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阻塞性睡眠呼吸暂停和夜间低氧血症与心肌梗死昼夜节律的关联。

Association of Obstructive Sleep Apnea and Nocturnal Hypoxemia With the Circadian Rhythm of Myocardial Infarction.

作者信息

Liu Xiaochen, Wang Bin, Hao Wen, Qiu Yuyao, Guo Qian, Guo Yingying, Xin Qingjie, Fan Jingyao, Que Bin, Gong Wei, Zheng Wen, Wang Xiao, Nie Shaoping

机构信息

Center for Coronary Artery Disease, Division of Cardiology Beijing Anzhen Hospital, Capital Medical University Beijing China.

Division of Cardiology Qingdao Municipal Hospital, Shandong Province Qingdao China.

出版信息

J Am Heart Assoc. 2025 Feb 4;14(3):e036729. doi: 10.1161/JAHA.124.036729. Epub 2025 Jan 27.

DOI:10.1161/JAHA.124.036729
PMID:39868516
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC12074749/
Abstract

BACKGROUND

The circadian rhythm of myocardial infarction (MI) in patients with obstructive sleep apnea (OSA) remains disputable and no studies have directly evaluated the relationship between nocturnal hypoxemia and the circadian rhythm of MI. The aim of the current study was to evaluate the association of OSA and nocturnal hypoxemia with MI onset during the night.

METHODS

Patients with MI in the OSA-acute coronary syndrome (ACS) project (NCT03362385) were recruited. The time of MI onset was identified by patient's report of the chest pain that prompted hospital admission. All patients underwent an overnight sleep study using a type III portable sleep monitoring device after clinical stabilization during hospitalization. The difference in circadian variation of MI onset was evaluated between patients with moderate/severe OSA and non/mild OSA and those with or without nocturnal hypoxemia. Nocturnal hypoxemia was evaluated using 3 variables, including oxygen desaturation index, minimum oxygen saturation, and total sleep time with saturation <90%.

RESULTS

Among 713 patients enrolled, 398 (55.8%) had moderate/severe OSA (apnea-hypopnea index ≥15 events·h - 1). Compared with the non/mild OSA group, the MI onset was significantly increased in the moderate/severe OSA group between midnight to 5:59 am in 6-hour epochs analysis (26.9% versus 18.4%, =0.008). Only in patients with both moderate/severe OSA and nocturnal hypoxemia, including oxygen desaturation index ≥15, minimum oxygen saturation ≤86%, and total sleep time with saturation <90% ≥2%, the incidence of MI onset between midnight to 5:59 am was significantly increased. Moderate/severe OSA (adjusted odds ratio 1.66 [95% CI, 1.13-2.43]; =0.01) and nocturnal hypoxemia (oxygen desaturation index ≥15 model, adjusted odds ratio 1.80, [95% CI, 1.21-2.66]; minimum oxygen saturation ≤86% model, adjusted odds ratio 1.70 [95% CI, 1.16-2.47]; =0.006; total sleep time with saturation <90% ≥2% model, adjusted odds ratio 1.54 [95% CI, 1.04-2.27]; =0.03) significantly predicted MI occurrence from midnight to 6:00 am.

CONCLUSIONS

A peak of incident MI onset between midnight to 5:59 am was observed in patients with moderate/severe OSA, especially in those presenting with nocturnal hypoxemia.

摘要

背景

阻塞性睡眠呼吸暂停(OSA)患者心肌梗死(MI)的昼夜节律仍存在争议,且尚无研究直接评估夜间低氧血症与MI昼夜节律之间的关系。本研究的目的是评估OSA和夜间低氧血症与夜间MI发作的相关性。

方法

招募OSA-急性冠状动脉综合征(ACS)项目(NCT03362385)中的MI患者。MI发作时间通过患者报告促使其住院的胸痛来确定。所有患者在住院期间临床病情稳定后,使用III型便携式睡眠监测设备进行整夜睡眠研究。评估中度/重度OSA患者与非/轻度OSA患者以及有或无夜间低氧血症患者之间MI发作昼夜变化的差异。使用3个变量评估夜间低氧血症,包括氧去饱和指数、最低氧饱和度和饱和度<90%的总睡眠时间。

结果

在纳入的713例患者中,398例(55.8%)患有中度/重度OSA(呼吸暂停低通气指数≥15次事件·小时⁻¹)。在6小时时段分析中,与非/轻度OSA组相比,中度/重度OSA组在午夜至凌晨5:59之间MI发作显著增加(26.9%对18.4%,P=0.008)。仅在同时患有中度/重度OSA和夜间低氧血症的患者中,包括氧去饱和指数≥15、最低氧饱和度≤86%以及饱和度<90%的总睡眠时间≥2%,午夜至凌晨5:59之间MI发作的发生率显著增加。中度/重度OSA(调整优势比1.66[95%CI,1.13-2.43];P=0.01)和夜间低氧血症(氧去饱和指数≥15模型,调整优势比1.80,[95%CI,1.21-2.66];最低氧饱和度≤86%模型,调整优势比1.70[95%CI,1.16-2.47];P=0.006;饱和度<90%的总睡眠时间≥2%模型,调整优势比1.54[95%CI,1.04-2.27];P=0.03)显著预测了午夜至凌晨6:00之间MI的发生。

结论

在中度/重度OSA患者中,尤其是伴有夜间低氧血症的患者,观察到午夜至凌晨5:59之间MI发作出现高峰。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4845/12074749/c5ceb3deec9f/JAH3-14-e036729-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4845/12074749/40ff3ed5ab8c/JAH3-14-e036729-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4845/12074749/9ec189fa749f/JAH3-14-e036729-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4845/12074749/2956478ef8d6/JAH3-14-e036729-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4845/12074749/c5ceb3deec9f/JAH3-14-e036729-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4845/12074749/40ff3ed5ab8c/JAH3-14-e036729-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4845/12074749/9ec189fa749f/JAH3-14-e036729-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4845/12074749/2956478ef8d6/JAH3-14-e036729-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4845/12074749/c5ceb3deec9f/JAH3-14-e036729-g001.jpg

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