Boyu Zhang1,2, Yingzhe Wang3,4, Bei Wang1,2, Ying-Hua Chu5, Yanfeng Jiang3,4, Mei Cui6, He Wang1,2,7, Xingdong Chen3,4. 1. Institute of Science and Technology for Brain-Inspired Intelligence, Fudan University, Shanghai, China. 2. Key Laboratory of Computational Neuroscience and Brain-Inspired Intelligence (Fudan University), Ministry of Education, Shanghai, China. 3. State Key Laboratory of Genetic Engineering, Human Phenome Institute, and School of Life Sciences, Fudan University, Shanghai, China. 4. Fudan University Taizhou Institute of Health Sciences, Taizhou, China. 5. MR Collaboration, Siemens Healthcare Ltd., Shanghai, China. 6. Department of Neurology, Huashan Hospital, Fudan University, Shanghai, China. 7. Human Phenome Institute, Fudan University, Shanghai, China.
Abstract
BACKGROUND: High blood pressure (BP) is a common risk factor for cerebral small vessel disease including white matter hyperintensity (WMH). Whether increased BP exacerbates WMH by impacting cerebral vascular morphologies remains poorly studied. PURPOSE: To determine the relationships among high BP, cerebrovascular morphologies, and WMH in elderly individuals. STUDY TYPE: Cohort. SUBJECTS: Eight hundred sixty-three participants (54.2% female) from the Taizhou Imaging Study without clinical evidence of neurologic disorders were included in the analyses. FIELD STRENGTH/SEQUENCE: 3.0 T; time-of-flight magnetic resonance angiography (TOF MRA); T2 fluid-attenuated inversion recovery (FLAIR); T1 magnetization-prepared rapid gradient-echo; gradient echo T2*-weighted; diffusion tensor imaging; pulsed arterial spin labeling. ASSESSMENT: Cerebrovascular morphologic measurements were quantified based on the TOF MRA images, including vessel density, radius, tortuosity, and branch number. WMH lesion volumes (WMHV) and WMH lesion counts (WMHC) were calculated automatically based on the T2 FLAIR images. STATISTICAL TESTS: Multivariable linear regression analysis and path analysis with a linear single-mediator model were employed. A P value <0.05 was considered statistically significant. RESULTS: Higher BP, especially diastolic BP, was significantly correlated with lower cerebrovascular density (β = -104) and lower branch numbers (β = -0.02). Although decreased tortuosity (β = -1.25) and increased radius (β = 93.8) were correlated with BP, no significant relationship of tortuosity (β = -4.6 × 10-4 , P = 0.58) or radius (β = 0.03, P = 0.08) with BP in small vessels was found. The proportion of small vessels decreased as BP increased (SBP: β = -6.6 × 10-4 ; DBP: β = -9.0 × 10-4 ). Similarly, increased WMHV and WMHC were associated with decreased vessel density (volumes: β = -24, counts: β = -127), decreased tortuosity (volumes: β = -0.08, counts: β = -0.53), and increased radius (volumes: β = 12.6, counts: β = 86.6). Path analyses suggested an association between high BP and WMHs that were mediated by cerebrovascular morphologic changes. DATA CONCLUSION: Structural alterations of cerebral vessels induced by high BP are correlated with WMH. This result suggested that elevated BP might be one of the pathophysiological mechanisms involving in the co-occurrence of cerebrovascular alteration and small vessel disease. LEVEL OF EVIDENCE: 1 Technical Efficacy Stage: 1.
BACKGROUND: High blood pressure (BP) is a common risk factor for cerebral small vessel disease including white matter hyperintensity (WMH). Whether increased BP exacerbates WMH by impacting cerebral vascular morphologies remains poorly studied. PURPOSE: To determine the relationships among high BP, cerebrovascular morphologies, and WMH in elderly individuals. STUDY TYPE: Cohort. SUBJECTS: Eight hundred sixty-three participants (54.2% female) from the Taizhou Imaging Study without clinical evidence of neurologic disorders were included in the analyses. FIELD STRENGTH/SEQUENCE: 3.0 T; time-of-flight magnetic resonance angiography (TOF MRA); T2 fluid-attenuated inversion recovery (FLAIR); T1 magnetization-prepared rapid gradient-echo; gradient echo T2*-weighted; diffusion tensor imaging; pulsed arterial spin labeling. ASSESSMENT: Cerebrovascular morphologic measurements were quantified based on the TOF MRA images, including vessel density, radius, tortuosity, and branch number. WMH lesion volumes (WMHV) and WMH lesion counts (WMHC) were calculated automatically based on the T2 FLAIR images. STATISTICAL TESTS: Multivariable linear regression analysis and path analysis with a linear single-mediator model were employed. A P value <0.05 was considered statistically significant. RESULTS: Higher BP, especially diastolic BP, was significantly correlated with lower cerebrovascular density (β = -104) and lower branch numbers (β = -0.02). Although decreased tortuosity (β = -1.25) and increased radius (β = 93.8) were correlated with BP, no significant relationship of tortuosity (β = -4.6 × 10-4 , P = 0.58) or radius (β = 0.03, P = 0.08) with BP in small vessels was found. The proportion of small vessels decreased as BP increased (SBP: β = -6.6 × 10-4 ; DBP: β = -9.0 × 10-4 ). Similarly, increased WMHV and WMHC were associated with decreased vessel density (volumes: β = -24, counts: β = -127), decreased tortuosity (volumes: β = -0.08, counts: β = -0.53), and increased radius (volumes: β = 12.6, counts: β = 86.6). Path analyses suggested an association between high BP and WMHs that were mediated by cerebrovascular morphologic changes. DATA CONCLUSION: Structural alterations of cerebral vessels induced by high BP are correlated with WMH. This result suggested that elevated BP might be one of the pathophysiological mechanisms involving in the co-occurrence of cerebrovascular alteration and small vessel disease. LEVEL OF EVIDENCE: 1 Technical Efficacy Stage: 1.