White matter hyperintensities had a correlation with the cerebral perfusion level, but no correlation with the severity of large vessel stenosis in the anterior circulation

OBJECTIVE: The contribution of large vessel stenosis to the development of white matter hyperintensities (WMHs) has not been fully elucidated. This study aims to explore the correlation between ipsilateral white matter hyperintensities (WMHs) and the severity of large vessel stenosis in the anterior circulation and cerebral perfusion level, as well as analyze the factors influencing WMHs. METHODS: A cross‐sectional study of 150 patients with unilateral anterior circulation large vessel stenosis of ≥50% was conducted. The severity of ipsilateral WMHs was assessed by Fazekas scale on T2‐weighted image and/or fluid‐attenuated inversion recovery MR imaging, vascular stenosis severity was evaluated on computed tomography angiography images, and the level of cerebral perfusion was rated according to a staging system for abnormal cerebral perfusion based on CTP results. The relationships between the stenosis severity, cerebral perfusion level and ipsilateral WMHs severity were analyzed. A multivariate logistic regression analysis was performed to determine the factors independently influencing WMHs. RESULTS: Among 150 patients (mean age, 63.12 ± 10.55 years), there was a statistically significant positive correlation between cerebral perfusion level and the severity of DWMHs and PWMHs (Gamma = 0.561, p < .001; Gamma = 0.600, p < .001), and a positive correlation between cerebral perfusion level and the severity of vascular stenosis (Gamma = 0.495, p < .001).While, there was no statistically significant correlation between the severity of vascular stenosis and the severity of DWMHs and PWMHs (Gamma = 0.188, p = .08; Gamma = 0.196, p = .06). The multivariate logistic regression analysis results demonstrated that age (OR = 1.047, 95% CI 1.003–1.093; p = .035), stroke/TIA history (OR = 2.880, 95% CI 1.154–7.190; p = .023) and stage II of cerebral perfusion (OR = 2.880, 95% CI 1.154–7.190; p = .023) were independent influencing factors on ipsilateral DWMHs. Age (OR = 1.051, 95% CI 1.009–1.094; p = .018), and stage II of cerebral perfusion (OR = 12.871, 95% CI 3.576‐46.322; p < .001) were factors independently influencing ipsilateral PWMHs. CONCLUSION: White matter hyperintensities may be attributed to cerebral hypoperfusion secondary to vascular stenosis but not directly to the severity of stenosis in the large vessels of anterior circulation. Moreover, longitudinal studies with sequential imaging exams may further reveal the impact of cerebral perfusion secondary to vascular stenosis on the development and progression of WMHs.