Hemodynamic Factors Affecting Carotid Sinus Atherosclerotic Stenosis.

Purpose Carotid atherosclerotic plaque occurs predominantly at the outer wall of the carotid sinus, and computational fluid dynamics (CFD) plays an important role in explaining plaque formation. The present study investigated the hemodynamic factors affecting carotid atherosclerotic stenosis. Methods Sixteen patients with normal carotid arteries and 16 with symptomatic stenotic carotid sinus underwent 3-dimensional angiographic imaging evaluations and were studied with CFD to simulate the complete 3-dimensional blood flow and hemodynamic parameter distribution in the carotid bifurcations. The hemodynamic parameters, including wall shear stress (WSS), dynamic and total pressure, total pressure gradient, strain rate, velocity, and velocity angle, were investigated. Results The atherosclerosis-prone outer lateral walls of the carotid sinus and the external carotid artery at its start had significantly (P < 0.05) low dynamic pressure, WSS, strain rate, and total pressure gradient but high static pressure. The blood flow near these walls with flow separation had significantly (P < 0.05) decreased velocity and dynamic pressures but a high velocity angle. The carotid divider had significantly (P < 0.05) elevated dynamic and total pressure, WSS, strain rate, and total pressure gradient but reduced static pressure. Additional stenosis occurred at the downstream area of stenosis with significantly (P < 0.05) decreased dynamic pressure, WSS, strain rate, and total pressure gradient similar to the wall at the sinus and the start of the external carotid artery. Conclusion Significantly decreased vascular WSS, dynamic pressure, strain rate, and total pressure gradient are key to atherosclerotic plaque formation at the carotid sinus. Highlights • Hemodynamic stresses affect carotid atherosclerotic plaque formation. • Deceased hemodynamic stresses promote carotid atherosclerotic plaque formation. • WSS, dynamic pressure, strain rate, and total pressure are key to atherosclerotic plaque formation. [ABSTRACT FROM AUTHOR]