在冠状动脉再血管化后,CPAP可能在睡眠呼吸暂停中促进内皮炎症环境
Yuksel Peker1, Yeliz Celik2, Afrouz Behboudi3
1Koç University School of Medicine, Istanbul, Turkey; University of Gothenburg, Gothenburg, Sweden; Brigham & Women's Hospital, Boston, MA, USA; University of Pittsburgh School of Medicine, Pittsburgh, PA, USA; Lund University, Lund, Sweden.
EBioMedicine
|February 25, 2024
概括
针对阻塞性睡眠呼吸暂停 (OSA) 的持续正气道压力 (CPAP) 治疗可能会增加心血管风险,因为它会增加血管蛋白-2 和减少VEGF-A. 这些变化可能会抵消心血管疾病患者CPAP治疗的预期好处.
科学领域:
- 心脏病学 心脏病学
- 睡眠医学 睡眠医学
- 肺部医学 肺部医学
背景情况:
- 持续的正气道压力 (CPAP) 并没有在阻塞性睡眠呼吸暂停 (OSA) 患者中持续降低心血管风险.
- 通过CPAP治疗增加了血管蛋白-2的增加,这是一个与心血管风险相关的内皮标记物.
- 这项研究研究了CPAP在OSA患者中存在心血管疾病的潜在炎症效应.
研究的目的:
- 调查CPAP在患有OSA和心血管疾病的患者中预期不到的炎症作用.
- 评估内皮和肺上皮生物标记物的变化.
- 确定生物标志物变化和心血管结果之间的关联.
主要方法:
- 一个随机的12个月的试验,比较CPAP与OSA患者冠状动脉再血管化后的常规护理.
- 测量了血管蛋白-2,Tie-2,E-selectin,VEGF-A和sRAGE的血水平.
- 评估了生物标志物水平与心血管疾病/死亡率之间的关联.
主要成果:
- 在CPAP组中,血管蛋白-2仍然升高,VEGF-A下降.
- 在通常治疗组中,血管蛋白-2 降低,VEGF-A 仍然升高.
- 较高的12个月抗血管素-2水平与增加的死亡率相关;较高的CPAP水平与更糟糕的心血管结果相关.
结论:
- 与常规护理相比,CPAP疗法增加了促炎性血管蛋白-2并降低了心脏保护性VEGF-A.
- 这些生物标志物的改变可能会抵消CPAP治疗OSA预期的心血管益处.
- 需要进一步的研究来了解这些发现的临床影响.
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