Brief Review

New Approaches to Abdominal Aortic Aneurysm Rupture

Risk Assessment
Engineering Insights With Clinical Gain
Timothy M. McGloughlin, Barry J. Doyle

Abstract—Abdominal aortic aneurysm (AAA) rupture remains a significant cause of death in the developed world. Current
treatment approaches rely heavily on the size of the aneurysm to decide on the most appropriate time for clinical
intervention and treatment. However, in recent years, several alternative rupture risk indicators have been proposed. This
brief review examines some of these new approaches to AAA rupture risk assessment, from both numeric and
experimental aspects and also what the future may hold for AAA rupture risk. Although numerically predicted wall
stress, finite element analysis rupture index, rupture potential index, severity parameter, and geometric factors, such as
asymmetry, have all been developed and show promise in possibly helping to predict AAA rupture risk, validation of
these tools remains a significant challenge. Validation of biomechanics-based rupture indicators may be feasible by
combining in vitro modeling of realistic AAA analogues with both retrospective and prospective monitoring and
modeling of AAA cases. Peak wall stress is arguably the primary result obtained from numeric analyses; however, as
the majority of ruptures occur in the posterior and posterior-lateral regions, the role of posterior wall stress has also
recently been highlighted as potentially significant. It is also known that wall stress alone is not enough to cause rupture,
as wall strength plays an equal role. Therefore, should a biomechanics-based rupture risk be implemented? There have
been some significant steps, both numerically and experimentally, toward answering this and other questions relating
to AAA rupture risk prediction, yet regardless of the efforts that are under way in several laboratories, the introduction
of a numerically predicted rupture risk parameter into the clinicians’ decision-making process may still be quite some
time away. (Arterioscler Thromb Vasc Biol. 2010;30:1687-1694.)
Key Words: aneurysms 䡲 risk factors 䡲 experimental modeling 䡲 numerical modeling 䡲 review 䡲 rupture risk

A pproximately 81 million people in the United States are

currently living with one of the many forms of cardio-
vascular disease. Of this affected population, it is estimated
that about 900 000 will die each year. Abdominal aortic
aneurysm (AAA) is a dilation of the aorta beyond 50% of the
normal vessel diameter, and it accounts for approximately
15 000 deaths per year in the United States.1 AAA rupture
risk is typically determined by size, and it has been shown
that in the 5 years following AAA diagnosis, rupture
occurs in approximately 2% of AAAs less than 4 cm in
diameter and in more than 25% of AAAs larger than 5
cm.2,3 Current clinical practice is to surgically repair large
AAAs (diameter ⬎5.5 cm) if the patient is fit for surgery
or to regularly monitor (eg, every 6 months) smaller AAAs
(diameter ⬍5.5 cm) with ultrasound, with referral for
surgery if the growth rate exceeds 1 cm/year or the
diameter exceeds 5.5 cm.3 However, surgeons need to
compare the risk of rupture with the risk of repair, as it has
been reported that only 25% of AAAs rupture in a patient’s
lifetime,4,5 and there can be serious complications with
both open repair and endovascular aneurysm repair.
Recent research has cast doubt over the suitability of
surgical repair based solely on the maximum diameter crite-
rion.6 –17 It is known that small AAAs can rupture and large
AAAs can remain stable; therefore, many believe that factors
other than size should be considered. Some interesting
rupture risk parameters have recently emerged as alternatives
to AAA size. AAA wall stress,7,8 vessel asymmetry,11 finite
element analysis rupture index (FEARI),12 rupture potential
index (RPI),9 severity parameter (SP),10 growth of intralumi-
nal thrombus,18 and a method of determining AAA growth
and rupture based on mathematical models19,20 have all been
proposed as useful adjuncts to AAA size, yet all require
extensive validation before they can be clinically accepted.
Several of these newer approaches to rupture risk rely on
biomechanics and numeric models to quantify the threat. In
particular, finite element analysis (FEA) has been extensively
used to determine the distribution of wall stress in the

Received on: February 6, 2010; final version accepted on: May 10, 2010.
