Evaluation of stenosis and hematocrit for platelet activation and plaque injury in atherosclerosis blood vessels

Atherosclerosis of lower extremity is often accompanied by thrombosis and plaque injury. Currently, there is a lack of comprehensive hemodynamics study that combines platelet activation related to thrombosis and plaque injury in atherosclerosis. Thus, we first analyze the mechanism of platelet activation and plaque injury and further investigate the effects of stenosis and hematocrit through hemodynamic results. An Euler–Euler method is used for the mixed fluid containing red blood cells (RBCs) coupled with a Lagrangian approach for the transport of plasma particles. To more realistically implement this mathematical model, we employ user-defined functions to incorporate platelet level of activation (LOA), vessel specific Windkessel model, RBCs form factor, and platelet form factor into the simulation calculation framework. Our results suggest that in a narrow larynx, high wall shear stress activates platelets. Subsequently, platelets accumulate downstream of the stenosis due to the reflux caused by the stenosis or hyperviscous blood stasis on account of increased hematocrit. The stenosis rises from 0.00% to 70.01%, or the hematocrit from 0.55 to 0.65, and increases LOA by 5.00% or 34.41%, respectively, in conclusion high stenosis and high hematocrit predispose to thrombosis and plaque injury. Therefore, it is necessary to regularly check the degree of stenosis in patients with atherosclerosis, especially in those with high hematocrit caused by related disease. The results obtained could provide a theoretical basis for the diagnosis and treatment of lower limb atherosclerosis.