Hindawi Publishing Corporation

Advances in Mechanical Engineering

Volume 2014, Article ID 908357, 7 pages
http://dx.doi.org/10.1155/2014/908357

Research Article
Hemodynamics Modeling and Simulation of
Anterior Communicating Artery Aneurysms
Jianjun Li,1 Shengzhang Wang,1 Gang Lu,2 and Xiaolong Zhang2
1
2

Department of Mechanics and Engineering Science, Fudan University, Shanghai 200433, China
Department of Radiology, Huashan Hospital Affiliated to Fudan University, Shanghai 200012, China

Correspondence should be addressed to Shengzhang Wang; szwang@fudan.edu.cn and Xiaolong Zhang; xlzhang56@hotmail.com
Received 9 April 2014; Accepted 16 May 2014; Published 17 July 2014
Academic Editor: Aike Qiao
Copyright 2014 Jianjun Li et al. This is an open access article distributed under the Creative Commons Attribution License, which
permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
It is a general agreement that hemodynamics plays very important role in the initiation, growth, and rupture of cerebral aneurysms
and hemodynamics in the anterior communicating artery aneurysms is considered the most complex in all cerebral aneurysms
and it is difficult to find some reasonable relationship between the hemodynamics parameters and the rupture risk. In this paper,
the 3D geometries of four anterior communicating artery aneurysms were generated from the CTA data and the computational
models with bilateral feeding arteries for the four aneurysms were constructed. The blood flow was simulated by computational
fluid dynamics software and the hemodynamics parameters such as velocity, wall shear stress, and oscillatory shear index were
calculated. The following results were observed: one of the four models only needs the left feeding artery; the max normalized wall
shear stress locates at the aneurysmal neck of the largest aneurysm; the max oscillatory shear index locates at the aneurysmal sac of
the largest aneurysm. The conclusion was drawn that the anterior communicating artery aneurysm has higher rupture risk from the
hemodynamics viewpoint if the max wall shear stress locates at the neck and the max oscillatory shear index locates at the dome.

1. Introduction
Cerebral aneurysms are pathologic dilations of the cerebral
arteries generally occurring in the anterior and posterior
regions of the circle of Willis. Rupture of a cerebral aneurysm
causes subarachnoid hemorrhage with an associated high
mortality and morbidity rate [1]. The mechanisms responsible for the initiation, evolution, and rupture of cerebral
aneurysms are not well understood until now. However, it
is widely accepted that hemodynamic characteristics such as
wall shear stress (WSS), velocity, vorticity, flow impingement,
and pressure play an important role in the progression of
aneurysms [2].
According to several large studies [35], the proportion
of the anterior communicating artery (AcomA) aneurysm
in all cerebral aneurysms is more than 25%. Because of
the complexity of the geometry and the flow conditions,
hemodynamics in the AcomA aneurysms is considered the
most complex in all cerebral aneurysms [6]. Aneurysms in
the AComA are more likely to have asymmetric A1 segments

[7] and furthermore to have exclusive filling angiographically

from one A1 segment in up to 78% of cases [8]. Tarulli and
Fox [9] performed a radiological examination and found
that A1 dominance configuration is strongly associated with
the presence of AComA aneurysms for 105 patients with
intracranial aneurysms at that location. Hassan et al. [10]
performed a sensitivity study using idealized computational
models of the anterior communicating artery and found that
aneurysms located in the AComA with differences of 50%
or more between the two A1 areas are subjected to more
flow stresses. Experimentally, an AComA aneurysm can be
produced in hypertensive rats by unilateral ligation of the
common carotid artery [11], further supporting a causative
relationship between increased flow and aneurysm formation. A computational study found a possible correlation
between AComA aneurysm formation, growth, and rupture
with A1 dysplasia or hypoplasia. Increased WSS was found
in the bifurcation when the diameter of the nondominant A1
segment decreased [12]. Previous in vitro modeling provided
evidence of this effect. Using a silicone replica of a lethal

