Biomedical Engineering Reference
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Fig. 8.45
3D plaque samples re-constructed from in vivo MR images showing progression and
regression (
a
) One sample showing plaque growth. (
b
)One sample showing plaque reduction. Scan
time interval: 18-months.
Red
:lumen;
yellow
:lipid;
dark blue
:calcification;
light blue
:outerwall.
(Image from Yang et al. 2010)
is less prone to atherosclerosis. Flow shear stress and plaque wall stress fields were
obtained for correlation analysis. These were taken at baseline time and follow-up
scan time (18-months later). Their results found that wall thickness increase cor-
relates positively with flow shear stress, the overall correlation was rather weak.
There were 26 cases that showed the negative correlation with plaque wall stress,
and it was suggested that both fluid and structural forces should be considered as
possible mechanisms governing plaque progression. There was increased plaque
progression in the posterior quadrants of the ICA, corresponding to disturbed flow
region, and lipid rich necrotic core regions were associated with higher flow shear
stress values.
In an attempt to reduce the computational modelling burden of creating the
models, the lipid core can be treated as a singular entity referred to as a no-com-
ponent lipid pool. Figure
8.46
compares plaque wall stress and flow shear stress
distributions from the no-component model and the model with components us-
Fig. 8.46
Comparison of plaque wall stress (
PWS
) and flow shear stress distributions on a bifur-
cation cut surface and a longitudinal cut surface from no-component model and model with com-
ponents showing good agreement for flow shear stress and reasonable agreement for PWS (
a
)
PWS on a Longitudinal Cut, No-Component Model, (
b
) PWS on a Longitudinal Cut, Model with
Component, (
c
) flow shear stress on a Longitudinal Cut, No-Component Model and (
d
) PWS on a
Longitudinal Cut, Model with Component. (Image adapted from Yang et al. 2010)
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