Epicardium facing side Pericardium facing side

LAD 1
LCx
LM LCx LM

Rigid Wall 0.1

LM
LAD

LM LCx
LCx
LAD 0.01
LAD
Epicardium facing side Pericardium facing side
LAD

LM LCx
LM
LCx

Fig. 6. Comparison of TAWSS (with logarithmic scale in [Pa]) between the FSI (top) and the rigid-wall models (bottom).
750 M. Malv et al. / International Communications in Heat and Mass Transfer 39 (2012) 745751
physiologically realistic ow in the correct phase relationship with
vessel motion when simulating coronary artery hemodynamics. Ana-
lyzing the inuence of dynamic curvature on coronary artery hemo-
dynamics they show that during systole, when high curvature
variations appear, their effect on the ow patterns and the wall
shear stress is dominated by the ow wave. On the contrary, due to
the smaller curvature changes during diastole, only minor effects of
curvature variation on the high and relatively constant diastolic
ow occur, as reported also in ref. [58]. Our results are conrmed by
their ndings, since the WSS we computed is strongly dependent by
the inow waveform (see Fig. 5), even neglecting the cardiac motion.
Moreover, the results of the study of Pivkin et al. [24] indicate that the
combined effect of pulsatile inow and dynamic geometry depends
strongly on the phase difference between the ow wave and arterial
motion. Neglecting the cardiac motion, it can be accepted as reported
by Theodorakakos et al. [25]. They investigated the effect of myocar-
dial motion on pulsating blood ow distribution of a stenotic LAD cor-
onary artery focusing their attention on the WSS distribution and
ow pattern. Their main conclusion is in fact that the spatial WSS
distribution along the LAD does not vary essentially in the presence
and absence of cardiac motion while the uid dynamics is consider-
ably affected by pulsatile ow. Moreover, the WSS values which
they evaluated in presence of myocardium motion are qualitatively
comparable with those found in this study.
This work, even showing improvements with respect to other pre-
vious studies, is affected by some assumptions and simplications.
First of all, the heart motion which could have a great impact on
coronary hemodynamics was not included in this work. This simpli-
cation could affect our results which are focused on the WSS compar-
ison between rigid and compliant walls. In this work, the WSS for the
FSI computation is evaluated taking into account only the wall dis-
placements due to the blood ow. The computed displacements
were found to be small. In reality the arterial compliance could be
greater than what we found a cause of the myocardiac motion. Al-
though its effect is still debated in literature [20,2325,58,59], in fu-
ture works, this movement must be included. In absence of real
data, a constant arterial wall thickness was assumed. In this way,
the solid model was strongly approximated. In future work, in order
to evaluate wall compliance, the coronary wall should be modeled
starting from patient specic data. Lastly, for the solid part, we
modeled the arterial wall with the approach used by Delno et al.
[45]. Studies on the sensitivity of wall stress to the material model
for pathological coronary artery showed that anisotropic material
models predicted higher wall stresses [12] than those assuming iso-
tropic material but not signicant qualitative differences were found
in the WSS distribution. Anyway the constitutive law of Delno may
affect the computed diameter variations of the coronary tree,
suggesting the use of more realistic material property models such
as the three-layered characterization of the arterial wall proposed
by Holzapfel et al. [60].
5. Conclusions
FSI and CFD modeling of a human healthy LCA bifurcation was car-
ried out under physiological velocity and pressures waveforms to in-
vestigate the effect of the arterial wall compliance on coronary
hemodynamics. Results show a WSS spatial distribution comparable
with previous studies on FSI. Comparison of computational results be-
tween rigid and compliant arterial wall showed not only remarkable
qualitative discrepancies in the WSS distribution, but also relevant
differences in the WSS proles. Signicant differences were found
comparing TAWSS, especially on its spatial distribution. These results
conrm that for WSS evaluation in LCA atherogenesis, arterial wall
compliance can be neglected only in rst approximation since, for
an accurate WSS computation, wall displacements can play an impor-
tant role.
