Thomas Owen, Cain John, Nasralla Mehran, Jackson Alan
Salford Royal NHS Foundation Trust, Salford, United Kingdom.
Salford Royal NHS Foundation Trust, Salford, United Kingdom; Wolfson Molecular Imaging Centre, School of Medicine, University of Manchester, Greater Manchester, United Kingdom.
J Stroke Cerebrovasc Dis. 2019 May;28(5):1252-1260. doi: 10.1016/j.jstrokecerebrovasdis.2019.01.020. Epub 2019 Feb 13.
To test the hypotheses that changes in the aortic pulse-wave produced by arterial stiffening are (1) propagated into cerebral small vessels, (2) associated with reduced compliance of small cerebral arterial vessels, and (3) associated with the presence of dilated perivascular spaces (PVS).
Fifteen volunteers and 19 patients with late-onset depression (LOD) were prospectively recruited, of which 6 fulfilled the criteria for treatment-resistant depression (TRD). Aortic pulse-wave velocity (PWV) was determined using Carotid-Femoral Doppler. Pulse-wave analysis (PWA) was performed using a SphygmoCor system. White-matter lesion load and PVS were scored on established MRI scales. Cerebral arterial and aqueductal cerebrospinal fluid (CSF) flow patterns were studied using quantitative phase-contrast angiography.
Depressed patients had more PVS (P < .05) and prolongation of the width of the arterial systolic pulse-wave in the carotid arteries (P < .01). There was no significant group difference for any PWV or PWA measurement. TRD patients showed more PVS than other LOD patients (P < .05). The fractional width of the arterial systolic peak correlated significantly with augmentation index (AIx) and heart rate-corrected augmentation index (AIx75; R = 0.302, P < .01and R = 0.363, P < .01 respectively). Arterial-aqueductal delay showed a negative correlation with estimated aortic systolic pressure (PWVsys; R = 0.293; P < .01), AIx (R = -0.491; P < .01) and AIx75 (R = -0.310; P < .01). PVS scores correlated with AIx (R = 0.485; P < .01) and AIx75 (R = -0.292; P < .01).
Our findings support the hypothesis that increased arterial pulsatility resulting from central arterial stiffness propagates directly into cerebral vessels and is associated with the development of microvascular angiopathy, characterized by dilated PVS and decreased compliance of small arterial vessels.
为验证以下假设:动脉僵硬度引起的主动脉脉搏波变化(1)会传播至脑小血管;(2)与脑小动脉血管顺应性降低有关;(3)与血管周围间隙(PVS)增宽有关。
前瞻性招募了15名志愿者和19名晚发性抑郁症(LOD)患者,其中6名符合难治性抑郁症(TRD)标准。使用颈股多普勒测定主动脉脉搏波速度(PWV)。使用SphygmoCor系统进行脉搏波分析(PWA)。根据既定的MRI量表对白质病变负荷和PVS进行评分。使用定量相位对比血管造影术研究脑动脉和导水管脑脊液(CSF)流动模式。
抑郁症患者的PVS更多(P < 0.05),颈动脉动脉收缩期脉搏波宽度延长(P < 0.01)。在任何PWV或PWA测量中,两组之间均无显著差异。TRD患者的PVS比其他LOD患者更多(P < 0.05)。动脉收缩期峰值的分数宽度与增强指数(AIx)和心率校正增强指数(AIx75)显著相关(分别为R = 0.302,P < 0.01和R = 0.363,P < 0.01)。动脉-导水管延迟与估计的主动脉收缩压(PWVsys;R = 0.293;P < 0.01)、AIx(R = -0.491;P < 0.01)和AIx75(R = -0.310;P < 0.01)呈负相关。PVS评分与AIx(R = 0.485;P < 0.01)和AIx75(R = -0.292;P < 0.01)相关。
我们的研究结果支持以下假设:中心动脉僵硬度导致的动脉搏动性增加直接传播至脑血管,并与微血管病的发展有关,其特征为PVS增宽和小动脉血管顺应性降低。