Numerical analysis of pulsatile blood flow and vessel wall mechanics in different degrees of stenoses.

Hemodynamics factors and biomechanical forces play key roles in atherogenesis, plaque development and final rupture. In this paper, we investigated the flow field and stress field for different degrees of stenoses under physiological conditions. Disease is modelled as axisymmetric cosine shape stenoses with varying diameter reductions of 30%, 50% and 70%, respectively. A simulation model which incorporates fluid-structure interaction, a turbulence model and realistic boundary conditions has been developed. The results show that wall motion is constrained at the throat by 60% for the 30% stenosis and 85% for the 50% stenosis; while for the 70% stenosis, wall motion at the throat is negligible through the whole cycle. Peak velocity at the throat varies from 1.47 m/s in the 30% stenosis to 3.2m/s in the 70% stenosis against a value of 0.78 m/s in healthy arteries. Peak wall shear stress values greater than 100 Pa were found for > or =50% stenoses, which in vivo could lead to endothelial stripping. Maximum circumferential stress was found at the shoulders of plaques. The results from this investigation suggest that severe stenoses inhibit wall motion, resulting in higher blood velocities and higher peak wall shear stress, and localization of hoop stress. These factors may contribute to further development and rupture of plaques.