From Centre for Applied Biomedical Engineering Research, Department of Mechanical and Aeronautical Engineering, and the Materials and Surface
Science Institute, University of Limerick, Ireland.
Both authors contributed equally to this work.
Correspondence to Timothy M. McGloughlin, MSG-014, MSSI Building, University of Limerick, Limerick, Ireland. E-mail tim.mcgloughlin@ul.ie
© 2010 American Heart Association, Inc.
Arterioscler Thromb Vasc Biol is available at http://atvb.ahajournals.org DOI: 10.1161/ATVBAHA.110.204529

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1688 Arterioscler Thromb Vasc Biol September 2010
aneurysm and has revealed some interesting correlations with
both AAA asymmetry11 and AAA geometry.21 Overall AAA
wall stress has been shown to be independent of maximum
diameter,5–16 hence the general understanding that more than
size alone should be considered in rupture risk evaluation.
This article reviews some of the more recent advances in both
numeric and experimental engineering methodologies used to
investigate the possible rupture risk of patient-specific AAAs.
Computational AAA Rupture Risk
The law of Laplace states that there is a linear relationship
between diameter and wall stress and is often applied to AAA
to calculate the mechanical stress acting on the vessel wall.
However, the law of Laplace is based on cylindrical geome-
tries, whereas AAAs are complex structures, and therefore
the law fails to predict realistic wall stresses. Stringfellow
et al22 applied FEA to the problem to determine wall stress
and paved the way for the extensive research into numerically
predicted AAA wall stress that is currently being performed.
It was concluded in this article that FEA (and therefore
computational modeling) is a versatile tool for use in the
study of vascular mechanics and may be potentially more
useful than size alone in determining the clinical significance of
AAAs.22 That work, however, used idealized AAA models,
whereas actual AAAs are typically highly irregular structures,
and the wall stress is not evenly distributed.5,6,9,11–16,21,23 Since
the late 1980s, the use of FEA has proven to be a very
useful method in determining patient-specific AAA wall
stress6 – 8,11–17,22–24 and has also been coupled with computa-
tional fluid dynamics to provide more accurate estimations of
the AAA wall stress though fluid-structure interaction tech-
niques.25–27 However, there are still mixed opinions as to the
possibly insignificant increase in wall stress accuracy when
using fluid-structure interaction compared with the very
significant increase in computational time. The use of com-
putational fluid dynamics has proven effective in analyzing
the hemodynamics of AAAs and has resulted in a new tapered
graft28 design that may help reduce the blood flow problems
and biomechanical performance associated with traditional
stent-graft designs.29
Numeric modeling has repeatedly highlighted the pitfalls
of solely using the diameter criterion. Fillinger et al7,8
demonstrated that peak wall stress may be a better indicator
of rupture than diameter, and it has since been reported by
several groups that equivalent diameter AAAs may have
largely different rupture potentials.5,9,12 Also, it has previ-
ously been shown30 –32 that AAA wall strength can vary
significantly within a particular aneurysm, and therefore to
fully understand the likelihood of rupture based on peak wall
stress, the AAA wall strength must also be considered. A
biomechanics-based rupture-prediction tool was recently de-
veloped by the authors,12 whereby FEA-computed peak wall
stress is coupled with the wall strength of that region
determined by mechanical testing.30 –32 This method is termed
the FEARI and is based on the definition of material failure;
that is, an AAA will rupture when the local stress exceeds the
local strength. The FEARI returns a simple rupture index by
dividing the peak wall stress by the strength at that location
with values close to 1, indicating a high rupture risk, and 0,
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indicating a low rupture risk (Figure 1). When FEARI results
were compared between electively repaired (n⫽42) and
ruptured (n⫽10) AAA cases, FEARI was significantly higher
in the ruptured group (FEARI⫽1.01⫾0.43 vs 0.66⫾0.3,
P⫽0.018). The FEARI predictive tool indicated that not all of
the cases examined may have required surgical intervention
and revealed that AAAs with similar diameters may have
markedly different rupture potentials, therefore implying that
maximum diameter is not a “one-size-fits-all” approach to
AAA management. The FEARI method relies on mechanical
testing of AAA tissue and therefore is dependent on the
accuracy of the mechanical test to represent patient-specific
tissue strength. A significant limitation of this rupture index is
the low numbers of tissue samples tested. The strength
component of the model is based on published literature,
specifically tensile test data obtained from 149 AAA tissue
samples harvested from 69 patients.30 –32 Mechanical data for
AAA tissue are difficult to obtain, primarily because the
majority of AAA cases are repaired using minimally invasive
techniques, and therefore the abdomen is not opened. Also,
excised tissue samples are usually harvested from the anterior
regions of the AAA, as there are increased surgical complex-
ities and risks associated with tissue removal from the
posterior regions of the aneurysm. If a large, multicenter
study could actively seek AAA tissue for mechanical testing,
the population-based accuracy of the model could be further
enhanced, thus improving the FEARI.
