J. Biomedical Science and Engineering, 2013, 6, 38-46 JBiSE
http://dx.doi.org/10.4236/jbise.2013.612A006 Published Online December 2013 (http://www.scirp.org/journal/jbise/)
A parameterized analysis of the mechanical stress for
coronary plaque fibrous caps
Ramses Galaz, Catherine Pagiatakis, Emmanuel Gaillard, Rosaire Mongrain*
Department of Mechanical Engineering, McGill University, Montreal, Canada
Email: *rosaire.mongrain@mcgill.ca
Received 31 October 2013; revised 28 November 2013; accepted 8 December 2013
Copyright © 2013 Ramses Galaz 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.
The fibrous cap is a protective layer of connective
tissue that covers the core of an atherosclerotic
plaque. The rupture of this layer has been commonly
associated with acute myocardial infarctions. The
thickness of the fibrous cap, the percentage of stenos-
ed area, and the stiffness of the core were studied
(commonly associated with vulnerable plaque char-
acteristics) to quantify their effects on the cap’s me-
chanical stress state by performing analyses using
computational fluid-structure interaction (FSI) me-
thods. The mechanical stress levels are significantly
increased within the fibrous cap structure at the up-
stream side of the plaque. As expected, the highest
stresses occurred for a severe stenosis and a thin fi-
brous cap. Interestingly, a weak structural support
such as a soft lipid pool beneath the fibrous cap al-
lowed for the hemodynamic pressure gradient forces
to displace the fibrous cap in the direction of the flow,
resulting in higher strains and thus higher mechani-
cal stresses in the upstream portion of the plaque cap,
potentially increasing the risk of cap rupture. The
peak stress behavior of the most critical cases (thin
fibrous cap and soft lipid core) at various degrees of
stenosis was analyzed. For mid-range stenosis from
43% to 75%, there was a plateau region revealing
that mild and moderate plaques were quickly exposed
to the high stress condition of severe plaques. In con-
clusion, the particular combi nation of a mild to severe
stenosis, a thin fibrous cap and a soft lipid core re-
sulted in the highest mechanical stresses calculated at
the proximal side of the plaque. Mild and moderate
plaques can be subjected to stresses similar to severe
plaques, possibly contributing to their rupture.
Keywords: Coronary Atherosclerotic Plaque; Fibrous
Cap; Stenosis Severity; Lipid Core; Fluid-Structure
Atherosclerosis is a chronic inflammatory response in the
arterial walls that narrows the lumen of vessels by the
gradual deposition of fatty substances, cholesterol crys-
tals, cellular waste products and calcium minerals, and
the growth of connective tissue [1,2]. These localized
pathological lesions are known as atheromatous plaques.
Covering the plaque’s core is the fibrous cap, which is a
layer of fibrous connective tissue and smooth muscle
cells that prevents the core’s highly thrombogenic con-
tents from coming into contact with blood. The rupture
of the fibrous cap, either by mechanical or by biological
factors, may trigger a biological response of platelet ac-
tivation and subsequently thrombus formation. It is esti-
mated that two thirds to three quarters of all arterial
thrombi are caused by plaque rupture [3]. This event
could potentially occlude the vessel and prevent blood
perfusion downstream, resulting in an acute myocardial
infarction. Clinicians have established from histopatho-
logical studies that ruptured plaques share certain mor-
phological and biological features that would make them
more vulnerable to rupture. Unstable lesions with a large
and soft lipid core, many inflammatory cells, and a thin
fibrous cap are typically associated with acute coronary
syndromes [4-6]. It is now recognized that plaque vul-
nerability leading to rupture is an important cause of
myocardial infarction, and sudden cardiac death.
The characteristics of culprit lesions suggest the con-
tribution of mechanical factors in plaque vulnerability for
rupture. From a mechanical point of view, plaque rupture
would occur when the stresses within the fibrous cap
tissue surpass the ultimate strength of the material.
