期刊
BIOMECHANICS AND MODELING IN MECHANOBIOLOGY
卷 20, 期 3, 页码 1069-1085出版社
SPRINGER HEIDELBERG
DOI: 10.1007/s10237-021-01431-x
关键词
Cross-bifurcation stenosis; Wall shear stress; Oscillatory shear index; Stress phase angle; Endothelial cell function
Atherosclerosis initiation is related to abnormal hemodynamic parameters at arterial bifurcations, with severe stenosis causing significant localized changes in hemodynamic parameters. Mild stenosis has minor impact on hemodynamic parameters.
Atherosclerosis is initiated by endothelial injury that is related to abnormal values of hemodynamic parameters such as wall shear stress (WSS), oscillatory shear index (OSI) and stress phase angle (SPA), which are more common in arterial bifurcations due to the complex structure. An experimental model of human carotid bifurcation with accurate geometrical and mechanical features was set up, and using realistic pulsatile flow rates, the inlet and outlet pressure pulses were measured for normal and stenosed models with 40% and 80% severities at common carotid (CCA), internal carotid (ICA) and external carotid (ECA) arteries. Based on the obtained experimental data, fluid-structure models were developed to obtain WSS, OSI, and SPA and evaluate pathological consequences at different locations. Mild severity had minor impact, however, inducing severe 80% stenosis in each branch led to considerable localized changes of hemodynamic parameters both in the stenosis site and other locations. This included sharp increases in WSS values accompanied by very low values close to zero before and after the peaks. Severe stenosis not only caused significant changes in the local artery, but also in other branches. OSI and SPA were less sensitive to stenosis, although high peaks were observed on bifurcation site for the stenosis at ECA. The interconnection of arteries at carotid bifurcation results in altered pressure/flow patterns in all branches when a stenosis is applied in any site. Such effect confirms pathological findings that atherosclerotic plaques are observed simultaneously in different carotid branches, although with different degrees of plaque growth and severity.
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