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stitutive model Watton et al.,
2009c
). The collagen fabric adapts to restore home-
ostasis and a small perturbation to the geometry alters the spatial distribution of
hemodynamic stimuli that act on the lumenal layer of the artery. This enables sub-
sequent degradation of elastin to be linked to deviations of hemodynamic stimuli
from homeostatic levels via evolution equations. As the elastin degrades and the
collagen fabric adapts (via G&R) an IA evolves. Watton et al. (
2009a
) adopted this
approach to investigate the evolution of IAs assuming degradation of elastin was
linked to high WSS or high WSSG. Given that a region of elevated WSS occurs
downstream of the distal neck of the model IA and elevated spatial WSSGs occur
in the proximal/distal neck regions, this approach led to IAs that enlarged axially
along the arterial domain, i.e. it did not yield IA with characteristic 'berry' topolo-
gies. Consequently, Watton et al. (
2011a
) linked elastin degradation to low WSS and
restricted the degradation of elastin to a localized region of the arterial domain: this
yielded IAs of a characteristic saccular shape that enlarged and stabilized in size.
Although interesting insights were obtained in both studies, an inherent limitation
was that the IAs evolved on a cylindrical section of artery and consequently the spa-
tial distribution of hemodynamic stimuli is non-physiological. This motivated the
application of the FSG modeling framework to patient-specific vascular geometries.
For a detailed description of the model methodology, we refer the interested reader
to Watton et al. (
2011b
,
2012
). Here we briefly illustrate the application of the FSG
modeling framework to 4 clinical cases.
12.3.2 Examples of FSG Models of IA Evolution
Figure
12.5
(upper row) illustrates 4 clinical cases depicting IAs. The IA is removed
(as in Fig.
12.1
(b)) and replaced with a short cylindrical section on which IA evo-
lution is simulated. The cylindrical section is smoothly reconnected to the upstream
and downstream sections of the parent artery (middle row; see Selimovic et al.,
2010
, for methodology). In all four cases, IA inception is prescribed, i.e. an initial
degradation of elastin is prescribed in a localized region of the domain, the collagen
fabric adapts to restore homeostasis and a small localized outpouching of the artery
develops. This perturbs the hemodynamic environment: subsequent degradation of
elastin is linked to low levels of WSS. It can be seen that the modeling framework
gives rise to IAs with different morphologies, i.e. IAs with: asymmetries in geome-
tries (a
3
,
d
3
); well-defined necks (b
3
); no neck (c
3
). For an in depth analysis of
simulation results for case (a
3
), e.g., evolution of elastin strains, collagen strains,
concentrations of constituents and evolving diastolic/systolic geometries, the inter-
ested reader is referred to Watton et al. (
2011b
). Interestingly, for this particular
case, which depicts an IA at (perhaps) a relatively early stage of formation (crudely
inferred from its small size), the qualitative asymmetries of the simulated IA (see
(a
3
)) are in agreement with the patient aneurysm (a
1
) and thus (tentatively) support
the modeling hypotheses for elastin degradation (low WSS drives degradation) and
collagen adaption.
