Neurosciences and Mental Health Research Institute, School of Medicine, Cardiff University, Cardiff CF24 4HQ, United Kingdom; Institute of Life Sciences, Swansea University Medical School, Swansea University, Singleton Park, Swansea SA2 8PP, United Kingdom.
Neurosciences and Mental Health Research Institute, School of Medicine, Cardiff University, Cardiff CF24 4HQ, United Kingdom.
Brain Behav Immun. 2017 Feb;60:233-239. doi: 10.1016/j.bbi.2016.10.017. Epub 2016 Oct 18.
Stress influences the risk of cardiovascular disease. Acute mental stress can induce both low-grade inflammation and endothelial dysfunction. The relationship between inflammatory responses to stress and future endothelial function is unexplored. Knowledge on the impact of other cardiovascular risk factors, such as dyslipidaemia, on such relationships is also limited We investigated the relationship between inflammatory responses to an acute mental stress challenge and endothelial function plus the influence of dyslipidaemia on the associations. Interleukin-6 (IL-6), tumor necrosis factor α (TNFα) and fibrinogen were assessed at baseline, immediately following standardized behavioural tasks and 45 min post-task in 158 participants. Blood pressure and heart rate responses were measured. Flow-mediated dilatation (FMD) was measured 3years later. Fibrinogen and IL-6 increased post-stress (p⩽0.001 & 0.003) but TNFα was unchanged (p=0.09). An independent negative association between FMD and change in fibrinogen at 45 min (β=-0.047 p=0.016) remained after multiple adjustment (baseline fibrinogen, baseline diameter, reactive hyperaemia, age, gender and other cardiovascular risk factors). There was no association between FMD and change in IL-6 or TNFα. There were no differences in the responses to stress between those with and without dyslipidaemia. However, there was an interaction between the presence of dyslipidaemia and immediate change in fibrinogen with stress which was associated with FMD. Those participants with dyslipidaemia who had a greater change in fibrinogen had lower FMD. We conclude that elevated fibrinogen responses to stress are associated with future endothelial dysfunction which may reflect increased cardiovascular risk.
压力会影响心血管疾病的风险。急性精神压力可引起低度炎症和内皮功能障碍。应激时炎症反应与未来内皮功能之间的关系尚不清楚。关于其他心血管危险因素（如血脂异常）对这些关系的影响的知识也有限。我们研究了急性精神压力挑战引起的炎症反应与内皮功能之间的关系，以及血脂异常对这些关联的影响。在 158 名参与者中，在基线、标准化行为任务后立即以及任务后 45 分钟测量白细胞介素 6 (IL-6)、肿瘤坏死因子 α (TNFα) 和纤维蛋白原。测量血压和心率反应。3 年后测量血流介导的扩张 (FMD)。应激后纤维蛋白原和 IL-6 升高（p ⩽ 0.001 和 0.003），但 TNFα 不变（p = 0.09）。在多因素调整后，FMD 与 45 分钟时纤维蛋白原变化之间仍存在独立的负相关（基线纤维蛋白原、基线直径、反应性充血、年龄、性别和其他心血管危险因素）。FMD 与 IL-6 或 TNFα 变化之间没有关联。血脂异常者和无血脂异常者的应激反应无差异。然而，血脂异常的存在与应激时纤维蛋白原的即时变化之间存在相互作用，这与 FMD 有关。血脂异常患者纤维蛋白原变化较大者，FMD 较低。我们的结论是，应激时纤维蛋白原的升高与未来的内皮功能障碍有关，这可能反映出心血管风险增加。
