补充氧暴露对 ST 段抬高型心肌梗死心肌损伤的影响。
Effect of supplemental oxygen exposure on myocardial injury in ST-elevation myocardial infarction.
机构信息
Department of Research and Evaluation, Ambulance Victoria, Melbourne, Australia Department of Epidemiology and Preventive Medicine, Monash University, Melbourne, Australia.
Department of Epidemiology and Preventive Medicine, Monash University, Melbourne, Australia Department of Cardiology, Alfred Hospital, Melbourne, Australia Hypertension and Cardiac Disease Research Group, Baker IDI Heart and Diabetes Institute, Melbourne, Australia Department of Cardiology, Western Health, Melbourne, Australia.
出版信息
Heart. 2016 Mar;102(6):444-51. doi: 10.1136/heartjnl-2015-308636. Epub 2016 Jan 6.
OBJECTIVE
Supplemental oxygen therapy may increase myocardial injury following ST-elevation myocardial infarction (STEMI). In this study, we aimed to evaluate the effect of the dose and duration of oxygen exposure on myocardial injury after STEMI.
METHODS
Descriptive analysis of data from a multicentre, prospective, randomised, controlled trial of 441 patients with STEMI randomised to supplemental oxygen therapy or room air breathing. The primary endpoint was myocardial infarct size as assessed by cardiac biomarkers, troponin (cTnI) and creatine kinase (CK). Oxygen therapy was commenced by paramedics, and continued for up to 12 h postintervention in hospital. Supplemental oxygen exposure was calculated as the area under the dose×time curve for oxygen administration over the first 12 h, and then assessed for its association with cTnI/CK release using multivariable linear regression.
RESULTS
The median supplemental oxygen exposure was 1746 L (IQR: 960-2858). After adjustment for potential confounders, every 100 L increase in oxygen exposure in the first 12 h was associated with a 1.4% (95% CI 0.6% to 2.2%, p<0.001) and 1.2% (95% CI 0.7% to 1.8%, p<0.001) increase in the mean peak cTnI and CK, respectively. Excluding patients who developed cardiogenic shock, recurrent myocardial infarction or desaturations (SpO2<94%) during admission, every 100 L increase in oxygen exposure was associated with a 1.2% (95% CI 0.2% to 2.1%, p=0.01) and 1.0% (95% CI 0.3% to 1.7%, p=0.003) increase in the mean peak cTnI and CK, respectively. The median supplemental oxygen exposure of 1746 L would result in a 21% (95% CI 3% to 37%) increase in infarct size according to the cTnI profile.
CONCLUSIONS
Supplemental oxygen exposure in the first 12 h after STEMI was associated with a clinically significant increase in cTnI and CK release.
目的
氧疗可能会增加 ST 段抬高型心肌梗死（STEMI）后的心肌损伤。本研究旨在评估 STEMI 后氧暴露的剂量和时间对心肌损伤的影响。
方法
对 441 例 STEMI 患者进行多中心、前瞻性、随机、对照试验的数据分析，这些患者被随机分配接受补充氧疗或室内空气呼吸。主要终点是通过心脏标志物肌钙蛋白（cTnI）和肌酸激酶（CK）评估心肌梗死面积。氧疗由护理人员开始，并在入院后最多 12 小时内继续进行。补充氧暴露被计算为前 12 小时内氧给药的剂量×时间曲线下面积，然后使用多变量线性回归评估其与 cTnI/CK 释放的关系。
结果
中位数补充氧暴露为 1746 L（IQR：960-2858）。在调整了潜在混杂因素后，前 12 小时内每增加 100 L 氧暴露与 cTnI 和 CK 的平均峰值分别增加 1.4%（95%CI 0.6%至 2.2%，p<0.001）和 1.2%（95%CI 0.7%至 1.8%，p<0.001）有关。排除入院期间发生心源性休克、复发性心肌梗死或血氧饱和度（SpO2<94%）下降的患者后，每增加 100 L 氧暴露与 cTnI 和 CK 的平均峰值分别增加 1.2%（95%CI 0.2%至 2.1%，p=0.01）和 1.0%（95%CI 0.3%至 1.7%，p=0.003）有关。根据 cTnI 谱，中位数为 1746 L 的补充氧暴露将导致梗死面积增加 21%（95%CI 3%至 37%）。
结论
STEMI 后前 12 小时内的氧暴露与 cTnI 和 CK 释放的临床显著增加有关。
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