Conict of interest statement
None of the authors of this work has conict of interest with other
people and organizations.
Acknowledgments
This study was supported by the Spanish Ministry of Science and
Technology through research project DPI2010-20746-C03-01 and
CIBER-BBN, an initiative funded by the VI National R &D & i Plan
20082011, Iniciativa Ingenio 2010, Consolider Program, CIBER Ac-
tions and nanced by the Instituto de Salud Carlos III with assistance
from the European Regional Development Fund and by the research
project PI07/90023. The authors gratefully acknowledge Roderic I.
Pettigrew and Ahmed M. Gharib (Laboratory of Integrative Cardiovas-
cular Imaging Science, National Institute of Diabetes Digestive and
Kidney Diseases, National Institute of Health, Bethesda, Maryland,
USA).
References
[1] WHOROE, World health organization regional ofce for Europe, European Health
Report for 2002 in European Series 97 (2002).
[2] ECDS, British Heart Foundation of Health Promotion Research Group, http://
www.heartstats.org.
[3] J. Ohayon, G. Finet, M. Gharib, D. Herzka, P. Tracqui, J. Heroux, G. Rioufol, M. Kotys,
A. Elagha, R. Pettigrew, Necrotic core thickness and positive arterial remodeling
index: emergent biomechanical factors for evaluating the risk of plaque rupture,
American Journal of Physiology. Heart and Circulatory Physiology 295 (2008)
H717H727.
[4] T. Asakura, T. Karino, Flow patterns and spatial distribution of atherosclerotic le-
sions in human coronary arteries, Circulation Research 66 (4) (1990) 10451066.
[5] C.G. Caro, J.M. Fitz-Gerald, R.C. Schroter, Atheroma and arterial wall shear: obser-
vation, correlation and proposal of a shear dependent mass transfer mechanism
for atherogenesis, Proceedings of the Royal Society of London (1971) 109159.
[6] G. Giannoglou, J. Soulis, T.M. Fermakis, D. Fermakis, G. Louridas, Haemodynamic
factors and the important role of local low static pressure in coronary wall thick-
ening, International Journal of Cardiology 86 (1) (2002) 2740.
[7] G. Giannoglou, J. Soulis, T. Fermakis, G. Zioupos, G. Giannakoulas, G. Louridas,
Wall shear stress differences between proximal and distal left coronary artery bi-
furcations, Abstract of European Heart Journal (Abstr. Suppl. 23) (2002) 686.
[8] F. Gori, A. Boghi, Three-dimensional numerical simulation of blood ow in two
coronary stents, Numerical Heat Transfer, Part A: Applications: An International
Journal of Computation and Methodology 59 (4) (2011) 231246.
[9] R. Balossino, F. Gervaso, F. Migliavacca, G. Dubini, Effects of different stent designs
on local hemodynamics in stented arteries, Journal of Biomechanics 41 (2008)
10531061.
[10] S. Morlacchi, C. Chiastra, D. Gastaldi, G. Pennati, G. Dubini, F. Migliavacca, Sequen-
tial structural and uid dynamic numerical simulations of a stented bifurcated
coronary artery, Journal of Biomechanical Engineering 133 (2011) 121010.
[11] C. Chiastra, S. Morlacchi, S. Pereira, G. Dubini, F. Migliavacca, Computational uid
dynamics of stented coronary bifurcations studied with a hybrid discretization
method, European Journal of Mechanics B/Fluids (2012).
[12] R. Torii, N. Wood, N. Hadjiloizou, A. Dowsey, A. Wright, A. Hughes, J. Davies, D.
Francis, J. Mayet, G. Yang, S. McG, X.Xu. Thom, Fluidstructure interaction analysis
of a patient-specic right coronary artery with physiological velocity and pressure
waveforms, Communications in Numerical Methods in Engineering 55 (2009)
565580.
