[Hypoxia and inflammation are risk factors for acute myocardial injury in patients with coronavirus disease 2019]

Beijing Da Xue Xue Bao Yi Xue Ban. 2020 Dec 28;53(1):159-166. doi: 10.19723/j.issn.1671-167X.2021.01.024.
[Article in Chinese]

Abstract

Objective: To investigate the risk factors for acute myocardial injury in coronavirus disease 2019 (COVID-19) patients.

Methods: This is a retrospective analysis of a COVID-19 cohort, in which 149 confirmed COVID-19 patients enrolled were divided into the group of myocardial injury (19 cases) and the group of non-myocardial injury (130 cases). Myocardial injury was defined according to Fourth universal definition of myocardial infarction released by European Society of Cardiology (ESC) in 2018, that cardiac troponin (cTn) was above 99th percentile of the reference level. Clinical information and results of laboratory tests of the eligible patients were collected. Factors associated with myocardial injury in COVID-19 patients were evaluated.

Results: Compared with the group of non-injury, the patients in the group of injury were older and had a larger proportion of severe or critical cases (P < 0.05), higher respiratory rate and lower percutaneous oxygen saturation (SpO2) without oxygen therapy on admission (P < 0.05). All inflammatory indexes except for tumor necrosis factor α (TNF-α) showed significant elevation in the patients of the group of injury (P < 0.05). Analyzed by Spearman correlation test, we showed that the levels of circulatory cTnI were in positive correlation with the levels of high-sensitivity C-reactive protein (hs-CRP), ferritin, receptor of interleukin-2 (IL-2R), interleukin-6 (IL-6) and interleukin-8 (IL-8) (ρ > 0, P < 0.05). Lower SpO2 without oxygen therapy on admission (OR: 0.860, 95%CI: 0.779-0.949, P=0.003) and higher plasma IL-6 levels (OR: 1.068, 95%CI: 1.019-1.120, P=0.006) were independent risk factors for acute myocardial injury in the patients with COVID-19 by multivariate Logistic regression analyses.

Conclusion: Hypoxic state and inflammation may play a key role in the pathogenesis of acute myocardial injury in COVID-19 patients.

目的: 寻找新型冠状病毒肺炎(coronavirus disease 2019,COVID-19)患者发生急性心肌损伤的危险因素。

方法: 本研究为单中心COVID-19住院患者的回顾性队列研究,共纳入149例COVID-19确诊患者,依据2018年欧洲心脏病学会年会发布的第四版心肌梗死全球统一定义中关于心肌损伤的诊断标准,将患者分为心肌损伤组(19例)及非心肌损伤组(130例)。收集全部入组患者的临床信息及实验室化验结果,并分析COVID-19患者发生急性心肌损伤的危险因素。

结果: 与非心肌损伤组患者相比,心肌损伤组患者年龄更大,危重症患者比例更高(P < 0.05),入院时呼吸频率更快,未吸氧状态外周血氧饱和度(percutaneous oxygen saturation,SpO2)偏低(P < 0.05)。心肌损伤组患者除肿瘤坏死因子α(tumor necrosis factor α,TNF-α)外,其余炎症因子水平均高于非心肌损伤组(P < 0.05)。多因素Logistic回归分析发现,入院时未吸氧状态SpO2水平偏低(OR=0.860,95%CI:0.779~0.949,P=0.003)及血白细胞介素-6(interleukin-6,IL-6)水平升高(OR=1.068,95%CI:1.019~1.120,P=0.006)为COVID-19患者发生急性心肌损伤的独立危险因素。

结论: 低氧状态及炎症在COVID-19患者发生急性心肌损伤的病理生理过程中起到了重要作用。

Keywords: Acute myocardial injury; Betacoronavirus; Inflammation; Interleukin-6.

MeSH terms

  • Biomarkers
  • COVID-19*
  • Humans
  • Hypoxia
  • Inflammation
  • Retrospective Studies
  • Risk Factors
  • SARS-CoV-2

Substances

  • Biomarkers