在急性心肌梗塞后睡眠呼吸障碍的炎症和纤维化
Jan Pec1, Stefan Buchner2, Henrik Fox3
1Department of Internal Medicine II, University Hospital Regensburg, 93053 Regensburg, Germany.
Biomedicines
|January 23, 2024
概括
在急性心肌梗塞 (AMI) 后的睡眠呼吸障碍 (SDB) 与更高的炎症和纤维化有关. 这表明SDB恶化了心脏在AMI后的恢复.
科学领域:
- 心脏病学 心脏病学
- 睡眠医学 睡眠医学
- 生物标志物 生物标志物
背景情况:
- 急性心肌梗塞 (AMI) 后的炎症驱动不良组织重塑.
- 聚原III氨基终端 (PIIINP) 表示原合成,并预测心脏衰竭后AMI.
- 睡眠呼吸障碍 (SDB) 可能促进炎症和纤维化,减少心肌的救援.
研究的目的:
- 为了调查SDB是否会提高循环中的炎症生物标志物 (hs-CRP) 和AMI后纤维化 (PIIINP).
- 通过皮肤冠状动脉干预 (PCI) 后与没有SDB的AMI患者的生物标志物水平进行比较.
主要方法:
- 用PCI治疗的88名首次AMI患者的横截面分析.
- 基于呼吸暂停-呼吸暂停指数 (AHI) 的分层;SDB定义为AHI≥15h-1 .
- 在PCI后3-5天测量hs-CRP和PIIINP水平.
主要成果:
- 患有SDB的患者表现出明显更高的hs-CRP (18.3 mg/L与5.8 mg/L) 和PIIINP (0.49 U/mL与0.33 U/mL) 水平.
- 在多变量分析中,SDB独立预测了更高的hs-CRP (p=0.028) 和PIIINP (p<0.001).
- 阻塞性SDB,而不是中央SDB,与高hs-CRP和PIIINP相关.
结论:
- 在AMI之后阻塞性SDB独立地与hs-CRP和PIIINP的增加有关.
- 结果突出了SDB作为伴随性疾病的作用,表明炎症加剧和心肌纤维化.
- 在AMI后,SDB管理可能对改善结果至关重要.
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