Objectives Fluid-attenuated inversion recovery (FLAIR) vascular hyperintensity (FVH) is a marker of hemodynamic impairment linked to poor outcomes. However, its underlying vascular pathology remains unclear. We aimed to evaluate the relationships between FVH, infarction, and vascular lesion burden, and explore whether infarction and vascular lesion burden can discriminate FVH presence and burden. Materials and methods A total of 253 consecutive patients with middle cerebral artery lesions who underwent vessel wall imaging were retrospectively enrolled. Multivariate logistic regressions were performed to identify discriminatory factors for FVH presence or burden; area under the curve (AUC), sensitivity and specificity assessed the discriminatory ability of combined models. Results Infarction, severe stenosis, and vascular wall marked enhancement were independently associated with FVH (ORs 2.995, 4.074, 2.141; all p < 0.05). Infarction, severe stenosis, max wall thickness, and max vascular lesion length were independently correlated with higher FVH burden (ORs 2.966, 8.785, 2.344, 1.049; all p < 0.05). The combined model (infarction + severe stenosis + marked enhancement) discriminated FVH presence with an excellent AUC of 0.803 (95% CI: 0.749–0.850, p < 0.001; sensitivity 76.6%; specificity 76.7%). The combined model (infarction + severe stenosis + max wall thickness + max vascular lesion length) discriminated higher FVH burden with an AUC of 0.801 (95% CI: 0.746–0.848, p < 0.001; sensitivity 80.8%; specificity 70.9%). Conclusion Infarction and vascular lesion burden are key factors associated with FVH. Our findings suggest a pathophysiological link between FVH and underlying vessel wall pathology, positioning FVH as a potential integrative MRI biomarker. Key Points <Emphasis Type="BoldItalic">Question</Emphasis> While FLAIR vascular hyperintensity (FVH) indicates hemodynamic compromise and slow collateral flow, how the underlying vascular lesion burden contributes to FVH formation remains unclear. <Emphasis Type="BoldItalic">Findings</Emphasis> Infarction, severe stenosis, and vascular lesion burden features effectively distinguished both FVH presence and higher burden, with combined models demonstrating excellent discriminatory performance. <Emphasis Type="BoldItalic">Clinical relevance</Emphasis> FVH may serve as a valuable and readily accessible biomarker on conventional MRI that integrates infarction and specific vascular characteristics, suggesting its potential to enhance risk stratification and guide personalized therapeutic decisions in clinical practice. Graphical Abstract

FLAIR vascular hyperintensity: association with infarction and vascular lesion burden in patients with middle cerebral artery stenosis

期刊论文
发表日期：

2026年3月12日

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Chunxiu Jiang,
Yuxin Li,
Caihong Li,
Yaoming Qu,
Jianbin Zhu,
Xianlong Wang,
Zhibo Wen

摘要

Objectives

Fluid-attenuated inversion recovery (FLAIR) vascular hyperintensity (FVH) is a marker of hemodynamic impairment linked to poor outcomes. However, its underlying vascular pathology remains unclear. We aimed to evaluate the relationships between FVH, infarction, and vascular lesion burden, and explore whether infarction and vascular lesion burden can discriminate FVH presence and burden.

Materials and methods

A total of 253 consecutive patients with middle cerebral artery lesions who underwent vessel wall imaging were retrospectively enrolled. Multivariate logistic regressions were performed to identify discriminatory factors for FVH presence or burden; area under the curve (AUC), sensitivity and specificity assessed the discriminatory ability of combined models.

Results

Infarction, severe stenosis, and vascular wall marked enhancement were independently associated with FVH (ORs 2.995, 4.074, 2.141; all p < 0.05). Infarction, severe stenosis, max wall thickness, and max vascular lesion length were independently correlated with higher FVH burden (ORs 2.966, 8.785, 2.344, 1.049; all p < 0.05). The combined model (infarction + severe stenosis + marked enhancement) discriminated FVH presence with an excellent AUC of 0.803 (95% CI: 0.749–0.850, p < 0.001; sensitivity 76.6%; specificity 76.7%). The combined model (infarction + severe stenosis + max wall thickness + max vascular lesion length) discriminated higher FVH burden with an AUC of 0.801 (95% CI: 0.746–0.848, p < 0.001; sensitivity 80.8%; specificity 70.9%).

Conclusion

Infarction and vascular lesion burden are key factors associated with FVH. Our findings suggest a pathophysiological link between FVH and underlying vessel wall pathology, positioning FVH as a potential integrative MRI biomarker.

Key Points

Question While FLAIR vascular hyperintensity (FVH) indicates hemodynamic compromise and slow collateral flow, how the underlying vascular lesion burden contributes to FVH formation remains unclear.

Findings Infarction, severe stenosis, and vascular lesion burden features effectively distinguished both FVH presence and higher burden, with combined models demonstrating excellent discriminatory performance.

Clinical relevance FVH may serve as a valuable and readily accessible biomarker on conventional MRI that integrates infarction and specific vascular characteristics, suggesting its potential to enhance risk stratification and guide personalized therapeutic decisions in clinical practice.

Graphical Abstract