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Aortic Hemodynamics and their Role in Aneurysm Location
157
[15]. In both conditions infrarenal abdominal shear stress is decreased [16], which suggests
that these altered hemodynamic conditions may play a role in AAA formation in these
patients. The role of hemodynamics in AAA is, however, mostly a suggested one, only
supported by increased aneurysm incidence in patients with aberrant aortic hemodynamics. It
is difficult to directly demonstrate that shear stress is actually involved in the initial phase of
aneurysm formation since shear is not a quantity that is easily measured on post-mortem
tissue. Shear stress needs to be calculated using numerical techniques (Computational Fluid
Dynamics (CFD) or Fluid-Structure Interaction (FSI) simulations) and for these calculations
to be trustworthy, in vivo measurements are indispensable. Many computational studies have
therefore investigated hemodynamics in a (human) setting where the aneurysm is already
present.
HEMODYNAMICS IN HUMAN ANEURYSM
Idealized axisymmetric [17-21] and asymmetric models [22] as well as patient-specific
AAA geometries [23-25] have been used to simulate blood flow in the dilated abdominal
aorta. As one could expect, flow recirculation is in almost all cases reported distal to the
aneurysm neck, giving rise to high shear at the tip and low WSS values in the aneurysmal sac.
These results were confirmed in more advanced FSI models, that allow for a simulation of the
blood flow as well as the structural displacement of the wall [26-28]. However, CFD and FSI
techniques have not just been used to compute the AAA flow field as such. In a new
emerging technique [29] the output of an instantaneous, short-term CFD simulation
(providing WSS and pressure in all nodes of the computational domain) is used as input for a
long-term analytical growth and remodeling model. The analytical model mimics the
degradation of the wall over time, taking into account elastin degradation and collagen
turnover. This results in a remodeled abdominal geometry, which is then again used as the
input for a new CFD simulation in an iterative way. These models are still in an initial phase,
but have a great potential to increase our knowledge on human AAA formation [5]. In any
case, the outcome of these studies depends on a thorough understanding of the interaction
between hemodynamic shear stress patterns and the vascular biology and aortic wall
remodeling. In humans, studies that could increase our understanding on this matter are
hampered by (i) the fact that the disease is asymptomatic and one therefore has no access to
baseline data and (ii) the long period it takes for an aneurysm to develop. To overcome these
problems, mouse models of aneurysm formation are often used.
ANEURYSM FORMATION RESEARCH IN MICE:
WHY THE ANGIOTENSIN II-INFUSED APOE
-/-
MOUSE MODEL?
Using transgenic, knock-in and knock-out techniques many researchers have attempted to
create mouse models developing aneurysm. Genetically engineered mice that were deficient
in receptors for low density lipoprotein (LDL) [30] and apolipoprotein E (ApoE) [31, 32],
commonly referred to as LDL
-/-
and ApoE
-/-
mice, were originally used as a model for
atherosclerosis but in some cases were reported to develop abdominal aneurysms as well.
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158
Many other genetically engineered mice have been reported to develop aortic aneurysm in the
abdominal aorta [33-36], the ascending aorta [37-40], or both locations [41-45]. Chemical
methods have been used to induce abdominal aneurysms in mice by targeted injection of
elastases [
46, 47] and calcium chloride [48, 49]. Due to the specific targeting of the
abdominal aorta, no ascending aortic aneurysms have been observed in these chemically
induced mouse models.
In 2000, genetic and chemical methods were combined when Daugherty et al. discovered
that continuous infusion of the peptide hormone angiotensin II (using a subcutaneous osmotic
pump) into ApoE
-/-
mice leads to AAA formation in the suprarenal abdominal aorta, with an
increased incidence in male animals
[50]. AAAs were also observed when angiotensin II was
infused into LDL
-/-
deficient mice and even in regular C57Bl/6 mice without any genetic
defect [51], albeit with a much lower incidence in the latter. Hyperlipidemic mouse models
such as ApoE
-/-
mice develop AAAs in the suprarenal region and not - as in the human case -
infrarenally. Since the location of the aneurysm is not determined by the induction method,
this makes ApoE
-/-
mice a specifically well-suited model to investigate what processes play a
role in the initial phase of AAA formation, and over the course of time this mouse model has
become the preferred model of choice to study AAA formation. Barisione et al.
