Stenosis hemodynamics and its effect on platelet accumulation inside stenosed dog carotid arteries

We investigated the in vivo effect of % stenosis, trans-stenotic pressure, and shear stress (SS) on platelet accumulation (PA) in canine mechanically injured and stenosed carotid arteries (SCA). In 10 dogs, intimai damage and controlled variations in stenosis were produced on the carotid artery. Blood flow through the stenosis, trans-stenotic pressure, and stenosis geometry were measured. A NaI gamma detector collimated over the SCA detected autologous radio-labeled PA as platelet mediated thrombi formed in the SCA. The SS was obtained from the finite difference solution of the Navier-Stokes equations. As the flow declined during thrombus formation, the radioactive count accumulated in an inverse fashion. The rate of flow decline directly correlated with the rate of PA during thrombus formation (r2 > 0.9). Compared to the undamaged and unstenosed artery, the PA increased by 52±34% due to mild stenosis (40-60%). PA increased by 94±66 % due to severe stenosis (60-70 %) and by 145156% due to critical stenosis (70-80%) (p > 0.01). The platelet accumulation produced totally occlusive thrombus formation at levels of stenosis higher than 70±5 % (diameter narrowing) and for trans-stenotic pressure gradients higher than 50±5 mmHg producing SS greater than 100 ±10 Pa. The PA was maximum at the stenotic portion of the vessel where the SS is the highest (p < 0.001). In vivo platelet mediated thrombosis increases with SS and occurs at the stenotic portion of the stenosis where the SS is the highest. Severe stenoses produce critical levels SS that potentiate thrombosis and leads to life threatening arterial occlusion.