[13] Y. Huo, J. Choy, M. Svendsen, A. Sinha, G. Kassab, Effects of vessel compliance on
ow pattern in porcine epicardial right coronary arterial tree, Journal of Biome-
chanics 42 (2009) 594602.
[14] Y. Huo, G. Kassab, Effects of vessel compliance and hematocrit on wall shear
stress in a model of the entire coronary arterial tree, Journal of Applied Physiolo-
gy 107 (2009) 500505.
[15] F. Gijsen, J. Wentzel, A. Thury, B. Lamers, J. Schuurbiers, P. Serruys, A. van der
Steen, A new imaging technique to study 3-d plaque and shear stress distribution
in human coronary artery bifurcations in vivo, Journal of Biomechanics 40 (2006)
23492357.
[16] J. Soulis, M. Fermakis, G. Giannoglou, G. Louridas, Wall shear stress in normal left
coronary artery tree, Journal of Biomechanics 39 (2006) 742749.
[17] L. Goubergrits, E. Wellnhofer, U. Kertzscher, K. Affeld, C. Petz, C. Hege, Coronary
artery wss proling using a geometry reconstruction based on biplane angiogra-
phy, Annals of Biomedical Engineering 37 (4) (2007) 682691.
[18] P. Bovendeerd, P. Borsje, T. Arts, F.V. de Vosse, Dependence of intramyocardial
pressure and coronary ow on ventricular loading and contractility: A model
study, Annals of Biomedical Engineering 34 (12) (2006) 18331845.
[19] S.D. Ramaswamy, S.C. Vigmostad, A. Wahle, Y.G. Lai, M.E. Olszewski, K.C. Braddy,
T.M.H. Brennan, J.D. Rossen, M. Sonka, K.B. Chandran, Fluid dynamics analysis in
a human anterior descending coronary artery with arterial motion, Annals of Bio-
medical Engineering 32 (2004) 16281641.
 M. Malv et al. / International Communications in Heat and Mass Transfer 39 (2012) 745751
[20] E. Weydahl, J. Meister Jr., Dynamic curvature strongly affects wall shear rates in a
coronary artery bifurcation model, Journal of Biomechanics 34 (2001)
11891196.
[21] A. Delno, J. Moore, J. Meister Jr., Lateral deformation and movement effects on
ow through distensible tube models of blood vessels, Biorheology 31 (1994)
533547.
[22] S. Waters, T. Pedley, Oscillatory ow in a tube of time-dependent curvature on ve-
locity proles in a model of the coronary arteries, Journal of Biomechanics 29
(1999) 469474.
[23] M. Prosi, K. Perktold, Z.D.M. Friedmanc, Inuence of curvature dynamics on pul-
satile coronary artery ow in a realistic bifurcation model, Journal of Biomechan-
ics 37 (2004) 17671775.
[24] I. Pivkin, P. Richardson, D. Laidlaw, G. Karniadakis, Combined effects of pulsatile
ow and dynamic curvature on wall shear stress in a coronary artery bifurcation
model, Journal of Biomechanics 38 (2005) 12831290.
[25] A. Theodorakakos, M. Gavaises, A. Andriotis, Z. Zifan, P. Liatsis, I. Pantos,
E. Efstathopoulos, D. Katritsis, Simulation of cardiac motion on non-
Newtonian, pulsating ow development in the human left anterior descending
coronary artery, Physics in Medicine and Biology 53 (2008) 48754892.
[26] A. Figueroa, I. Vignon-Clementel, K. Jansen, T. Hughes, C. Taylor, A coupled mo-
mentum method for modeling blood ow in three-dimensional deformable arter-
ies, Computer Methods in Applied Mechanics and Engineering 195 (2006)
56855706.
[27] M. Scotti, J. Jimenez, S. Muluk, E. Finol, Wall stress and ow dynamics in
abdominalaortic aneurysms: nite element analysis vs. uidstructure interac-
tion, Computer Methods in Biomechanics and Biomedical Engineering 11 (3)
(2008) 301322.
