长期COVID-19患者的交感神经过度驱动,血管功能障碍和运动能力降低:对心血管后续的长期研究
Bruna E Ono1,2, João E Izaias1,2, Artur O Sales1,2
1D'Or Institute for Research and Education (IDOR), Rio de Janeiro, RJ, Brazil.
概括
长期COVID患者表现出持续的交感过度激活,血管和心脏问题,以及感染后两年的运动能力降低. 这些心血管后果需要有针对性的治疗策略来解决.
科学领域:
- 心血管医学 心血管医学
- 传染性疾病 传染性疾病
- 运动生理学 运动生理学
背景情况:
- 严重的COVID-19与神经血管,心脏和运动能力受损有关.
- 长期COVID中这些变化的长期持续性尚未得到充分理解.
- 这项研究调查了长期COVID患者感染后2年的心血管和运动能力变化.
研究的目的:
- 为了测试长期COVID患者表现出持续的交感过度驱动,大动脉硬化,内皮功能障碍,心脏变化和运动能力下降的假设.
- 在SARS-CoV-2感染后2年评估心血管和功能后果.
主要方法:
- 评估了18名长期COVID患者和19名对照患者,医院出院后大约2年.
- 测量了肌肉交感神经活动 (MSNA),手臂动脉流介导扩张 (BAFMD),大动脉-大腿脉冲波速 (CFPWV),心脏功能 (心声学) 和峰值氧气吸收 (峰值V̇O2).
- 评估了循环中的 ангиотензин II,内皮细胞衍生的细胞外囊泡 (EV) 和氧化应激标志物.
主要成果:
- 与对照组相比,长期COVID患者的MSNA,CFPWV,心率和内皮细胞衍生的EV都较高,心脏功能 (E/A比率,LVEF,LVGLS) 和峰值V̇O2较低.
- 在长期COVID患者中观察到氧化应激标志物 (碳酸) 的增加和抗氧化能力的降低 (SOD).
- 峰值V̇O2与MSNA,LVGLS和碳基相反相关,与BAFMD和SOD直接相关.
结论:
- 长期COVID患者在急性疾病后2年表现出持续的交感过度激活,血管和心脏功能障碍,以及减弱的运动能力.
- 由内皮细胞衍生的EV增加和氧化压力有助于长期COVID的病理生理学.
- 迫切需要制定策略来解决这些持续的心血管后果.
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