Associations between arterial stiffness, depressive symptoms and cerebral small vessel disease: cross-sectional findings from the AGES-Reykjavik Study.
Associations between arterial stiffness, depressive symptoms and cerebral small vessel disease: cross-sectional findings from the AGES-Reykjavik Study.
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DOI：
10.1503/jpn.140334
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发表时间：
2016-04
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影响因子：
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通讯作者：
T. V. van Sloten;G. Mitchell;S. Sigurdsson;M. van Buchem;P. Jonsson;M. Garcia;T. Harris;R. Henry;A. Levey;C. Stehouwer;V. Gudnason;L. Launer
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作者：
T. V. van Sloten;G. Mitchell;S. Sigurdsson;M. van Buchem;P. Jonsson;M. Garcia;T. Harris;R. Henry;A. Levey;C. Stehouwer;V. Gudnason;L. Launer
动脉硬化可能通过脑微血管损伤导致抑郁，但证据很少。因此，我们研究了动脉硬化是否与抑郁症状有关，以及脑小血管疾病是否有助于这种关联。这项横断面研究包括AGES-Reykjavik研究第二轮检查的参与者子集，该研究于2007年至2011年进行。测定动脉僵硬度（颈-股动脉脉搏波速度[CFPWV]）、抑郁症状（15项老年抑郁量表[GDS-15]）和脑小血管疾病（MRI）。脑小血管病变的表现包括较高的白色高信号体积、皮质下梗死、脑微出血、Virchow-Robin间隙和较低的总脑实质体积。结果：我们的分析包括2058名参与者（平均年龄79.6岁，59.0%为女性）。校正潜在混杂因素后，较高的CFPWV与较高的GDS-15评分相关（β 0.096，95%置信区间[CI] 0.005-0.187）。对白色高信号体积或皮质下梗死的额外调整减弱了CFPWV和GDS-15评分之间的关联，其变得不显著（p > 0.05）。正式的调解测试表明，白色物质高信号体积和皮质下梗死的衰减效果有统计学意义。Virchow-Robin间隙、脑微出血和脑萎缩不能解释CFPWV与抑郁症状之间的关系。局限性我们的研究受到其横断面设计的限制，这排除了任何关于因果中介的结论。抑郁症状通过自我报告问卷进行评估。结论：动脉僵硬度越大，抑郁症状越多;这种关联部分由白色物质高信号体积和皮质下梗死引起。这项研究支持了动脉硬化导致抑郁症部分通过脑小血管疾病的假设。
BACKGROUND Arterial stiffness may contribute to depression via cerebral microvascular damage, but evidence for this is scarce. We therefore investigated whether arterial stiffness is associated with depressive symptoms and whether cerebral small vessel disease contributes to this association. METHODS This cross-sectional study included a subset of participants from the AGES-Reykjavik study second examination round, which was conducted from 2007 to 2011. Arterial stiffness (carotid-femoral pulse wave velocity [CFPWV]), depressive symptoms (15-item geriatric depression scale [GDS-15]) and cerebral small vessel disease (MRI) were determined. Manifestations of cerebral small vessel disease included higher white matter hyperintensity volume, subcortical infarcts, cerebral microbleeds, Virchow-Robin spaces and lower total brain parenchyma volume. RESULTS We included 2058 participants (mean age 79.6 yr; 59.0% women) in our analyses. Higher CFPWV was associated with a higher GDS-15 score, after adjustment for potential confounders (β 0.096, 95% confidence interval [CI] 0.005-0.187). Additional adjustment for white matter hyperintensity volume or subcortical infarcts attenuated the association between CFPWV and the GDS-15 score, which became nonsignificant (p > 0.05). Formal mediation tests showed that the attenuating effects of white matter hyperintensity volume and subcortical infarcts were statistically significant. Virchow-Robin spaces, cerebral microbleeds and cerebral atrophy did not explain the association between CFPWV and depressive symptoms. LIMITATIONS Our study was limited by its cross-sectional design, which precludes any conclusions about causal mediation. Depressive symptoms were assessed by a self-report questionnaire. CONCLUSION Greater arterial stiffness is associated with more depressive symptoms; this association is partly accounted for by white matter hyperintensity volume and subcortical infarcts. This study supports the hypothesis that arterial stiffness leads to depression in part via cerebral small vessel disease.