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anterior communicating artery aneurysm and imaging of
fluid slip streams, it was observed that with symmetrical
flow conditions slip streams rarely enter the aneurysm, but
with asymmetric alterations in flow complicated flow patterns
were identified within the aneurysm [13].
Castro et al. [14] performed a patient population
study that included twenty-six computational hemodynamics
models of AComA aneurysms, which showed interesting
associations between flow patterns and aneurysm rupture.
Karmonik et al. [15] showed that hemodynamic patterns
changed when flow rates at the A1 segments are altered with
respect to the baseline defined by PC-MRI flow measurements in the same patient, but keeping the total flow rate
unchanged. The maximum change observed in the aneurysm
average WSS when increasing the right AComA flow rate to
68% was as high as 43%. According to the data presented
in that paper, the model only included the A1 and A2
segments of the AComA; therefore, it is not clear if those
differences would be so relevant when normalized flow rates
are imposed at the ICAs. However, it is clear that using
patient-specific inflow conditions would help in minimizing
the effects of model assumptions. Recently, Hodis et al.
[16] performed a CFD analysis of the hemodynamics of an
AComA that spontaneously ruptured immediately following
three-dimensional rotational angiography. Subsequent digital subtraction angiography allowed for the localization of the
point of rupture within the aneurysm dome. CFD analysis
demonstrated a concentrated jet that impinged directly at
the site of rupture. The authors reported that peak systolic
pressure and WSS were both maximal near the rupture
location.
In this paper, the 3D geometries of four AComA
aneurysms were generated from the CTA data and the
computational models for the four aneurysms with bilateral
feeding arteries and four outlet arteries were constructed.
The blood flow in the four aneurysms was simulated by
CFD software and the hemodynamics parameters such as
velocity, wall shear stress, and oscillatory shear index were
calculated. By analyzing and comparing the difference of
the hemodynamics in the four AComA aneurysms, the
association between hemodynamics parameters and rupture
risks in the AComA aneurysms was concluded.

2. Materials and Methods

Four patients suffering from AComA aneurysm were
obtained from Huashan Hospital affiliated to Fudan
University and the patient data is demonstrated in Table 1.
2.1. Geometry Model. 3DRA data can only construct the
unilateral internal carotid artery (ICA) but the AComA
aneurysm has bilateral feeding ICAs. In order to have the
bilateral ICAs of the AComA aneurysms, the geometries of
the four aneurysms were constructed from the CTA data.
After image processing such as segmentation and smoothing,
the final geometrical models are shown in Figure 1. The
sizes of the four aneurysms are demonstrated in Table 2 and

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Table 1: The patient data of the four aneurysms.

AComA-1
AComA-2
AComA-3
AComA-4

Age
65
43
55
61

Gender
F
M
M
M

Status
Unruptured
Unruptured
Unruptured
Unruptured

Table 2: The geometric sizes of the four aneurysms.

AComA-1
AComA-2
AComA-3
AComA-4

Width
(mm)

Height
(mm)

AR (/)

9.19
3.96
12.54
6.12

6.77
3.52
7.37
5.78

0.74
0.89
0.59
0.94

Table 3: The numbers of elements and nodes in the computational

grids of the models.

AcomA-1
AcomA-2
AcomA-3
AcomA-4

Elements
9,072,472
4,456,469
3,444,603
7,356,194

Nodes
1,539,297
759,975
587,457
1,249,728

Elements/mm3
1,813
1,810
1,834
1,818

definition of the size, width () and height (), is shown in

Figure 2.
2.2. Numerical Model. The computational grids for the four
models were generated by mesh generator software ICEMCFD 12.1 (Ansys Inc., Canonsburg, PA, USA). The meshes
composed by tetra elements were specified in terms of the
size as follows: the value between 0.2 mm and 0.3 mm was
set to the max element size of the four aneurysm models,
and the average element number per cubic millimeter in the
four models was about 1800 in order to obtain the meshindependent results. The geometry of the original aneurysm
was divided into two parts, the aneurysm sac part and the
parent artery part, by the interface at the aneurysm neck, but
the parameters for the mesh generation of the two parts were
the same. Figure 5 shows the computational grid of the model
AcomA-4 and Table 3 demonstrates the numbers of elements
and nodes in the computational grids of the four models.
The vessel wall was assumed rigid with no deformation
because of lack of information about the wall thickness and
material properties. The pulsatile velocity shown in Figure 3
was imposed at the inlets of the models and the flow rate
of each inlet depended on the cross-section area. As Castro
et al. reported that the phase shift between the pulsatile
velocities at the two inlets had little effect on the numerical
results [17], no phase shift was assumed to the pulsatile
velocities at the two inlets. The boundary conditions at the
four outlets were traction free and the flow rate at each
outlet was assigned according to its cross-section area and the
total flow rate satisfied mass conservation. Figure 4 shows the
multiply inlets and outlets in the model AcomA-4.