Therefore, identifying the critical stress state within the
diseased tissue could potentially elucidate plaque me-
chanical failure mechanisms. Numerous studies have
demonstrated that plaque component material properties
*Corresponding author.
R. Galaz et al. / J. Biomedical Science and Engineering 6 (2013) 38-46 39
and lesion morphology influence the mechanical stress
distribution within the fibrous cap tissue and could play
an important role in plaque rupture [7-11].
While there is an agreement in the scientific community
that mechanical factors influence the site and mode of
tissue failure, it is not yet fully understood to which ex-
tent the different factors, specifically fluid and solid
stresses, affecting the initiation and progression of such
failure. A histopathological study of patients who had
died during physical exertion showed that ruptures were
commonly located in the midcap regions of the plaques
whereas patients who died at rest showed shoulder rup-
ture predominance [12,13]. Changes in cardiac output
induce non-uniform changes in both the fluid and solid
stress states and therefore, these findings suggest that
mechanical factors influence plaque rupture, and that
different rupture mechanisms may occur in different pa-
tient cases as a result of altered stress states. For example,
it has been proposed that lateral plaque shoulder ruptures
are the results of cyclic tensile stress induced by the
pressure wave [13] and that the high shear stress up-
stream of the plaque induces fibrous cap thinning [14].
While significant work has been done in order to
evaluate the stresses within unstable plaques, the quanti-
fication of the relative effect of unstable plaque charac-
teristics (core size and stiffness, fibrous cap thickness,
etc.) on the mechanical stress state of the diseased vessel
has not systematically been done. Therefore, the objec-
tive of this study was to evaluate the role of 3D me-
chanical stress as a factor that might contribute to the
vulnerability of plaques for rupture, emphasizing the
morphological and material property features. The phy-
sical interaction between blood flow and the tissue is
examined by using FSI computational models of syn-
thetic and standardized geometries of coronary arteries
with varying degrees of stenosis. The performed analysis
quantifies the effect of the thickness of the fibrous cap,
the stiffness of the core and the degree of luminal nar-
rowing on the plaque cap mechanical stress. These three
variables have been described by pathologists and clini-
cians as those might increase plaque vulnerability for
rupture [4-6].
2.1. Geometry of Stenosed Coronary Artery
The simplified synthetic geometry of the coronary artery
was cylindrical, with dimensions corresponding to those
of the proximal third portion of the major epicardial
coronary arteries. This location is where most plaque
ruptures are observed and where the risks of obstructing
blood flow to large regions downstream of the myocar-
dium are the highest [15]. The dimensions of the ideal-
ized stenosed coronary artery were: 3 mm for the lumen
diameter of the artery, 0.5 mm for the artery wall thick-
ness, 20 mm for the total length of the artery segment
and 15 mm for the length of the stenosis at its base
(which corresponds to a slightly diffuse thickening). The
center of the stenosis was coincident with the center of
the segment (see Figure 1).
The stenosis geometry was modeled as an eccentric
blister type protrusion using a symmetrical Gaussian
curve along the longitudinal axis and different heights to
mimic different degrees of stenosis (see Figure 2).
Fibrous Cap
Lipid Core
Figure 1. Schematic of the idealized stenosed coronary artery.
Lc is the length of the coronary artery segment (here of the
cylinder) (=20 mm), Ls the length of the stenosis (=15 mm), D
the coronary artery lumen diameter (=3 mm), Tw the coronary
artery wall thickness (=0.5 mm), and TFC the fibrous cap thick-
(a) (b)
Fi gure 2. The ten different stenosis severities used in this study.
(a) Longitudinal view, and (b) Radial view.