Another biomechanics-based rupture index has also been
suggested9 and may be more clinically applicable than
FEARI. The RPI, which was developed by the Vorp group at
the University of Pittsburgh, uses a combination of experi-
mental tensile testing and statistical modeling to predetermine
the wall strength on a patient-specific basis,33 with wall stress
then predicted using FEA. Although both FEARI and RPI are
similar in their working hypotheses, RPI uses a more sophis-
ticated technique to determine wall strength. The strength of
AAA tissue is calculated using parameters such as age, sex,
smoking status, family history of AAA, normalized diameter,
and the maximum thickness of the intraluminal thrombus.
RPI was reported to possibly identify high rupture risk AAAs
a priori better than either diameter or peak wall stress alone
(Figure 2).9 The potential of RPI to become a useful rupture-
prediction tool may be significant, although the approach
requires extensive validation before it can be considered in a
clinical setting.
Kleinstreuer and Li10 have reported a novel rupture risk
tool that incorporates 8 weighted biomechanical parameters
that return a dimensionless SP. They reported that their SP
may be clinically applicable and were able to show how the
SP values of 3 different AAA cases available in literature
were similar to the actual clinical decisions of either “waiting
for repair” or “possible rupture.” The same authors have also
reported, in a separate publication,34 an equation that can
predict the maximum wall stress of an AAA to within 9.5%
of that computed using FEA. The 9.5% difference was
obtained by applying their new equation to 10 different
AAAs previously reported in the literature. This novel equa-
tion is an adaption of the law of Laplace, which takes into
account geometric ratios and parameters, as well as the
 McGloughlin and Doyle
maximum vessel diameter and the blood pressure of the
patient. The accuracy of these 2 approaches10,34 reduces
greatly with geometric complexities, and also these tools fail
to pinpoint the location of peak stress, which is vital to
comprehensively determine the likelihood of rupture.5 As
with all computational tools, there is a need to determine the
clinical feasibility of using such methods to assess rupture
potential.
More than 3 decades ago, Darling et al4 reported that 82%
of AAA ruptures occur along the posterior and posterior-
lateral wall. As the majority of ruptures occur in the posterior
regions, the wall stress acting on these regions may have
clinical relevance. This hypothesis encouraged research into
the influences on posterior wall stress, and it was found that
the asymmetry of the AAA is strongly related to the posterior
wall stress distribution.11 In that report, the authors developed
a simple method of measuring AAA asymmetry and observed
that inflection points, which are regions where the curvature
changes from concave to convex, were deemed to be the
likely regions of peak or high wall stress, observations that
have been noted in other studies.5,12–17 The work postulated
that asymmetry could become a useful addition to diameter in
determining AAA severity. Others have also recently exam-
ined the role of geometry on AAA wall stress21 by measuring
the tortuosity instead of the asymmetry in 19 patient-specific
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New Approaches to AAA Assessment 1689
Figure 1. A, Anterior view of a represen-
tative patient-specific AAA stress distri-
bution with peak stress indicated (black
triangle). B, Peak stress location corre-
sponds to the anterior region of the an-
eurysm; therefore, wall strength for that
region can be determined from
population-mean tensile test data. C,
FEARI results for 42 repaired and 10
ruptured AAA cases. Horizontal line at
1.0 indicates rupture. Preliminary results
using the FEARI show that many
repaired AAA may not have presented a
high rupture risk; equally, several rup-
tured cases appear to have low rupture
risk indices. Clearly, the approach needs
further investigation and validation
before clinical applicability is
established.
