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An evidence of brain-heart disorder: mental stress-induced myocardial ischemia regulated by inflammatory cytokines.
Neurological Research ( IF 1.9 ) Pub Date : 2020-06-23 , DOI: 10.1080/01616412.2020.1783879
Meiyan Liu 1 , Jianyang Liu 1 , Lijun Zhang 1 , Wan Xu 1 , Dongfang He 1 , Wanlin Wei 2 , Yingbin Ge 3 , Chaitu Dandu 4
Affiliation  

Objective

Underlying Coronary Artery Disease (CAD) complicated by Mental Stress-Induced Myocardial Ischemia (MSIMI) has been linked with an increased risk for adverse cardiovascular events and even sudden death. However, the underlying mechanisms of MSIMI remain unknown. In this study, we investigated cytokine levels at baseline inflammation status and during acute inflammatory responses to mental stress in patients with known CAD who presented with MSIMI.

Method

77 patients with known CAD were recruited and all underwent echocardiography before and during arithmetic stress task. MSIMI was diagnosed by new or worsening wall motion abnormalities greater than or equal to a 5% reduction of left ventricle ejection fraction. Inflammatory markers were measured both before and immediately after the Mental Stress (MS) by ELISA kits. Repeated measures models were used to report the responses and mixed linear regression models were used to report the differences between MSIMI negative and positive patients.

Result

MS induced a significant increase in Stromal Cell-Derived Factor-1α (SDF-1α) and Monocyte Chemoattractant Protein-1 (MCP-1) in all subjects; 20.78% of the patients with known CAD developed MSIMI during the arithmetic task. MSIMI positive patients had significantly lower baseline levels of Interleukin-1β (IL-1β) and Tumor Necrosis Factor-α (TNF-α), but a higher response in levels of SDF-1α than MSIMI negative patients.

Conclusion

MS can induce acute inflammatory responses. MSIMI is associated with lower levels of IL-1β and TNF-α at baseline and higher levels of SDF-1α in response to MS.



中文翻译:

脑-心脏疾病的证据:精神应激诱导的心肌缺血由炎症细胞因子调节。

目的

潜在的冠状动脉疾病(CAD)并伴有精神压力诱发的心肌缺血(MSIMI)与心血管不良事件甚至猝死的风险增加有关。但是,MSIMI的基本机制仍然未知。在这项研究中,我们调查了患有MSIMI的已知CAD患者在基线炎症状态和对精神压力的急性炎症反应期间的细胞因子水平。

方法

招募了77名已知CAD的患者,并在进行算术压力任务之前和期间均接受了超声心动图检查。通过新的或恶化的壁运动异常(大于或等于左心室射血分数降低5%)诊断出MSIMI。通过ELISA试剂盒在精神压力(MS)之前和之后立即测量炎症标志物。重复测量模型用于报告反应,混合线性回归模型用于报告MSIMI阴性和阳性患者之间的差异。

结果

MS诱导所有受试者的基质细胞衍生因子-1α(SDF-1α)和单核细胞趋化蛋白-1(MCP-1)显着增加;在计算任务期间,有20.78%的已知CAD患者发展了MSIMI。MSIMI阳性患者的白细胞介素-1β(IL-1β)和肿瘤坏死因子-α(TNF-α)的基线水平显着降低,但SDF-1α水平的应答率高于MSIMI阴性患者。

结论

MS可引起急性炎症反应。MSIMI与基线时较低的IL-1β和TNF-α水平以及较高的SDF-1α水平相关。

更新日期:2020-08-05
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