Biomedical Engineering Reference
In-Depth Information
We adopted a steady flow analysis to reduce the cost of the computational
simulations. The similarity of the spatial WSS/WSSG distributions for steady and
pulsatile flow [
95
-
97
] implies that this is a reasonable approach for the purposes of
investigating phenomenological hypotheses that explore the link between G&R
and deviations of the WSS/WSSG from homeostatic levels [
36
]. However, tem-
poral changes in WSS distribution during the cardiac cycle affect the functionality
of ECs: oscillatory shear is elevated in regions of disturbed flow and is associated
with proatherogenic patterns of gene expression [
98
,
99
]. A pulsatile flow analysis
yields additional quantification of the haemodynamic stimuli that act on ECs and
thus is necessary to explore more sophisticated G&R hypotheses related to the
haemodynamics.
Approximately 75 % of AAAs have an associated intraluminal thrombus (ILT)
[
100
]. ILT alters the stress distribution and reduces peak wall stress in AAA.
However, presence of ILT leads to regional wall weakening [
101
]: platelet acti-
vation, fibrin formation, binding of plasminogen and its activators, and trapping of
erythrocytes and neutrophils, leads to oxidative and proteolytic injury of the arterial
wall [
102
]. Consequently, ILT must play an important role in the aetiology of AAA
and thus the biochemomechanical roles of ILT must be understood and modelled
better [
103
]. However, incorporating a model for ILT evolution is challenging; it
would require integration of a model for thrombus evolution [
104
-
106
] combined
with a constitutive model describing its mechanical response [
107
-
109
]; this may
merit investigation with conceptual mathematical models with simpler geometries
first. We note also that our model does not include calcification of the arterial wall
which are often present in AAAs [
110
]. Calcifications influence stress distributions
[
111
] and thus may influence G&R and AAA evolution [
112
].
5 Conclusion
In order to sophisticate computational models to more accurately represent
mechanobiology, guidance is needed from experiments. In return, computational
models assist in the interpretation of experimental data and in the identification of
questions that need to be addressed by experiments. Moreover, they can play a
vital role in guiding our understanding of mechanobiology: they serve as an in
silico testbed for exploration of hypotheses; enable underlying mechanisms to be
evaluated with incomplete data sets and yield insight which would be impossible
from in vitro/vivo experimental set-up alone. We have extended the FSG model
proposed by [
35
] to link both growth and remodelling to cyclic deformation of
vascular cells and applied it to simulate the evolution of abdominal aortic aneu-
rysm. The model predicts an aneurysm that evolves with similar mechanical,
biological and morphological properties with those observed in vivo. Whilst in
need of further sophistications to more accurately reflect the underlying
mechanobiology, this computational framework has clear potential to be applied to
aid the design and optimisation of tissue engineered vascular constructs.
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