cases. In that study, the authors conclude that diameter does
statistically influence peak wall stress but that tortuosity may
also affect wall stress. Although clinicians do consider AAA
geometry when determining the likelihood of rupture, they
may often be interpreting the geometry with endovascular
aneurysm repair in mind rather than in relation to the effect on
wall stress. Geometry plays a vital role in wall stress
distributions, and the results of a patient-specific stress
analysis may serve as useful decision aides for the clinician.
Experimental validation of biomechanical approaches to
rupture assessment may be possible through the use of the
experimental methodologies developed and reported previ-
ously.13,17,35 It is now possible to create patient-specific
rubber AAA models36 that are nonuniform in wall strength35
similar to the in vivo situation.31 These models can then be
studied using the rupture technique reported by the au-
thors.13,17 Identifying the rupture locations of these experi-
mental models and comparing them with the numerically
predicted rupture site using biomechanical models may help
toward in vitro validation. Preclinical validation, however, is
difficult to achieve and significantly more costly. Retrospec-
tive clinical validation may be made possible by predicting
the rupture threat using the proposed biomechanics-based
indicator and applying this model to AAAs that have previ-
ously ruptured. By comparing the rupture prediction with the
1690 Arterioscler Thromb Vasc Biol September 2010
Figure 2. A, Contours of FEA-predicted wall stress. B, Noninva-
sively determined wall strength. C, Corresponding RPI for a
patient-specific AAA. Reprinted with permission from Vorp and
Vande Geest.61
actual clinical outcomes, it may be possible to show that
certain ruptured AAAs have significantly higher rupture risk
indices compared with electively repaired and monitored
cases.
It may also be possible to prospectively validate these tools
by monitoring the biomechanics-based rupture threat in
patients who are followed over time. Suitable candidates who
could be included are patients who have a small AAA
(diameter ⬍5 cm) and are regularly monitored for AAA
enlargement, patients who refuse surgery, and those patients
who are at high risk and advised against surgical intervention.
This cohort could be followed until their AAA either ruptures
or becomes symptomatic. Biomechanical rupture risk models
could be calculated at every time point using the CT images,
and values could be compared over time. Rupture indicators
could be inspected for correlation with growth patterns and
clinical events and may ultimately work toward the clinical
validation of these new tools.
There are of course some limitations to the clinical vali-
dation strategies of these biomechanical rupture risk param-
eters. Firstly, clinicians will always feel that large AAAs
should be treated if the patient is fit for surgery. Large AAAs
are an obvious clinical concern, with statistics placing them in
the high-risk category, regardless of biomechanical indices.
Conservative management of these cases could possibly
result in fatal circumstances, and therefore biomechanical
parameters should always be used in conjunction with not
only AAA size but also, and possibly more importantly,
clinical judgment. Computational rupture risk indices may be
reserved for small to medium-sized AAAs where regular
monitoring is involved before ever being considered for large
AAAs.