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R. Galaz et al. / J. Biomedical Science and Engineering 6 (2013) 38-46
2.2. Computational Model for the Structural
The stresses within the fibrous cap were analyzed using a
standard commercial structural mechanics software
(ANSYS, Canonsburg, PA, USA). Since mechanical de-
formations are not large, linear elastic and isotropic ma-
terial properties were used for both the coronary artery
wall and the fibrous cap. The stiffness of the fibrous cap
was initially assumed to be equal to the stiffness of the
coronary artery wall, Ea, and assigned a value of Ea =
800 kPa for the Young’s modulus (calculated using the
Lame equations for the specified vessel dimensions and a
maximum luminal diameter expansion of 5%). The ma-
terial was assumed to be incompressible due to the high
water content in the tissue; therefore a Poisson’s ratio ν =
0.49 was used.
The necrotic lipid core stiffness, Ec, is modeled with a
very low Young’s modulus Ec 0 Pa, representing a soft
lipid core, to a very high value, Ec >> Ea, representing
very stiff plaque components such as fibrotic tissue cal-
cifications. In this study, the maximum value of the
plaque core stiffness was taken to be equal to that of the
arterial wall. The ratio between the stiffness of the lipid
core and that of the coronary artery wall was defined as γ,
the stiffness ratio (Eq.1).
2.3. Computational Model for the Fluid Domain
The fluid domain was modeled using a standard com-
mercial computational fluid dynamics package (ANSYS-
CFX, ANSYS Inc., Canonsburg, PA, USA). The income-
pressible and steady-state Navier-Stokes equations (Eq.2)
were used and the flow was assumed to be Newtonian.
 
 
uu u0
where ρ is the fluid density, u is the velocity, p is the
pressure and µ is the viscosity. The fluid was assigned a
viscosity of 3.6 MPa and a density of 1050 kg/m3 to
match the properties of blood. Physiological hemody-
namic conditions were applied as boundary conditions
with a fully-developed laminar inlet profile (parabolic)
corresponding to a maximum average phasic coronary
flow of 100 ml/min (Figure 3) [16] and a base inlet
pressure of 100 mmHg [17]. The same flow rate was
used in the different models to study the morphological
and material properties. At the fluid-solid interface, no-
slip boundary conditions were applied.
2.4. Coupling of Structural and Fluid Domains
A unidirectionally-coupled fluid-structure interaction
Inlet Velocity Profile
Radial Position [mm]
1.5 1 0.5 0 0.5 1 1.5
Velocity [cm·s
Figure 3. Fully developed inlet parabolic profile corresponding
to a maximum average phasic coronary flow of 100 mL/min.
(FSI) analysis was performed wherein the pressure gra-
dient results obtained from the fluid analysis were ap-
plied as an external load in the structural analysis. A
structural domain change would translate to a change in
the fluid domain in the same proportion. Due to their
small magnitudes, the changes in the fluid domain and
the corresponding changes in flow field were neglected,
allowing for the treatment of the problem using a unidi-
rectional framework. Both fluid and structural domains
were discretized into approximately 50,000 tetrahedral
elements, which was found to be sufficient based on a
mesh sensitivity analysis.
Using the above procedure, 80 parameterized FSI
analyses were performed for a sensitivity analysis to as-
sess the effect of plaque morphology and material prop-
erties on the magnitude of the mechanical stress within
the fibrous cap. The three main variables investigated
were the stenosis severity, the fibrous cap thickness, and
the stiffness ratio. Four different coronary artery stenosis
severities were selected: 36%, 51%, 75% and 91% and
four fibrous cap thicknesses varying from 200 to 500
microns and five stiffness ratios varying from 0.001 to 1
were taken. The results of the parameterized FSI analy-
ses were used to construct surface plots of the resulting
peak stress values within the plaque. The conditions,
with respect to the fibrous cap thickness and the stiffness
ratio, that produced the critical stress state were identi-
fied and utilized in a separate FSI analysis for the en
stenosis severities displayed in Figure 2, in order to as-
sess the impact of stenosis severity on the plaque’s me-
chanical stress.