[28] H. Gao, Q. Long, M. Graves, J. Gillard, Z. Li, Carotid arterial plaque stress analysis
using uidstructure interactive simulation based on in-vivo magnetic resonance
images of four patients, Journal of Biomechanics 42 (2009) 14161423.
[29] S. Tada, J. Tarbell, A computational study of ow in a compliant carotid
bifurcation-stress phase angle correlation with shear stress, Annals of Biomedical
Engineering 33 (9) (2005) 12021212.
[30] R. Torii, M. Oshima, T. Kobayashi, K. Takagi, T. Tezduyar, Fluidstructure interac-
tion modeling of aneurysmal conditions with high and normal blood pressures,
Computational Mechanics 38 (2006) 482490.
[31] R. Torii, M. Oshima, T. Kobayashi, K. Takagi, T. Tezduyar, Role of 0d peripheral vas-
culature model in uidstructure interaction modeling of aneurysms, Computa-
tional Mechanics 46 (2010) 4352.
[32] T. Tezduyar, S. Sathe, M. Schwaab, B. Conklin, Arterial uid mechanics modeling
with the stabilized space-time uidstructure interaction technique, Internation-
al Journal for Numerical Methods in Fluids 57 (2008) 601629.
[33] V. Calo, N. Brasher, Y. Bazilevs, T. Hughes, Multiphysics model for blood ow and
drug transport with application to patient-specic coronary artery ow, Compu-
tational Mechanics 43 (2008) 161177.
[34] D. Tang, C. Yang, J. Zheng, P. Woodard, G. Sicard, J. Saftz, C. Yuan, Mri-based
multicomponent fsi models for atherosclerotic plaques, Annals of Biomedical
Engineering 32 (7) (2004) 947960.
[35] D. Zeng, E. Boutsianis, M. Ammann, K. Boomsma, S. Wildermuth, D. Poulikakos, A
study on the compliance of a right coronary artery and its impact on wall shear
stress, Transactions of the ASME, Journal of Biomechanical Engineering 130
(2008) 041014104101411.
[36] B. Berthier, R. Bouzerar, C. Legallais, Blood ow patterns in an anatomically real-
istic coronary vessel: Inuence of three different reconstruction methods, Journal
of Biomechanics 35 (10) (2002) 13471356.
[37] Z. Ding, M. Friedman, Quantication of 3-d coronary arterial motion using clinical
biplane cineangiograms, Sensors 16 (5) (2000) 331346.
[38] J. Ohayon, M. Gharib, A. Garca, J. Heroux, S. Yazdani, M. Malv, P. Tracqui,
M. Martnez, M. Doblar, G. Finet, R. Pettigrew, Is arterial wall-strain stiffening
an additional process responsible for atherosclerosis in coronary bifurcations?:
an in vivo study based on dynamic ct and mri, American Journal of Physiology.
Heart and Circulatory Physiology 301 (2011) H1097H1106.
751
[39] K. Takizawa, J. Christopher, E. Tezduyar, S. Sathe, Space-time nite element com-
putation of arterial uidstructure interactions with patient-specic data, Com-
munications in Numerical Methods in Engineering 26 (2010) 101116.
[40] A. Joshi, R. Leask, J. Myers, M. Ojha, J. Butany, C. Ethier, Intimal thickness is not
associated with wall shear stress pattern in the human right coronary artery,
Arteriosclerosis, Thrombosis and Vascular Biology - Journal of the American
Heart Association 24 (2004) 24082413.
[41] I. Gradus-Pizlo, B. Bigelow, Y. Mahomed, S. Sawada, K. Rieger, H. Feigenbaum, Left
anterior descending coronary artery wall thickness measured by high-frequency
transthoracic and epicardial echocardiography includes adventitia, The American
Journal of Cardiology 91 (2003) 2732.
[42] B. Johnston, R. Johnston, S. Corney, D. Kilpatrick, Non-Newtonian blood ow in
human right coronary arteries: steady state simulations, Journal of Biomechanics
37 (9) (2004) 709720.
