在COVID-19后的6个月和12个月后的SARS-CoV-2感染患者中,内皮功能障碍和心血管风险
Paula Poyatos1,2, Neus Luque1, Gladis Sabater1,2
1Department of Pulmonary Medicine, Dr. Josep Trueta University Hospital de Girona, Santa Caterina Hospital de Salt and the Girona Biomedical Research Institute (IDIBGI), 17190, Girona, Spain.
后COVID-19患者显示持续的血管损伤和改变的内皮殖民地形成细胞 (ECFCs) 长达12个月. 较低的ECFC与较高的炎症相关,这表明它具有保护作用,需要进行后续检查.
科学领域:
- 心血管研究研究心血管研究
- 传染病免疫学 传染病免疫学
- 血管生物学 血管生物学
背景情况:
- 感染SARS-CoV-2会导致内皮损伤,这是心血管并发症的关键因素.
- 内皮殖民地形成细胞 (ECFC) 是血管损伤的生物标志物,但它们在COVID-19后果中的作用尚不清楚.
研究的目的:
- 调查COVID-19后ECFC和血管源生物标志物的长期变化.
- 确定这些变化是否与长期COVID综合征和心血管风险标志物相关.
主要方法:
- 招募了72名COVID-19后患者和31名健康对照,根据人口统计和并发症进行了匹配.
- 从外围血液中量化的ECFC和测量的血管原生生物标志物,托洛,NT-proBNP和费里水平.
主要成果:
- 感染后的6个月和12个月内,ECFC的产量持续增加 (82.8%与对照组的48.4%相比).
- 在12个月内观察到血管生成蛋白的显著下调和心血管风险标志物 (热素,NT-proBNP,费里丁) 的升高.
- 较低的ECFC计数与较高的费里水平相关,这表明ECFCs具有保护作用.
结论:
- 在SARS-CoV-2感染后,血管连续性持续长达12个月.
- 碳化合物可能起到对炎症和心血管风险的保护作用.
- 强调需要预防策略和长期患者监测.
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