Path-dependent hemodynamics of the stenosed carotid bifurcation.
Previous work using computational simulations and experimental flow visualizations has demonstrated marked differences in local flow patterns between stenosed carotid bifurcation models having the same stenosis severity but different stenosis geometries. Since local blood flow patterns are known to influence thrombosis and atherosclerotic plaque development and rupture, such differences may in turn reflect differences in thromboembolic and atherosclerotic potential, and hence risk of ischemic stroke. Towards testing this hypothesis, we tracked point particles, representing uniformly distributed blood elements, through concentrically and eccentrically stenosed carotid bifurcation models, and computed and compared various path-dependent hemodynamic parameters between the models. Our results suggest that residence time alone is not sensitive to stenosis geometry; however, notable differences between the stenosis models were observed with residence time indicators that incorporate shear-related phenomena, such as the transit times and levels of activation of platelets that exceed a given shear threshold. Specifically, these and other indicators, including the magnitude of platelet shear exposure and the size and density of local platelet and monocyte deposition, were found to be higher in the eccentric model. Experimental work is now required to assess the significance of these differences.
Imaging Research Laboratories, Robarts Research Institute, Department of Medical Biophysics, The University of Western Ontario, Ontario, Canada.
Mauro
M
Tambasco
David A
DA
Steinman
D001783:Blood Flow Velocity; D001792:Blood Platelets / Q000502:physiology; D001794:Blood Pressure; D017536:Carotid Artery, Common / Q000503:physiopathology*; D002342:Carotid Artery, External / Q000503:physiopathology; D002343:Carotid Artery, Internal / Q000503:physiopathology; D016893:Carotid Stenosis / Q000150:complications / Q000503:physiopathology*; D003198:Computer Simulation; D003324:Coronary Artery Disease / Q000150:complications / Q000503:physiopathology; D018056:Hemorheology / Q000379:methods*; D008955:Models, Cardiovascular; D009000:Monocytes / Q000502:physiology; D010316:Particle Size; D011673:Pulsatile Flow; D033081:Shear Strength; D020521:Stroke / Q000209:etiology / Q000503:physiopathology / Q000517:prevention & control