Experimental AAA Rupture Risk
Experimental methodologies do not receive the same atten-
tion as numeric techniques in relation to AAA rupture risk,
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partially because of the labor intensity of manufacturing
patient-specific AAA models, performing experiments, and
ensuring significance of results through repetition and accu-
racy. Numeric modeling, on the other hand, is relatively quick
to perform, and changes can be easily incorporated into
models through parameter-based modeling packages. None-
theless, computationally determined rupture-prediction must
be thoroughly validated before clinical acceptance and for
such an approach to demonstrate the level of robustness
needed for clinical adoption. It is at this stage that experi-
mental AAA rupture risk may play a key role. To facilitate
validation of numeric models, it is now possible to create
patient-specific experimental AAA models by rapid prototyp-
ing37 or injection molding,36,38 with the latter technique
shown to create repeatable anatomically correct benchtop
models for a variety of in vitro modeling applications.36 To
develop accurate representations of the AAA wall, a tech-
nique has been reported that can manufacture silicone AAA
models with random or controlled material properties, with
methods in place to nondestructively assess these material
properties.35 It has also recently been demonstrated that the
intraluminal thrombus, which may significantly influence the
rupture site, can be included in experimental models.39 These
benchtop AAA analogues can be used to determine rupture
locations and validate numerically predicted burst sites.
Experimental rupture modeling was initiated with idealized
AAA geometries17 and progressed to include realistic cases.13
This seminal work used high-speed photography to capture
the rupture site and showed that AAAs rupture at inflection
points and not at regions of maximum diameter. Similar
observations have been reported throughout numeric studies
in the literature, which have shown that inflection points
exhibit higher wall stresses than the maximum diameter
regions.6,11,12 Each experimental model was imaged using CT
before testing to generate accurate numeric reconstructions
for validation purposes using previously reported 3D recon-
struction techniques and the commercially available software
Mimics (Materialise).16,23,36 Rupture occurred at the location
of numerically predicted peak wall stress in 80% of cases and
at high, but not peak, stress regions in 10% of cases. These
sites were also shown to be regions of complex gaussian
surface curvature40 and correlated well with the stress pat-
terns observed using photoelastic stress analysis on the same
geometry.14 Good agreement was found among FEA-
predicted wall stress, experimental rupture site, numerically
predicted surface curvature, and experimental wall stress
(Figure 3). The remaining 10% of models examined in this
study had defects in the AAA wall, which shifted the rupture
location away from regions of elevated wall stress to that of
the defect. Wall defects are also likely to affect rupture
location in vivo, as it was shown that the location of peak wall
stress is not the rupture site in the presence of aortic blebs.41
The methods and techniques reviewed here represent some of
the more significant steps in assessing AAA rupture in vitro,
an area of research that, as mentioned previously, receives
minor attention.
The Future of AAA Rupture Risk
AAA rupture threat is currently the subject of intensive
research, with many aiming to prove that numeric models,
 McGloughlin and Doyle
Figure 3. Comparison of experimental rupture site (A), FEA wall
stress distribution (B), and the gaussian surface curvature (C) for
an example AAA case. Inflection points in C are shown as yel-
low regions. The virtual grid allows easy comparisons between
locations, with all models presented from the anterior view. The
qualitative agreement between the FEA wall stress (D) and the
photoelastic wall stress (E) for the same case is also shown.
and ultimately a biomechanics-based approach to rupture
prediction, may have clinical relevance. As the volume of
reports highlighting the inadequacies of the maximum diam-
eter criterion grow, clinicians may become more aware of the
ease with which alternative rupture risk parameters can be
incorporated into the decision-making process. Several of the
recently proposed risk indicators may be useful additional
tools for the clinician and complement the current use of
maximum diameter and growth rate. These new tools can
return recommendations in as little as a few hours after
medical imaging, depending on the tool used and the facilities
available. Validation of numeric models, in particular FEA,
has been performed in terms of quantitative wall stress
correlations using idealized geometries42,43 and also qualita-
tively by correlating rupture locations13,17 and regions of
curvature.14,15 However, the limitations of numeric modeling
should be noted. An important limitation of FEA is that the
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New Approaches to AAA Assessment 1691
approach does not take into account the hemodynamics of the
situation, which can affect the forces exerted on the aortic
wall. In recent years, many researchers have favored a
fluid-structure interaction approach to aneurysm model-
ing,25–27 yet the significant increase in computational time
compared with the relatively small increase in wall stress
accuracy remains in question. There are, however, many
drawbacks to patient-specific numeric wall stress predictions
that are applicable to all approaches. Aortic wall thickness
still remains elusive from traditional CT and MRI images.