The influence of plaque geometric features on solid
stresses in the vascular wall and fibrous cap were inves-
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R. Galaz et al. / J. Biomedical Science and Engineering 6 (2013) 38-46 41
tigated. More specifically, parameters that have been
clinically reported to influence plaque vulnerability for
rupture, namely fibrous cap thickness, plaque core com-
position, and stenosis severity were considered. All FSI
computations resulted in a stress concentration in the
arterial wall, at the proximal side of the plaque (Figure
3.1. Effect of Lipid Pool Stiffness and Fibrous
Cap Thickness: Sensitivity Analysis
The results of the sensitivity analysis are provided in
Figure 5. The surface plots display the relationship be-
tween the maximum principal stresses in the fibrous cap
as a function of stenosis severity, fibrous cap thickness
and stiffness ratio. As expected, the highest stresses oc-
curred under the condition of the thinnest plaque cap and
the lowest stiffness ratio for all characteristic plaque se-
verities. Moreover, under this critical condition, as steno-
sis severity increased, the magnitude of the maximum
principal stress also increased.
It can be observed in the surface plots that when the
stiffness ratio is greater than a value of approximately 0.3,
the maximum principal stresses in the fibrous cap appear
to become constant, and therefore independent of stiff-
ness ratio, stenosis severity, and fibrous cap thickness.
Below a stiffness ratio of about 0.3, as both the stiffness
ratio and the cap thickness decrease, the maximum
stresses increase. It is interesting to observe that as the
fibrous cap thickness decreases, the calculated stresses
become more sensitive to changes in stiffness ratio
(steeper variations). In other words, at low cap thickness
(for example, at the minimum value), the results show
that a small decrease in the stiffness of the plaque core
results in significant increase in the maximum principal
Blood Flow Direction
Figure 4. Longitudinal view of a typical mechanical stress
distribution obtained from the FSI analysis. All stenosis sever-
ities resulted in high stress concentrations in the arterial wall,
proximal to the stenosis.
Figure 5. Maximum principal stresses for four different steno-
sis severities: (a) 36%, (b) 51%, (c) 75%, and (d) 91%.
Copyright © 2013 SciRes. OPEN ACCESS
R. Galaz et al. / J. Biomedical Science and Engineering 6 (2013) 38-46
stresses present in the fibrous cap. When the stiffness
ratio is taken to be constant, a decrease in the plaque cap
thickness results in a more direct increase in stresses to-
wards the maximum value at the minimum plaque thick-
ness. It is important to note that the fibrous cap thick-
nesses considered in this study are above the value for
which plaques have been clinically observed to rupture
(approximately 65 microns) [18].
It can be observed that the magnitude of the stresses in
the fibrous cap appear to be independent of the stenosis
severity, even for severe area reductions, when the stiff-
ness ratio is in the range of 0.1 to 0.3. Moreover, when
the stiffness ratio decreases to a low level such that the
core is essentially a soft lipid pool, the magnitude of the
principal cap stresses still appears to be relatively con-
stant for intermediate stenoses, yet increases significantly
when the area reduction becomes severe.
3.2. Effect of Stenosis Severity
The effect of stenosis severity on the stress state of the
fibrous cap was investigated by performing FSI analyses
for ten different area reductions (ranging from 19% to
91%, Figure 2) under the critical stress condition of
small fibrous cap thickness and low lipid core stiffness
ratio. In Figure 6, the normalized principal stress in the
fibrous cap is plotted as a function of the percent area
reduction for the minimal cap thickness (200 microns)
and the minimal lipid core stiffness ratio (0.001), which
appeared from the sensitivity analysis to be the condition
for which the stresses were most sensitive to percent
The results displayed in Figure 6 show three distinct
regions where stresses increase with different rates as a
function of the area stenosis, which correspond to mild,
Percentage of stenosed area [%]
0 10 20 30 40 50 60 70 80 90 100
Normalized principal stress
Figure 6. Normalized principal stress for different stenosis
severities in the case of a fibrous cap thickness of 200 microns
and a stiffness ratio between the lipid core and the coronary
artery wall, γ, of 0.001.
intermediate and severe stenoses, based on the percent
area reduction. For both mild (19% to 43% area reduc-
tion) and severe (greater than 75% area reduction)
stenoses, the rate of increase of the peak stress with in-
creasing area reduction is significant, particularly for
severe stenoses which display a steep slope. However, in
the case of intermediate stenoses (43% to 75% area re-
duction), the plot displays a plateau region where there is
a relatively small increase in peak stress over the range
of lesion severity.