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3
AComA-2

AComA-1

AcomA-3

AcomA-4

Figure 1: The patient-specific models of four AComA aneurysms.

2.3. Numerical Scheme. The computational grid was imported into the commercial CFD package ANSYS CFX 12.1
(Ansys, Inc., Canonsburg, PA, USA) to simulate the blood
flow in the four models. Blood flow in the cerebral artery was
assumed to be incompressible and laminar and satisfied the
Navier-Stokes equation and continuity equation. The finite
volume method based on first order and second order upwind
scheme was employed to obtain the solution both for the
pressures and the velocities at each time step. The second
order backward Euler scheme with a time step = 0.001 s
was implemented for time discretization. The convergence
criterion of simulation was that the residuals of velocity and
mass were less than 15 . The blood flow in the two cardiac
cycles was performed for each simulation in order to obtain
stable results independent of initialization, and the data in the
second cycle was selected as the numerical results.

Figure 2: The size definition of the aneurysmal sac.

0.5

Velocity (m/s)

0.45
0.4

3. Results and Discussion

0.35
0.3
0.25
0.2
0.15
0.1
0

0.2

0.4

0.6

0.8
Time (s)

1.2

1.4

Figure 3: The velocity profile imposed at the inlets.

1.6

Ansys CFD-post 12.1 was utilized to process the numerical

results. The 3D flow patterns in the four model are presented
by the streamlines and the complexity and stability can be
easily recognized. Wall shear stress (WSS) is a very important
hemodynamics parameter and is considered to be related
to the initiation and rupture of the aneurysms; thus the
distributions of WSS and other derivative such as time
average wall shear stress (TAWSS) and oscillatory shear index
(OSI) on the four AComA models are analyzed.

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stress such as time average wall shear stress (TAWSS) and
oscillatory shear index (OSI):
TAWSS =

1

0

(1/)

1
0
OSI = (1
),

2
(1/) 0

Figure 4: Boundary conditions imposed at the inlets and outlets.

The two inlets (the right and left ICAs) were imposed by the pulsatile
velocities and the four outlets (the right and left MCAs and ACAs)
were imposed by traction free condition.

Figure 5: The computational grid of the model AcomA-4.

3.1. Streamlines. Figure 6 demonstrates the streamlines in the

four models; the red streamlines and the blue streamlines represent the flow coming from left and right ICA, respectively.
The flow direction in the anterior communicating artery is
determined by the pressure of the two anterior arteries. In
AComA-1, the flow direction in AComA is from left to right
and blood from the left A1 flows into the aneurysmal sac but
there is almost no vortex formation and the flow pattern is
very simple. In AComA-2, the flow direction in AComA is
from left to right; there is no flow in the right A1 and blood
from the left A1 flows into the aneurysmal sac and there is a
small vortex; therefore the AComA-2 model only needs the
left ICA as the feeding artery. In AcomA-3, the size of the
aneurysmal sac is the largest; the flow direction in AComA
is from right to left; blood from the right A1 flows into the
aneurysmal sac and there is complex flow pattern formation.
In AcomA-4, the flow direction in AComA is from left to
right; blood from the left A1 flows into the aneurysmal sac
and there is no vortex formation.
3.2. Wall Shear Stress. Wall shear stress is considered to be
one of the most important hemodynamic parameters related
to the initiation, growth, and rupture of cerebral aneurysms
[18]. There are several derivative parameters from wall shear

(1)