Numeric modeling relies heavily on the assumed wall thick-
ness of the model and is believed to be intrinsically related to
the wall stress. Many researchers use a uniform wall thick-
ness ranging from 1.5 to 2 mm6 – 8,11,12,14 –16,21,23–27 in their
analyses; however, the resulting wall stress is highly depen-
dent on this value. In a report by Venkatasubramaniam et al,44
it was shown that decreasing the wall thickness by 25%
results in a 20% increase in peak wall stress and vice versa.
It is also known that AAA wall thickness in vivo is nonuni-
form, ranging from 0.23 to 4.26 mm31; therefore, in terms of
patient-specific rupture-prediction, it is beneficial to incorpo-
rate nonuniform wall thickness into numeric models also. A
reliable and robust method to extract wall thickness data from
CT images is desirable and would significantly improve the
current use of numeric modeling in AAA rupture assessment.
Martufi et al45 recently described a method to determine wall
thickness from CT images; however, the approach is yet to be
validated. Arguably the most significant limitation of numeric
modeling today is the inability to translate these approaches
to the clinic. In a recent article, Neal and Kerckhoffs46 report
on the current progress in patient-specific modeling and
conclude that the incorporation of patient-specific modeling
into the workflow of the clinician will require, among other
things, regulatory approval by the relevant bodies, such as the
US Food and Drug Administration. This represents another
significant barrier to incorporating numeric modeling into
everyday AAA clinical assessment; however, this barrier
should not deter researchers from investigating the problem
and developing new exciting ways to quantify rupture risk.
Advances in medical imaging have enabled several new
approaches to be examined in relation to the better under-
standing of AAAs. A recent study by Tierney et al47 has
explored the feasibility of using acoustic radiation force
impulse (ARFI) imaging, which was developed at Duke
University, to examine AAA mechanical properties. An
artificially induced AAA model was analyzed using the ARFI
technique to study the effects of AAA on vascular elastic
pathology. The mechanical changes produced in the artifi-
cially induced aneurysm were found to be detectable using
ARFI imaging. The technique was then further applied in
another study48 to determine patient-specific AAA tissue
strength using a previously diagnosed AAA patient. This
preliminary investigation revealed that it was possible to
excite the diseased aortic wall. However, at these realistic
aortic depths, there are challenges in generating sufficient
radiation forces to measurably displace this tissue. The
technique appears to hold promise in determining patient-
specific AAA material properties but requires further inves-
tigation. The application of positron-emission tomography
1692 Arterioscler Thromb Vasc Biol September 2010
and CT to AAA assessment has gained interest recently49,50
after a preliminary investigation by Sakalihasan et al in
2002.51 It was demonstrated in 5 patients that high levels of
18F-fluorodeoxyglucose uptake in the AAA wall are associ-
ated with FEA-predicted wall stress (Figure 4).50 If indeed
metabolic activity can be definitively correlated to wall stress
in a much larger cohort of patients, positron-emission tomog-
raphy–CT could become a useful tool in AAA assessment.
Speelman et al52 recently examined the relationship between
circulating biomarkers and FEA-predicted wall stress. That
study analyzed matrix metalloproteinase-9, tissue inhibitor of the
metalloproteinases-1, ␣1-antitrypsin, and C-reactive protein, all
of which are biomarkers that are believed to reflect inflam-
mation and degeneration in the AAA wall53 and influence
AAA growth.54 The article reported, however, that there was
no correlation between FEA-predicted wall stress and bi-
omarker concentrations. Clearly there is a need to investigate
these hypotheses further, in larger cohorts, to determine
clinical applicability.