[43] B. Johnston, R. Johnston, S. Corney, D. Kilpatrick, Non-newtonian blood ow in
human right coronary arteries: Transient simulations, Journal of Biomechanics
39 (2006) 11161128.
[44] H. Demiray, A note on the elasticity of soft biological tissues, Journal of Biome-
chanics 5 (3) (1972) 309311.
[45] A. Delno, N. Stergiopulos, J. Moore Jr., J. Meister, Residual strain effect on the
stress eld in a thick wall nite element model of the human carotid bifurcation,
Journal of Biomechanics 8 (1997) 777786.
[46] D. Carmines, J. McElhaney, R. Stack, A piece-wise nonlinear elastic stress expres-
sion of human and pig coronary-arteries tested invitro, Journal of Biomechanics
24 (10) (1991) 899906.
[47] J. Rodriguez, C. Ruiz, M. Doblar, G. Holzapfel, Mechanical stresses in abdominal
aortic aneurysm: inuence of diameter, asymmetry and material anisotropy,
Journal of Biomechanical Engineering 130 (2008).
[48] J. Davies, Z. Whinnett, D. Francis, C. Manistry, J. Aguado-Sierra, K. Willson, R. Foale,
I. Malik, A. Hughes, K. Parker, J. Mayet, Evidence of a dominant backward-
propagating suction wave responsible for diastolic coronary lling in humans,
attenuated in left ventricular hypertrophy, Circulation 113 (2006) 17681778.
[49] A. Schaar, C. de Korte, F. Mastik, L. van Damme, R. Krams, P. Serruys, A. van der
Steen, Three-dimensional palpography of human coronary arteries, Herz 30
(2005) 125133.
[50] Y. Qiu, J. Tarbell, Numerical simulation of pulsatile ow in a compliant curved
tube model of a coronary artery, Journal of Biomechanical Engineering 122
(2000) 7785.
[51] S. Glagov, C. Zarins, D. Giddens, D. Ku, Haemodynamics and atherosclerosis. in-
sights and perspectives gained from studies of human arteries, Archives of Pa-
thology & Laboratory Medicine 112 (10) (1988) 10181031.
[52] A. Svindland, The localization of sudanophilic and brous plaques in the left main
coronary bifurcation, Atherosclerosis 48 (2) (1983) 139145.
[53] P. Grottum, A. Svindland, L. Walloe, Localization of atheroscerotic lesions in the
bifurcation of the main left coronary artery, Atherosclerosis 47 (1) (1983) 5562.
[54] D. Halon, D. Sapoznikov, B. Lewis, M. Gotsman, Localization o lesions in the coro-
nary circulain, The American Journal of Cardiology 152 (8) (1983) 921926.
[55] B. Fox, K. James, B. Morgan, A. Seed, Distribution of fatty and brous plaques in
young human coronary arteries, Atherosclerosis 41 (2,3) (1992) 337347.
[56] N. Westerhof, C. Boer, R. Lamberts, P. Sipkema, Cross-talk between cardiac muscle
and coronary vasculature, Physiological Reviews 86 (2006) 12631308.
[57] M. Zamir, The Physics of Coronary Blood Flow, (2005).
[58] J. Moore, N. Guggenheim, A. Delno, P. Doriot, P. Dorsaz, W. Rutishauser, J. Meister,
Preliminary analysis of the effects of blood vessel movement on blood ow patterns
in the coronary arteries, Journal of Biomechanics 116 (1994) 302306.
[59] S. Schilt, J. Moore Jr., A. Delno, J. Meister, The effects of time-varying curvature
on velocity proles in a model of the coronary arteries, Journal of Biomechanics
29 (1996) 469474.
[60] G. Holzapfel, G. Sommer, C.T. Gasser, P. Regitnig, Determination of layer-specic
mechanical properties of human coronary arteries with nonatherosclerotic inti-
mal thickening and related constitutive modeling (2005).