WSS is the frictional force exerted in parallel to the endothelial surface of the vessel wall by blood viscosity. It is considered a major parameter to assess the risk of atherosclerosis. Traditional color Doppler ultrasound imaging only measures the velocity component of blood flow along the direction of ultrasonic propagation, but it cannot image the blood flow perpendicular to the direction of ultrasonic propagation. This technique provides accurate data on the velocity component of blood flow only under the laminar flow condition. Hence, it is almost impossible to obtain the correct blood flow velocity component for calculating WSS in a complex blood flow state. The v-flow technique can provide directional information on blood flow velocity and help obtain accurate blood flow velocity components for WSS toward more accurate evaluation [13].
WSS is also considered an important cause of the development of carotid atherosclerosis. The measurement of WSS in the carotid artery is typically performed via magnetic resonance imaging or enhanced CT, with three-dimensional reconstruction and calculation by software. Comparatively, flow vector imaging can visualize and quantify the flow field and hemodynamics in the lumen of blood vessels, detect eddy currents and countercurrents, and detect WSS. Thus far, it has been widely used in the diagnosis, evaluation, and treatment of cardiovascular diseases [14–17]. Vector flow imaging (VFI) is an angle-independent technique that measures and visualizes the blood flow velocities in all directions, thereby providing intuitive and quantitative images of vortex formation. Assessment of disturbed blood flow patterns at the carotid bifurcation has the potential to allow a better understanding of the diagnostic value of complex flow patterns, enhancing the risk stratification efficiency [13, 18]. It can also evaluate hemodynamic changes during moderate to severe carotid stenoses [8]. Moerman et al. performed MRI imaging of the carotid bifurcations of patients scheduled for carotid endarterectomy surgery. This study compared local WSS metrics and histological characteristics of plaque vulnerability in carotid plaques, revealing that necrotic core sizes and macrophage activation areas are significantly larger in areas exposed to high time-averaged WSS or low-oscillatory shear index [19]. More recently, flow vector imaging to assess arteriosclerotic carotid artery stenosis hemodynamics has been increasingly studied[13], but less research has specifically focused on patients undergoing CAS.
Our findings that WSS is increased in the distal and lower in the proximal portions of carotid artery stenosis further suggests that decreased proximal WSS may aggravate intima-media thickening and promote plaque formation, and increased distal wall shear may increase the risk of plaque rupture. Compared with patients with carotid artery stenosis without ischemic symptoms, patients with ischemic symptoms had higher WSS proximal and at the narrowest portion of stenosis, indicating that the higher the WSS in the narrowest area, the greater the risk of plaque rupture and detachment. This is in line with the literature reporting that wall shear obtained by measuring peak systolic velocity at the narrowest portion of stenosis can be a better predictor of ischemic stroke than the degree of stricture [20, 21] .
The results also showed that the patients with 70–99% stenosis had higher WSS in the proximal and narrowest regions compared to patients with 50–69% stenosis, indicating a positive correlation between WSS and severity of stenosis, consistent with the literature [19]. After stenting, WSS decreased in the proximal and narrowest region, with a larger decrease in the narrowest region. There was no significant change in WSS of the proximal, narrowest, or distal regions six months post-operation compared with one week post-operation. In 1 of 28 cases, the shear stress of the proximal and narrowest regions increased significantly. In this single case, the blood flow velocity increased, the vortex ratio increased, and the degree of stenosis was 70%. The restenosis was indicated by angiography. Notably, the case’s gene analysis showed that the genotype for clopidogrel was CYP2C19 * 2/* 17, and the genotype for statins was SLCO1B1 * 1a/* 1b, apoe E3E4. The patient is currently under follow-up after being transitioned from clopidogrel to ticagrelor and having ezetimibe added as a lipid-lowering drug along with atorvastatin calcium.
At present, the application of blood flow vector imaging to measure WSS of the carotid arteries is rare in the clinical setting. Notably, this is a self-contrast study. The number of cases included in this study is small and only from a single center, which limits the generalizability of our results. WSS affects the morphology, intimal proliferation, differentiation, metabolism, and communication of endothelial cells [22]. By controlling the near-wall transport processes involved in atherosclerosis, such as low-density lipoprotein, nitric oxide, adenosine triphosphate, oxygen, monocyte chemoattractant protein-1, etc.[23]. Our study did not examine the relationships between shear stress, endothelial cells, and related biochemical mass transport models. Further studies are needed to understand the long-term value of shear stress testing post-CAS because the technique has yet to be compared to repeat cerebral angiography, particularly in regard to in-stent restenosis.
In conclusion, ultrasonic measurement of WSS provides important hemodynamic information in patients with carotid artery stenosis before stent implantation to help determine severity and treatment options. The therapeutic effect can be evaluated after stenting, providing key long-term follow-up value.