创伤后应激障碍通过神经和心脏炎症通路增加了主要心血管不良事件的风险
Antonia V Seligowski1, Simran S Grewal2, Shady Abohashem2
1Deparment of Psychiatry, Massachusetts General Hospital and Harvard Medical School, Boston, MA, USA; Cardiovascular Imaging Research Center, Massachusetts General Hospital and Harvard Medical School, Boston, MA, USA.
Brain, behavior, and immunity
|January 13, 2024
概括
创伤后应激障碍 (PTSD) 通过神经免疫通路与主要不良心血管事件 (MACE) 有关. 与压力相关的神经活动,心率变化和炎症介于PTSD患者心血管风险增加.
科学领域:
- 心脏病学 心脏病学
- 精神病学是一个精神病学.
- 神经科学是一个神经科学.
背景情况:
- 创伤后应激障碍 (PTSD) 与重大心血管不良事件 (MACE) 的风险增加有关.
- 将PTSD与MACE联系在一起的潜在机制仍然不完全理解.
- 新出现的证据表明神经免疫通路调解了压力综合征和心血管疾病之间的关系.
研究的目的:
- 调查神经免疫机制是否调解PTSD和MACE之间的关联.
- 测试一种假设,即高调节的神经免疫活动会增加患有PTSD的个体的MACE风险.
主要方法:
- 使用了一个大型的医院生物库队列 (N=118,827).
- 数据包括人口统计,诊断和病史.
- 参与者的子组提供了与压力相关的神经活动 (SNA),心率变化 (HRV) 和高灵敏性C反应蛋白 (hs-CRP) 的数据.
主要成果:
- 在调整传统风险因素后,PTSD独立预测MACE (HR=1.317,p=0.003).
- 创伤后应激障碍和MACE之间的关联被SNA,HRV和hs-CRP显著调解.
- 调解分析表明,神经免疫标记在这种关系中起着至关重要的作用.
结论:
- 神经免疫通路,包括SNA,HRV和hs-CRP,与PTSD患者中MACE风险增加有关.
- 这些发现突出了减少PTSD心血管风险的潜在治疗目标.
- 需要进一步的研究来证实针对这些神经免疫标记物的治疗相关性.
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