Intracranial hemodynamic relationships in patients with cerebral small vessel disease
Intracranial hemodynamic relationships in patients with cerebral small vessel disease
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DOI：
10.1212/wnl.0000000000009483
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发表时间：
2020-05-26
期刊：
影响因子：
9.9
通讯作者：
Wardlaw, Joanna M.
中科院分区：
文献类型：
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作者：
Blair, Gordon W.;Thrippleton, Michael J.;Wardlaw, Joanna M.
目的探讨轻度缺血性卒中患者的脑血管反应性(CVR)、血流、血管和脑脊液的搏动性及其与脑小血管病变(SVD)特征和MRI表现的独立关系。方法我们招募了轻度缺血性卒中患者，在高二氧化碳状态下用血氧水平依赖的MRI评估CVR，用相位对比MRI评估脑血管和脑脊液的搏动性，用结构磁共振脑成像定量白质高信号(WMH)和血管周围间隙(PVSS)。我们使用多元回归来确定与SVD特征相关的参数，并控制患者的特征。结果60例患者中有53例完成了完整的数据集(年龄68.0%+/-8.8岁，74%男性，75%高血压)。在控制了年龄、性别和收缩压后，较低的白质CVR与较高的WMH容量(WMH容量每对数值增加-0.01%/mm Hg，p=0.02)、基底节PVS(PVS评分每点增加-0.01%/mm Hg，p=0.02)和较高的静脉搏动(上矢状窦-0.03%/mm Hg，p=0.02，每单位脉动指数增加)相关，但与CBF无关(p=0.58)。枕大孔下部脑脊液每搏出血量与脑白质CVR较差(每毫升脑搏出量增加0.04%/mm Hg，p=0.04)和基底节PVS较严重(p=0.09)相关。结论较低的CVR、较高的静脉搏动性和较低的枕大孔脑脊液每搏输出量表明，动态血管功能障碍是PVS功能障碍和WMH发生的基础。进一步探索微血管功能障碍和脑脊液动力学可能会发现新的机制和干预靶点，以减少SVD病变的发展、认知能力下降和卒中。
Objective To investigate cerebrovascular reactivity (CVR), blood flow, vascular and CSF pulsatility, and their independent relationship with cerebral small vessel disease (SVD) features in patients with minor ischemic stroke and MRI evidence of SVD. Methods We recruited patients with minor ischemic stroke and assessed CVR using blood oxygen level-dependent MRI during a hypercapnic challenge, cerebral blood flow (CBF), vascular and CSF pulsatility using phase-contrast MRI, and structural magnetic resonance brain imaging to quantify white matter hyperintensities (WMHs) and perivascular spaces (PVSs). We used multiple regression to identify parameters associated with SVD features, controlling for patient characteristics. Results Fifty-three of 60 patients completed the study with a full data set (age 68.0% +/- 8.8 years, 74% male, 75% hypertensive). After controlling for age, sex, and systolic blood pressure, lower white matter CVR was associated with higher WMH volume (-0.01%/mm Hg per log10 increase in WMH volume,p= 0.02), basal ganglia PVS (-0.01%/mm Hg per point increase in the PVS score,p= 0.02), and higher venous pulsatility (superior sagittal sinus -0.03%/mm Hg,p= 0.02, per unit increase in the pulsatility index) but not with CBF (p= 0.58). Lower foramen magnum CSF stroke volume was associated with worse white matter CVR (0.04%/mm Hg per mL increase in stroke volume,p= 0.04) and more severe basal ganglia PVS (p= 0.09). Conclusions Lower CVR, higher venous pulsatility, and lower foramen magnum CSF stroke volume indicate that dynamic vascular dysfunctions underpin PVS dysfunction and WMH development. Further exploration of microvascular dysfunction and CSF dynamics may uncover new mechanisms and intervention targets to reduce SVD lesion development, cognitive decline, and stroke.