Experimental and numerical models demonstrate that the cumulative effect of shear stress and exposure duration in stenosed coronary vessels determines platelet activation and potential aggregation.
Arterial disease, characterized by arterial occlusion (stenosis), is a leading cause of cardiovascular diseases and a major healthcare problem in the Western world. One of the main mechanisms leading to vessel occlusion is thrombus formation, which may be initiated by platelet activation. Shear rates and flow patterns (fluid dynamics factors) and concentration of coagulation factors and platelet agonists (biological factors) modulate platelet function and may lead to platelet activation and aggregation. Here, we examine the flow-induced mechanisms leading to platelet activation in models of stenosed coronary vessels. Experimental and numerical methods were used to investigate and characterize the influence of the flow field on platelet activation. As it passes through pathological geometries characteristic of arterial stenosis, a platelet is exposed to varying levels of shear stress. The cumulative effect of the shear stress level and the duration of the platelet's exposure to it determine whether the platelet is brought beyond its activation threshold. Stress histories of individual platelets can be tracked within the flow field to locate the regions where activated platelets might be found and subsequently aggregate and/or adhere to the wall.
Einav et al. (Sat,) studied this question.