We found that such locations are
correlated to the vulnerable plaque phenotype, which is prone to rupture. Our
results demonstrate that at locations of high particle concentration, blood
particles change the shear stress distribution and magnitude. Therefore, the
non-Newtonian blood flow assumption provides new insights in the characterization of plaque built up.
These results are combined to in-vitro
experiments that suggest the influence of blood particles in the activity of
cytokines. An unbalance in pro and anti-inflammatory cytokines has been associated to an increase in inflammation and, consequently, in the volume of plaques forming. We anticipate our work to be a starting point for a more
sophisticated multi-scale model, which combines experimental findings and
computational modelling to characterize arterial segments affected by
atherosclerosis. Such model includes a coupling between the distending arterial
wall and the non-Newtonian blood flow.
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