[52]
measured AAA progression in angiotensin II-infused ApoE
-/-
mice at short intermediate
timepoints using high-frequency ultrasound, while Turner et al. [53] used a 9.4 Tesla micro-
MRI scanner to follow up AAAs on a weekly basis. However, these were purely
morphological studies that did not increase understanding on the underlying phenomena
causing the initial disease stages. Cigarette smoke inhalation was found to double AAA
incidence in angiotensin II-infused ApoE
-/-
mice [54] , and deficiency of the transcriptional
regulator Kruppel-like factor 15 (Klf15) was reported to induce both heart failure and aortic
aneurysm formation (72% abdominal, 28% thoracic aorta) [55]. A particularly interesting
study showed that systemic neutralization of TGF- nce of
normocholesterolemic C57BL/6 mice to angiotensin II-induced AAA formation and
markedly increases their susceptibility to the disease [56]. Using 4.7 Tesla micro-MRI to
visualize aneurysms in the same mouse model, Goergen et al. [57] hypothesized that the
suprarenal location of AAAs might be related to a local increase in vessel curvature. In a
follow-up study, the same authors demonstrated that AAAs correlate with aortic motion in
both angiotensin II-induced (suprarenal) and elastase-induced (infrarenal) AAAs [58].
Amirbekian et al. did a first attempt to investigate hemodynamics in these animals. They
reported that ApoE
-/-
mice (unlike humans) do not experience reversed flow in the infrarenal
aorta, and suggested a causal effect with the suprarenal location of their AAAs [59]. They
did, however, not calculate shear stress patterns in the aorta of these animals. Recently,
angiotensin II-infused ApoE
-/-
mice were reported to present ascending aortic aneurysms as
well [60], which makes them an even more interesting model to study aneurysm formation.
ASSESSING AORTIC HEMODYNAMICS IN MICE
It is not straightforward to study detailed aortic hemodynamics in mice, whose
cardiovascular system can be considered as a ten times faster and smaller version of the
human , readily available in the clinic, cannot
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Aortic Hemodynamics and their Role in Aneurysm Location
159
be used to obtain the geometries and boundary conditions that are needed as an input for
murine CFD simulations. Dedicated small animal imaging systems are required, which has
hampered the use of small animal CFD simulations for a significant period of time. Greve et
al.
[61] were able to compute shear stresses in the infrarenal aorta of C57BL/6 mice, basing
their geometry on 4.7 Tesla MRI images and measuring inlet boundary conditions with
Phase-Contrast MRI. They found that WSS in mice is generally much higher than human
WSS, a finding that was later confirmed via CFD simulations in mice of different size [62]
and from a theoretical point of view using allometric scaling laws
[63]. However, small
animal MRI is an expensive technique that (at that time) did not obtain a sufficient resolution
to include side branches into the model. Micro-CT can achieve better resolutions, but was for
a long time hampered by the lack of dedicated contrast agents to discriminate the mouse aorta
from surrounding tissues in micro-CT scans. In many studies this problem has been
circumvented by first creating a so-called vascular cast: a plastic replica of the aorta that is
scanned ex vivo to obtain the aortic geometry. Suo et al.
[64] performed CFD simulations in
the aortic arch of C57Bl/6 mice to demonstrate a link between zones experiencing low WSS
and zones with increased expression of VCAM-1 and ICAM-1 (both of which are shear
responsive genes), while Zhu et al. demonstrated that significant differences in aortic arch
WSS can exist between different mouse strains [65].
Still basing the geometry on a scanned cast, Feintuch et al. were the first to implement
mouse-specific inlet and outlet boundary conditions into their CFD model. They reported
small differences between flow ratios obtained from high-frequency ultrasound and PC-MRI
(7 Tesla) in the side branches of the aortic arch [66]. The most detailed CFD simulation in a
murine setting was presented by Huo et al. [67]. They modeled flow in the complete aorta
(from the ascending aorta to the iliac bifurcation) of a C5Bl/6 mouse and reported much more
complicated WSS patterns in the aortic arch compared to other aortic regions. More recently,
Hoi et al. simulated hemodynamics in LDL
-/-
mice with aortic regurgitation, a mouse model
for atherosclerotic plaque [68]. They found that locations of low and oscillatory shear stress
were consistent with plaque locations (although plaque data and CFD simulations were
obtained in different animals). Most of the hitherto described studies used vascular casts to
obtain the murine arterial geometry and thus had to sacrifice the animals. Moreover, none of
these studies attempted to link shear stress patterns in the murine aorta to aneurysm location.
Figure 1. Followed methodology to study the influence of mouse-specific hemodynamics on aneurysm
formation in vivo. Figure was made in the context of [70].
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Figure 2. Example of mouse-specific hemodynamics in the abdominal aorta. A, B: relative residence
time (RRT) and wall shear stress averaged over the cardiac cycle (TAWSS). C-F: flow patterns and
color-coded wall shear stress levels at 4 instants during the cardiac cycle. Disturbed flow occurs during
late systolic deceleration and causes elevated RRT near the trifurcation of right renal and mesenteric
arteries. Figure was made in the context of [70].