The contribution of MRI in assessing cardiovascular dis-
ease is also becoming evident. Not only can MRI provide
flexible medical imaging without the significant radiation
problems associated with CT,55 but it can also quantify blood
velocities with quantitative magnetic resonance flow imaging
using phase-contrast magnetic resonance angiography. How-
ever, although phase-contrast magnetic resonance angiogra-
phy is accurate in measuring velocities of the blood, the
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Figure 4. Comparison of the correlations
between positive 18F-fluorodeoxyglucose
uptake and FEA-predicted wall stress. A,
a, CT image of an AAA; b, positron-
emission tomography–CT images; c, FEA-
predicted wall stress of the same case. B,
a, FEA-predicted peak wall stress; b,
positron-emission tomography–CT
correlation showing positive 18F-
fluorodeoxyglucose uptake at location of
numerically predicted peak wall stress.
Reprinted with permission from Xu et al.50
approach cannot measure wall shear stress and is therefore
most powerful when used as a precursor for computational
models to provide useful inlet and outlet boundary conditions.
It has recently been suggested that the inlet boundary condi-
tion may have important implications in cerebral aneurysm
growth56 and also causes variations in skewness and recircu-
lation of flow throughout AAAs.57 Dynamic imaging has also
played a significant role in advancing AAA assessment.
Much effort has focused on the effects of reconstruction and
smoothing of computational models derived from both
CT23,58 and MRI datasets,59,60 yet the requirement of smooth-
ing is almost eliminated when reconstructions are based on
more advanced forms of dynamic imaging techniques. CT
scanners such as the Aquilion ONE 320-slice CT (Toshiba
America Medical Systems Inc) are now capable of capturing
entire organs in a fraction of a second, thus reducing exposure
to radiation (which is thought to cause as many deaths per
year as AAA rupture: ⬇15,000 deaths)55 and creating 3D
reconstructions of exquisite detail and accuracy. Numeric
models derived from advanced dynamic imaging modalities
may be one step closer to achieving a standardized platform
from which numeric models can be developed, an important
step if clinical approval of patient-specific modeling is
desired.
There is a clear need to revisit and revise the current
rupture risk parameters. Some useful adjuncts to AAA size
have recently emerged, and with further validation, they may
 McGloughlin and Doyle
become clinically feasible. Biomechanical aspects of AAA
rupture are important61 and may improve the current ap-
proach to AAA assessment if models can be rigorously
validated and if key opinion leaders can be convinced of the
benefits. In a 2006 survey62 of 392 vascular surgeons, more
than 92% of clinicians use maximum diameter and growth
rate to determine surgical intervention, as is the standard
current practice. Nineteen percent of clinicians were not
aware that the biomechanics of the problem may be influen-
tial in rupture risk, and an additional 69% were aware of
biomechanics-based rupture risk but were not familiar with
the approach.
Although there are some potential parameters that, once
fully validated and tested, could readily be implemented into
the clinical toolkit, it will be quite some time before use of
these tools becomes common practice. However, with re-
search efforts continuously striving to accurately understand
AAA rupture risk on a patient-specific basis, the gap between
experimental research and clinically feasible rupture risk
tools is becoming smaller by the day.
Acknowledgments
We acknowledge Prof David Vorp at the University of Pittsburgh,
not only for his role in our AAA research efforts but also for his
contribution to the field of AAA biomechanics. We also acknowl-
edge the Department of Vascular Surgery at the Health Service
Executive (HSE) Midwestern Regional Hospital, Limerick, Ireland,
in particular Eamon Kavanagh, Prof Pierce Grace, Dr Peter Coyle,
and Paul Burke.
Sources of Funding
This work was funded in part by Irish Research Council for Science,
Engineering and Technology grant RS/2005/340 and by US National
Heart Lung and Blood Institute grant R01-HL060670.
Disclosures
None.
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New Approaches to Abdominal Aortic Aneurysm Rupture Risk Assessment: Engineering
Insights With Clinical Gain
Timothy M. McGloughlin and Barry J. Doyle

Arterioscler Thromb Vasc Biol. 2010;30:1687-1694; originally published online May 27, 2010;
doi: 10.1161/ATVBAHA.110.204529
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