Spousal bereavement is associated with more pronounced ex vivo cytokine production and lower heart rate variability: Mechanisms underlying cardiovascular risk?
Spousal bereavement is associated with more pronounced ex vivo cytokine production and lower heart rate variability: Mechanisms underlying cardiovascular risk?
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DOI：
10.1016/j.psyneuen.2018.04.010
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发表时间：
2018-07-01
影响因子：
3.7
通讯作者：
Heijnen, Cobi
中科院分区：
文献类型：
--
作者：
Fagundes, Christopher P.;Murdock, Kyle W.;Heijnen, Cobi
失去配偶是一件压力很大的事情，会使人们面临额外的死亡风险。丧偶者的超额死亡率在配偶死亡后的前六个月最高，并随着时间的推移而下降。心脏病在这些死亡中所占比例最大。与应激性生活事件相关的心理应激可以增强炎症和降低心率变异性(HRV)。较低的心率变异性和较高的炎症反应都是心血管并发症和死亡率的危险因素。32名最近失去亲人的人(平均为死亡后89.68天，SD=17.09)和33名年龄匹配的对照完成了抽血、心电图和自我报告问卷。在调整和未调整的模型中，配偶丧亲与体外脂多糖刺激外周血白细胞产生的促炎细胞因子增加有关。此外，与对照组相比，配偶丧亲与较低的心率变异性相关。这项研究首次证明，在一个完全由寡妇和鳏夫组成的人群中，丧失亲人与更明显的体外细胞因子产生和较低的HRV有关。这些发现增加了越来越多的文献，揭示了与丧亲有关的心血管问题背后的机制。未来需要进行纵向研究，以确定这些风险之间的时间关系。了解这种紧张的生活事件背后的生物学机制，可以让研究人员为干预创造治疗目标，以减少或防止“心碎”的损失。
The loss of a spouse is a highly stressful event that puts people at excess risk of mortality. Excess mortality among those who are widowed is highest in the first six months after the death of a spouse and decreases over time. Heart disease accounts for the largest proportion of these deaths. The psychological stress associated with stressful life events can enhance inflammation and lower heart rate variability (HRV). Both lower HRV and higher inflammation are risk factors for cardiovascular morbidity and mortality. Thirty-two recently bereaved individuals (Mean = 89.68 days since death, SD = 17.09) and 33 age-matched comparisons completed a blood draw, EKG, and self-report questionnaires. In both adjusted and unadjusted models, spousal bereavement was associated with enhanced pro-inflammatory cytokine production by in vitro lipolysaccharide-stimulated peripheral blood leukocytes. Moreover, spousal bereavement was associated with lower HRV in comparison to the comparison group. This study is the first to demonstrate that bereavement is associated with a more pronounced ex vivo cytokine production and lower HRV in a population that exclusively consisted of widows and widowers. These findings add to the growing literature revealing the mechanisms that underlie bereavement-related cardiovascular problems. Future longitudinal studies are needed to determine the temporal relation between these risks. Understanding the biological mechanisms that underlie this stressful life event could allow researchers to create therapeutic targets for interventions to reduce or prevent the toll of a "broken heart."