In previous investigations of the role of mechanical fac-
tors on plaque vulnerability for rupture, much focus has
been put on 2D/3D structural finite element analyses
separate from fluid dynamic analyses. For example, stu-
dies have shown through 2D (cross-sectional views) and
3D finite element models that high stress regions corre-
spond to the culprit (rupture) zones in histopathological
studies and that the magnitudes of these stresses are af-
fected by plaque composition and morphology [19,20].
On the other hand, computational fluid dynamics analy-
ses have also correlated the location of high wall shear
stress to that of plaque ulceration [21].
However, when structural and fluid analyses are con-
sidered separately (and particularly in a 2D model), the
true state of the stress tensor is not fully represented for
either domains and the complex interactions between
plaque morphology, plaque composition and fluid and
solid forces on the global stress state cannot be evaluated.
Therefore, in order to obtain a better understanding of
the true physical events taking place in the diseased ves-
sel, it becomes necessary to use 3D models that incorpo-
rate the interactions between the fluid and structural do-
mains. These models would provide more accurate nu-
merical evidence on the spatial stress distribution and the
longitudinal component of the shear stress caused by
blood flow. Moreover, when combined with localized
anisotropic material properties and a mechanical failure
criterion, the analyses could define the proper orientation
and the extent of rupture propagation. The 3D numerical
results could serve as a basis to compare the spatial loca-
tion of the rupture with clinical evidence that often re-
ports plaque rupture locations, for example, at the up-
stream regions of the stenosis [22,23]. Tang and col-
leagues have developed 3D fluid-structure interaction
(FSI) models based on MRI scans and have displayed
that regions of localized maximum stresses, particularly
solid stresses, correspond well with the location of
plaque ulceration identified from histopathological eva-
luations. The magnitude of the stresses in ulcerated
plaques was also found to be higher than that of stable
plaques, and also displayed a general increasing trend in
unstable plaques with larger lipid pools and thinner
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R. Galaz et al. / J. Biomedical Science and Engineering 6 (2013) 38-46 43
plaque caps [17,24,25].
The idea that mechanical factors play a role in the
rupture of plaques has been agreed upon in the scientific
community although the exact mechanisms by which
these factors, specifically solid and fluid stresses, initiate
plaque damage, are unclear. From a mechanical perspec-
tive, it can be expected that the fibrous cap will rupture
when the solid stresses therein surpass the material’s
ultimate strength (Lee and Loree [26]). Consequently, the
global solid stress state within the fibrous cap is a central
factor in the study of plaque fracture mechanics; it is
affected by the fluid forces (cyclic pressure, pressure
gradients) exerted on and the morphology and material
properties of the tissue. Fluid shear stresses could affect
the surface of the plaque as well as activate endothelial
cells to produce and secrete degrading enzymes that
weaken the structure of the fibrous cap.
A stenosis impedes the flow of blood and induces an
energy loss which is reflected as a pressure drop across
the stenosis. This loss in energy is a result of inertial
pressure losses from geometrical changes, and viscous
effect. It is dissipated from the system in the form of heat
(carried away by flow advection), and in the form of ir-
reversible mechanical deformation, specifically of the
viscoelastic fibrous cap which is the most mechanically
solicited component of the plaque. The hemodynamic
pressure gradient exerts a force on and causes deforma-
tion of the plaque in the direction of the bulk flow, which
results in higher solid stresses at the proximal side of the
fibrous cap, compared to the distal side. This effect is
amplified when the fibrous cap of the plaque is thin and
has a weak structural support underneath it, as was
shown in our study for the case of a soft lipid core which
acts as a weak elastic foundation. This effect has also
been proposed by Doriot [27] and Li [11] using theoreti-
cal and numerical calculations with only 2D longitudinal
models of stenosed arteries.
