Introduction

High-risk plaque characterized by easily rupturing and leading to thrombosis or embolism, is the predominant risk factor of cerebrovascular events¹. Low-risk plaque needs conservative treatments like pharmacological interventions while high-risk plaque needs more active treatments like stent placement or endovascular thrombectomy. Therefore, to identify whether the plaque is a high-risk plaque is important. The current definition of high risk plaque is based on pathology, such as intraplaque hemorrhage, lipid core, inflammatory response². Imaging research on plaque can be generally classified into morphology and hemodynamics. Recently, morphological research has made a breakthrough with the development of high resolution vessel wall imaging (HRVWI), but hemodynamic research is still controversial and requires more research to confirm the vulnerable plaques. In this study, the combination of HRVMI and 4D flow MRI was used to explore the differences of wall shear stress (WSS) between high-risk and low-risk plaques and to identify whether WSS is a predictor of high-risk plaques and provide evidences for further clinical treatment.

Method

Forty-four patients with carotid sinus plaques were retrospectively enrolled in the study. All patients underwent CTA, HRVW, and 4D flow MRI. Twenty-eight patients with high-risk plaques and sixteen patients with low-risk plaques. High-risk plaque was defined as (1) no calcification seen on CT images; (2) the signal intensity in the plaque on HRVWIs is not homogeneous and enhanced significantly; (3) cerebrovascular events occurred in the ipsilateral brain parenchyma. Low risk plaque was defined as (1)calcification seen on CT images; (2) the signal intensity in the plaque on HRVWIs is not homogeneous and no enhancement; (3) no cerebrovascular events in the ipsilateral brain parenchyma. The stenosis rate of all plaques was 20%-50% (diagnosis based on HRVWI). 4D Flow MRI data were imported into post-processing software (Version 5.6.6, Circle Cardiovascular Imaging, Canada) to calculate volume (max, mean, min), axial WSS (max, mean, min), circumferential WSS (max, mean, min) and 3D WSS (max, mean, min).

Result

Table 1 displayed the demographics characteristics of patients with high-risk and low-risk plaque. The high-risk group showed significantly higher hypertension rate compared to the low-risk group. No significant differences in age, gender, height, weight, diabetes, drinking, smoking, hyperlipidemia and stenosed rate were found between groups. Volume: No difference of blood volume (max, mean, min) between two groups was found (Figure1d).
WSS: The axial, circumferential, and 3D WSS were all significantly higher in the high-risk plaque group than the low-risk group except for the minimum axial and circumferential WSS (Figure1a,b,c). Figure 2 showed the WSS distribution of one case in each group.

Discussion

WSS played an important role in the formation and development of atherosclerosis. In our study, WSS discrepancy calculated by 4D flow was still found between two groups when patients with similar stenosis degree confirmed by no difference of vascular volume measurements. Previous studies found that ulcer appeared exclusively at the high-WSS location and higher maximum WSS was also significantly associated with the presence of intraplaque hemorrhage^3,4. Gijsen et al. has reported a plaque in the high-WSS region increases strain over time, indicating that lipid deposition likely increases in high WSS⁵. These aforementioned studies were consitent with ours, but more details such as axial, circumferential and 3D WSS were shown in our study. Only comparisons of the minimum circumferential and axial WSS were significant different, and it should be further confirmed that high WSS was more likely to cause high risk plaque. WSS might affect the function of vascular endothelial and smooth muscle cells, and high WSS even induces specific changes in endothelial cell behavior, including modifying gene expression and expression of matrix metalloproteinases, which may contribute to the initialization and progression of atherosclerosis^6-8.

Conclusion

Higher WSS was found in patients with high-risk plaque than those with low-risk and may be related to atherosclerotic plaque rupture and cause thrombosis or embolism, leading to cerebrovascular events.

Acknowledgements

Supported by the Key Program National Natural Science Foundation of China (Grant No. 81730049)

References

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