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Войти в исследования Quantitative imaging in medicine and surgery · 2026
Differential associations of intracranial large artery phenotypes (calcification vs. stenosis) with topographical white matter hyperintensity patterns in minor stroke/transient ischemic attack (TIA).
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Li Jintao, Wen Jia, Cheng Kailin, Liu Yazhao, Li Shuen, Fu Xiaoli, Shi Zhu
Аннотация
BACKGROUND: White matter hyperintensity (WMH) is a common cerebrovascular complication of hypertension, associated with intracranial arterial diseases, including stenosis and calcification. However, the distinctive pathophysiological mechanism remains unclear. To address this critical knowledge gap, the present study was designed to investigate the impact of major intracranial arterial phenotypes, including stenosis and calcification, on WMH and the differences in WMH across distinctive topological regions.
METHODS: Consecutive stroke patients from an unicentric cohort were retrospectively enrolled. Major intracranial vessels evaluated included the intracranial segment of the C4-7 segments of internal carotid artery (ICA), M1 of the middle cerebral artery (MCA), V4 of the vertebral artery (VA) and the basilar artery (BA). Intracranial artery calcification (IAC) was determined on non-contrast computed tomography (NCCT) and classified into intimal-IAC and medial-IAC, and the number of involved arteries was recorded; intracranial artery stenosis burden (ICASB) was evaluated using computed tomography angiography (CTA); WMH severity was assessed using the Fazekas score, and categorized as none/mild, moderate and severe. Logistic regression models were constructed to evaluate the relationship between IAC, intracranial arterial stenosis (ICAS) with WMH.
RESULTS: Among the 503 enrolled patients (40.6% female; median age 71 years), a higher ICASB was independently associated with greater overall WMH severity [adjusted odds ratio (OR) 1.47 per unit increase, 95% confidence interval (CI): 1.31-1.66; P<0.001]. In stratified analyses by WMH topography, a greater number of arteries affected by medial-IAC was independently associated with severe periventricular-WMH (P-WMH) (aOR 1.42, 95% CI: 1.21-3.83; P=0.012), while a greater number of arteries with intimal-IAC showed a significant association with severe deep-WMH (D-WMH) (aOR 1.11, 95% CI: 1.09-2.76; P=0.014).
CONCLUSIONS: Intracranial arterial stenosis and calcification jointly contribute to WMH; each exhibited subtle heterogeneity in pathogenesis of P-WMH and D-WMH, with medial-IAC being more closely associated with P-WMH.
METHODS: Consecutive stroke patients from an unicentric cohort were retrospectively enrolled. Major intracranial vessels evaluated included the intracranial segment of the C4-7 segments of internal carotid artery (ICA), M1 of the middle cerebral artery (MCA), V4 of the vertebral artery (VA) and the basilar artery (BA). Intracranial artery calcification (IAC) was determined on non-contrast computed tomography (NCCT) and classified into intimal-IAC and medial-IAC, and the number of involved arteries was recorded; intracranial artery stenosis burden (ICASB) was evaluated using computed tomography angiography (CTA); WMH severity was assessed using the Fazekas score, and categorized as none/mild, moderate and severe. Logistic regression models were constructed to evaluate the relationship between IAC, intracranial arterial stenosis (ICAS) with WMH.
RESULTS: Among the 503 enrolled patients (40.6% female; median age 71 years), a higher ICASB was independently associated with greater overall WMH severity [adjusted odds ratio (OR) 1.47 per unit increase, 95% confidence interval (CI): 1.31-1.66; P<0.001]. In stratified analyses by WMH topography, a greater number of arteries affected by medial-IAC was independently associated with severe periventricular-WMH (P-WMH) (aOR 1.42, 95% CI: 1.21-3.83; P=0.012), while a greater number of arteries with intimal-IAC showed a significant association with severe deep-WMH (D-WMH) (aOR 1.11, 95% CI: 1.09-2.76; P=0.014).
CONCLUSIONS: Intracranial arterial stenosis and calcification jointly contribute to WMH; each exhibited subtle heterogeneity in pathogenesis of P-WMH and D-WMH, with medial-IAC being more closely associated with P-WMH.