Our numerical results were consistent with clinical
observations. Fujii et al. [22] have shown that most of
the ulcerated ruptured plaques in culprit lesions of acute
coronary syndrome patients were proximal to site of
minimal lumen dimension based on intravascular ultra-
sound imaging studies. Hiro et al. [23] have also reported
ultrasonographic longitudinal views of ruptured coronary
plaques, and most of them were also located in the
proximal region of the plaque.
4.1. Plaque Cap Principal Stresses
Thin fibrous caps and soft lipid cores have been clini-
cally associated with higher rupture risk. The values ob-
tained in this study for the maximum principal stresses
are consistent with similar studies. In a 2D (cross-sec-
tional) structural analysis, Finet et al. [8] obtained maxi-
mum principal stresses in coronary plaques between 100
kPa and 200 kPa (at a pressure of 110 mmHg, a cap
thickness of 200 microns and a core stiffness of 1 kPa)
for stenoses of approximately 50 - 60 percent area reduc-
tion. Our results gave maximum principal stresses of 85
kPa for similar conditions (baseline pressure of 100
mmHg, a cap thickness of 200 microns and a stiffness
ratio of 0.001). Arterial dimensions in Finet et al. were
greater than those in the present study and can account in
part for the differences in stress magnitude.
Tang et al. [24] performed FSI analyses on coronary
plaques for which the morphology was obtained from ex
vivo MRI of cadaveric samples. For an approximate area
reduction of 80%, a pressure of 100 mmHg the maxi-
mum principal stresses were found to range from 100 -
200 kPa at the interface of the lipid core and the lumen,
which again corresponds well to the 90 - 100 kPa stress
range found in the current study for the thin plaque cap
and the soft lipid core. A similar study by the same au-
thors [28], which also addressed the issue of cyclic bend-
ing, found principal stress values within the plaque cap
within the 50 - 80 kPa range.
4.2. Plaque Cap Thickness and Core Stiffness
Our results showed that plaque cap stresses were found
to be very sensitive to small changes in the core stiffness
at low stiffness ratios. These findings are similar to those
of [8] who showed that for a critical cap thickness of 50
microns, a small change from a core stiffness of 25 kPa
to 1 kPa could destabilize the plaque (specifically, in-
crease the circumferential cap stresses over a predefined
threshold corresponding to rupture initiation).
Virmani et al. [18,29] first introduced a critical cap
thickness below which coronary plaques are at high risk
for rupture. This value was found to be approximately 65
microns and has since been adopted by the American
Heart Association. Through computational studies, a cir-
cumferential fibrous cap stress of 300 kPa has also been
found to correspond to the threshold for coronary plaque
rupture [19] and is consistent with the critical cap thick-
ness. Previous studies have found a curvilinear/exponen-
tial relationship between the cap thickness and the
circumferential stresses [8,30], and that significant in-
crease in principal stress with a small decrease in cap
thickness occurs near this critical value. The results of
this study displayed a more direct relationship between
the stress and the cap thickness which seems to contra-
dict previous findings. It is important to note however,
that the minimum cap thickness considered in this study
is well above the critical value and the corresponding
principal stresses are also below the 300 kPa threshold.
The relative contribution/effect of plaque core compo-
sition and fibrous cap thickness has not been elucidated
thus far yet could have significant clinical implications.
