Key result
Blood rheology models alter end-diastolic WSS distribution, while vessel deformability impacts peak pressure phases.
Computational modeling demonstrates that both blood rheology (shear-thinning behavior) and vessel wall deformability significantly impact wall shear stress distribution in the carotid artery at different phases of the cardiac cycle.
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Carotid WSS models require phase-specific rheology and deformability inputs; extends simulation accuracy but leaves clinical translation open.
Hemodynamic factors, such as Wall Shear Stress (WSS), play a substantial role in arterial diseases. In the larger arteries, such as the carotid artery, interaction between the vessel wall and blood flow affects the distribution of hemodynamic factors. In the present study, both rigid-wall and deformable-wall models are developed in a 3D numerical simulation to assess the effectiveness of arterial rigidity on worsening hemodynamics, especially WSS. Two different rheological models (Newtonian and Carreau–Yasuda) have been employed to evaluate the influence of blood, non-Newtonian properties, as well. The importance of vessel wall deformability was compared with the rheological model of blood. Although the deformability changes hemodynamic factors under the steady state boundary condition, or at the last two phases of the cardiac cycle (when the blood flow in carotid looks like a steady condition), WSS distribution is mostly affected by the blood rheological model. In other words, the influence of shear-thinning behavior at the end-diastolic phase of the cardiac cycle is undeniable unlike the deferability. However, the effects of deformability, like the rheology of blood on WSS could not be neglected at the first two phases of the cardiac cycle when pressure reaches its highest values.
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Toloui et al. (2012) studied Hemodynamics of carotid bifurcation. Deformable-wall models and non-Newtonian blood rheology vs. Rigid-wall models and Newtonian blood rheology was evaluated on Wall Shear Stress (WSS) distribution. Blood rheological models primarily affect Wall Shear Stress distribution at the end-diastolic phase, while vessel deformability effects are significant during peak pressure phases.
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