Abstract :
In this study the hemodynamics in the early stages of the atherosclerotic process-when a neointimal hyperplasia or an intimal fibrocellular hypertrophy takes place-is theoretically investigated. A local, slight increase in the wall thickness of a canine femoral artery is simulated using an original two-dimensional mathematical model of arterial hemodynamics and the effects induced on the velocity field by the simulated mild stenosis-only 2% of area reduction-are analysed. The model incorporates: fluid non-linear inertial forces, viscoelastic wall motion, anatomical taper, unsteady flow, pressure propagation and reflections on both the proximal and distal vessel ends. Two different physiological pulsatile flows are considered: a basal flow condition and a light vasodilation state inducing in the vessel segment a limited increase in mean flow (50%). The distributions along the vessel during the cardiac cycle of both the velocity profile and wall shear stress, are shown. The shape of velocity distributions is strongly perturbed by the stenosis and disturbances are clearly evident whatever instant of the cardiac cycle is considered. After vasodilatation, during the phase of systolic deceleration, a vortex circulation appears in the post-stenotic region. The vortex persists for the whole diastolic phase, causing a very strong stress at the arterial wall: wall shear stress in the distal part of the simulated mild stenosis is at least five times the basal value. The reported results provide a coherent explanation of the critical role that hemodynamic factors may play in the early stages of atherogenic process.