The results of our study suggest that one of these vari-
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R. Galaz et al. / J. Biomedical Science and Engineering 6 (2013) 38-46
ables may play a more central role in the initiation of
plaque ulceration. The relatively constant principle
stresses when the stiffness ratio is above 0.3, independent
of both fibrous cap thickness and percent stenosis, sug-
gests that there may be a threshold for plaque stiffness
above the risk of rupture is reduced. Furthermore, the
fact that the maximum principal stresses at the minimum
core stiffness were well below the critical plaque rupture
stress, suggests that the thickness of the plaque cap may
have greater influence on plaque vulnerability for rupture
compared to core stiffness.
4.3. Stenosis Severity
One of the most interesting results of this study was a
quasi-constant region (plateau) of peak principal stress
with increasing stenosis severity for intermediate lesions
(the maximum principal stress was relatively insensitive
to percentage of stenosis). A similar observation was
reported in a clinical investigation by Li et al. [11] in the
carotid artery; they found that the peak principal stress
remained relatively constant for a degree of luminal
stenosis comprised between 40% and 60%, and for a
fibrous cap thickness ranging from 0.2 mm to 1 mm.
The clinical implications of these findings are worthy
of note. For intermediate stenoses, the results suggest
that the vulnerability to rupture may be insensitive to the
severity of the lumen reduction (above and below certain
thresholds) in terms of stress loading and the size of the
lipid pool.
4.4. Limitations
The minimum thickness of the fibrous cap in our model
was 200 microns although pathologists have reported
that the typical thickness at which fibrous caps fail is
around 65 microns [29]. This value facilitated the mesh-
ing of the fibrous cap and allowed to avoid being in a
situation of rupture. However, the computed stress could
be underestimated.
Another limitation of this model was that the me-
chanical properties of the fibrous cap were the same as
those of the artery wall. The mechanical properties of the
fibrous cap are still unknown, and they can vary from
patient to patient. The fact that the fibrous cap is mostly
composed of collagen fibers and some smooth muscle
cells is hint that it is reasonable to assume that its me-
chanical properties are similar to the artery wall. How-
ever, it should be somewhat stiffer since it has a higher
ratio of collagen although it was found in [17] that in-
creasing the stiffness of the fibrous cap by 100% has
minor effects (less than 2%) on the stress state within the
Finally, in order to obtain a more accurate model in
terms of anatomical structure and physiological condi-
tions, it becomes necessary to analyze realistic geome-
tries of the coronary arteries and include more realistic
material properties such as viscoelasticity and anisotropy
of the connective tissue. Furthermore, it has been shown
that cyclic bending of the arteries can have a significant
effect on the magnitude of the peak principal stresses
[28]. This idea is of particular importance for coronary
arteries which are subjected to such a loading due to the
cyclic contraction of the heart, and must be considered in
order to better understand the relative importance of
plaque morphology (size and cap thickness) and plaque
composition on its vulnerability to rupture.
Using FSI simulations, the 3D mechanical stress in dis-
eased coronary arteries was calculated for varying plaque
cap thickness, lipid core stiffness and stenosis severity
and evaluated as a factor that might contribute to a
plaque’s vulnerability to rupture. The peak principal
stresses were observed at the proximal side of the plaque
in all FSI analyses which was consistent with pathologi-
cal observations for plaque ulceration locations. The im-
portant findings of this investigation included the fact
that 3D mechanical stresses were observed to be more
sensitive to changes in fibrous cap thickness compared to
changes in core thickness which suggested that cap
thickness could play a more central role in plaque rupture
vulnerability compared to other morphological plaque
characteristics. It was also found that at a critical cap
thickness, a small change in plaque composition could
significantly change the peak principal stresses and thus
the plaque’s vulnerability to rupture. Furthermore, the
peak principal stresses of moderate stenoses (ranging
from 43% to 75% area reductions) were found to be
generally unaffected by stenosis severity (at a particular
cap thickness and core stiffness), displayed by a plateau
in the stresses as a function of severity. This observation
not only suggests that moderate and even mild plaques
could have the same vulnerability to mechanical failure
but that they can be subjected to stresses similar to se-
vere plaques that could contribute to their rupture.
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