Biomedical Engineering Reference
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Fig. 8.49  Simulation results of pulsatile flow through a stenotic carotid artery. ( a ) velocity vectors
showing the flow velocities within the artery and surface plot of principal stress distribution within
the plaque. (  Luminal stenosis was 70 % and the fibrous cap thickness was 1 mm ). ( b ) Surface
plot showing flow velocities within the artery and flow streamlines. The contour plot within the
plaque shows the strain distribution. (Luminal stenosis was 80 %, and the fibrous cap thickness
was 0.5 mm. White arrow shows the maximal plaque deformation, and star indicates the large flow
recirculation zone). (Image from Li et al. 2006)
hyperelasticity of the human tissue. Luminal stenosis (  ϕ ) was varied from 10 to
95 %, and the fibrous cap thickness (  d ) was varied from 0.1 to 2 mm. The flow field
and stress/strain distribution within the plaque were calculated for every degree of
luminal stenosis and fibrous cap thickness used.
Velocity vectors and stress distribution in a vessel with a 70 % degree of luminal
stenosis are shown in Fig. 8.49a . The fibrous cap thickness is 1.0 mm. Reverse
flow occurs distal to the plaque, which is a fluid dynamics characteristic produced
by separated flows (see Chap. 4). The principal stress contours are shown in the
fibrous cap and the lipid pool, and high stress concentrations are found within the
fibrous cap. This occurs at the shoulder regions of the plaque where the oncoming
fluid tends to build up pressure. In Fig. 8.49b the luminal stenosis is 80 %, and the
fibrous cap thickness is 0.5 mm.
The plaque is deformed with a maximum deformation of 2.44 mm because of
the large luminal stenosis (80 %) and thin fibrous cap (0.5 mm). Severe stenosis
and 100 % eccentricity lead to high flow velocity, high pressure at the throat of the
stenosis, and a large recirculation region.
Li et al. (2006) showed that when the plaque changed from concentric to eccen-
tric, the maximal plaque stress was slightly increased. This effect was smaller when
compared with the effect of thinning the fibrous cap. It is suggested that plaque ec-
centricity does not play a major role in plaque vulnerability.
Kock et al. (2008) studied longitudinal 2D FSI models from MRI scans to predict
plaque rupture risk and examinations of correlations between local stress variation
and morphology. Blood-flow was simulated in a Navier-Stokes model, and treated
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