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在COVID-19冲击患者中可逆心肌缩和扩张
Matthew J Fata1, Steven M Hollenberg2, Brent Klinkhammer3
1Hackensack University Medical Center, Hackensack, NJ.
Critical care explorations
|June 13, 2025
概括
COVID-19的冲击会导致可逆性心肌压缩和心室扩张,类似于细菌性败血症. 心声图显示,幸存者左心室喷射率有所改善,这表明共享的病原遗传机制.
科学领域:
- 心脏病学 心脏病学
- 传染性疾病 传染性疾病
- 关键护理医学 关键护理医学
背景情况:
- 细菌和真菌感染引起的败血症冲击通常呈现为左心室喷射率 (LVEF) 降低和左心室 (LV) 轻度扩张.
- 这些心脏异常在几天内在幸存者中是可逆的.
- 研究了住院COVID-19患者的休克,以评估心脏功能.
研究的目的:
- 调查COVID-19冲击患者心肌功能障碍和心室扩张的可逆性.
- 为了比较COVID-19冲击对心脏的影响与细菌和真菌的败血症冲击.
主要方法:
- 分析了368名住院COVID-19患者的队列.
- 在急性休克期间,十五名患有心声图确定抑郁的LVEF的患者接受了连续心声图.
- 使用辛普森规则测量左心室喷射分数 (LVEF) 和LV体积,并通过配对t-test进行分析.
主要成果:
- 平均LVEF从急性休克期间的35.3%增加到随访时的43.8% (p=0.031).
- 静脉末透缩体积从182毫升降至152.1毫升 (p=0.025),静脉末透缩体积从120.2毫升降至90.1毫升 (p=0.025).
- 索引中风体积没有显著变化 (29.6毫升对31.7毫升,p=0.522).
结论:
- 随着LVEF降低和心室扩张的COVID-19冲击显示了心肌抑郁和扩张的可逆性.
- 这些发现与细菌和真菌败血症休克中观察到的结果相似,这表明共享的病原遗传机制.
- 由于COVID-19引起的败血性休克可能与细菌或真菌败血症共享心肌功能障碍途径.
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