HEMODYNAMICS IN THE ANGIOTENSIN II –
INFUSED APOE
-/-
MOUSE MODEL
Ford et al. investigated hemodynamics in existing AAAs in the angiotensin II-infused
ApoE
-/-
model, basing their geometry on reconstructed ultrasound images and neglecting side
branches [69]. Their results are in line with what was reported in human existing AAAs: flow
recirculation and low shear stresses were found in the aneurismal sac. However, they only
investigated hemodynamics in existing aneurysms. In order to study the potential influence of
hemodynamics on the initial stages of aortic aneurysm (or any other cardiovascular disease),
one ideally wants to image the animal at baseline (before aneurysm induction) and compare
those baseline hemodynamics to the location of the aneurysm at end stage. We therefore
proposed a novel methodology [70], depicted in Figure 1. Entirely mouse-specific CFD
simulations were obtained through combined in vivo imaging of both the aortic geometry (via
contrast-enhanced micro-CT) and blood velocities (via high-frequency ultrasound). Velocities
were first converted to volumetric flows and the error in the flow balance was redistributed
over all flow waveforms, which eventually resulted in a set of flow waveforms that could be
imposed as mouse-specific, measurement-based boundary conditions in the CFD simulations.
After the baseline scans were obtained, aneurysms were induced. The end-stage
(aneurysmatic) geometry was then projected onto the baseline geometry and a distance map
was calculated between both to quantify aneurysm location. The developed methodology has
shown to be robust, and can be used to obtain a detailed insight in the normal and
pathophysiological behavior of blood velocity in the murine aorta, as well as the shear stress
patterns that are associated with it. Moreover, it is tailored to the specific hemodynamic
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Aortic Hemodynamics and their Role in Aneurysm Location
161
conditions of each animal, and it can be used to compare different time points in the onset of
any cardiovascular disease as all measurements are obtained in vivo. In a first longitudinal
study, the methodology was applied in the abdominal aorta of male ApoE
-/-
mice
[70]. A
detailed example of mouse-specific abdominal hemodynamics is shown in Figure 2.
Disturbed flow (usually occurring during systolic deceleration near the trifurcation of
mesenteric and right renal arteries), was quantified using the so-called relative residence time
(RRT) and time-averaged wall shear stress (TAWSS). We did not find an overt relationship
between these parameters and AAA location in the four animals that developed an AAA. In
most cases, however, AAAs seemed to occur proximal to the regions experiencing low and
oscillatory shear stress (Figure 1, right panel). However, intermediate data that would allow to
elucidate if there was a causal effect were lacking. Our methodology was then extended to
include the entire aorta into the model, from the heart to the iliac bifurcation and including 7
side branches
[71]. This allowed us to set up a second longitudinal study, in which mice were
scanned at several intermediate time points and aneurysm formation was studied in both the
ascending and the abdominal aorta. Baseline CFD simulations were compared to aneurysm
growth following the same methodology as in Figure 1. For the first time, aneurysm
development at two different locations could thus be compared in one longitudinal study.
Preliminary findings indicate that both aneurysm types evolve differently over time (Trachet
et al, unpublished data, 2012
[72]): while the abdominal aneurysm appears abruptly in
between scans, the ascending aneurysm grows gradually. Interestingly, RRT was found to be
markedly elevated in the ascending aorta, at the very same location where ascending aortic
aneurysm developed later on. In the abdominal region, RRT distribution did not show an
overt relationship with AAA location, which was not the case in the previous study either.
CONCLUSION
This review presents on overview of existing studies on hemodynamics in aneurysm
formation in humans and mice. Most studies in literature focus on the flow field in existing
aneurysms, due to (i) limited access to baseline data in humans and (ii) limited in vivo small
animal imaging modalities in mice. Recent technological improvements have, however,
allowed us to propose a novel methodology to obtain mouse-specific hemodynamics in mice,
and to relate the outcome of these simulations to end stage aneurysm formation in the same
animals. The obtained findings are promising, but still limited by a number of shortcomings,
the most important being the small number of studied animals and the fact that aneurysm
location is currently derived from the aortic lumen, while aortic aneurysm is essentially a
disease of the aortic wall. Further research is needed to fully elucidate the role of shear stress
in aneurysm location, and further advancements in (in vivo) animal imaging technology and
image processing techniques (e.g. allowing us to include aortic wall properties into the
model) might contribute to achieve that goal.
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