(2)

where represents the vector of wall shear stress and is

the cardiac cycle.
Figure 7 shows the distribution of TAWSS on the four
models. We focus on the aneurysmal sac and the parent vessel
connecting to the aneurysm. In AComA-1 model, the max
TAWSS locates at the neck of the aneurysm. In AComA-2
model, the max TAWSS locates at the downstream bifurcation
of the left A1. In AComA-3 model, the max TAWSS locates
at the downstream bifurcation of the right A1. In AComA-4
model, the max TAWSS locates at the neck of the aneurysm.
The value of max TAWSS on the four models varies from
4.9 Pa to 14.6 Pa. Figure 8 shows the distribution of OSI on
the four models. The value range of OSI is from 0 to 0.5 and
the higher OSI region indicates flow direction change during
a cardiac cycle. In the four models, the max OSI locates at
higher curvature of the dome of the aneurysmal sac.
Because the value of wall shear stress depends on the
geometry and the inlet boundary conditions of the aneurysm
models, NTAWSS (the normalized TAWSS) is defined to
investigate the relative variations of TAWSS on the four
models in order to reduce the influence of the geometry.
Figure 9 shows the distributions of NTAWSS and OSI on the
aneurysmal sacs of the four models:
NTAWSS
=

TAWSS
.
max TAWSS on the aneurysmal sac

(3)

Higher WSS is considered to trigger a mural-cellmediated pathway, which could be associated with the
growth of the aneurysm, while higher OSI will trigger an
inflammatory-cell-mediated pathway, which could be associated with the rupture of the aneurysm [19]. If the aneurysm
has higher WSS at the aneurysmal neck, then it has very high
possibility to grow larger. Meanwhile, if the aneurysm has
higher OSI at the aneurysmal dome, then the endothelium
will degenerate. Both the higher WSS at the aneurysmal neck
and the higher OSI at the aneurysm dome will reduce the
thickness of the aneurysmal wall, weaken the mechanical
property, and increase the rupture risk of the aneurysm. In
AComA-3 and AComA-4, the max OSI locates at the dome
and the max NTWSS loacates at the neck; therefore both may
have the higher rupture risk. Actually, the clinician usually
assesses the higher rupture risk for AComA-3 because it has
the largest aneurysm in the four models, but it is difficult
for the clinician to assess the rupture risk of the AComA-4
depending only on the size.

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Figure 6: The streamlines in the four AcomA aneurysms.

TAWSS

10.0
9.0
8.0
7.0

5.0

(Pa)

6.0

4.0
3.0
2.0
1.0
0.0

Figure 7: The distributions of TAWSS on the four AcomA aneurysms.

4. Conclusions
In this paper, four models of the AComA aneurysms were
constructed from CTA image data. The models had the bilateral feeding arteries as inlets and four downstream arteries
as the outlets. Imposing the pulsatile velocity at the inlets

and traction free condition at the outlets, the blood flows in

the four models were simulated by CFD software. Analyzing
the flow pattern and the distribution of hemodynamics
parameters, we have the following conclusions. (1) Unilateral
feeding artery model for some AComA aneurysm such as
the model AComA-2 is accurate enough. (2) If we assess

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OSI

0.5
0.5
0.4
0.3
0.3
0.3
0.2
0.2
0.1
0.1
0.0

Figure 8: The distributions of OSI on the four AcomA aneurysms.

AComA-1

AComA-2

AComA-3

AComA-4

NTAWSS
1.0
0.9
0.8
0.7
0.6
0.5
0.4
0.3
0.2
0.1
0.0
OSI

0.5
0.5
0.4
0.3
0.3
0.3
0.2
0.2
0.1
0.1
0.0

Figure 9: The distributions of NTAWSS on the four AcomA aneurysmal sacs.

the rupture risk of an AComA aneurysm only depending

on geometric parameters or one hemodynamics parameter,
there will be some contradictory conclusions. (3) An AComA
aneurysm may have higher rupture risk if the max WSS
locates at the aneurysm neck and the the max OSI (larger than
0.3) locates at the dome of the aneurysmal sac. The conclusion
(3) coincides with the clinician assessment because it is the
largest one in the four aneurysms, but it needs more cases to
prove in the future.

Conflict of Interests
The authors declare that there is no conflict of interests for
publication of this research.

Acknowledgment
The research was supported by the National Natural Science
Foundation of China (Grant nos. 11102042 and 81371308).

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