Cordeanu Elena-Mihaela, Duthil Nicolas, Severac Francois, Lambach Hélène, Tousch Jonathan, Jambert Lucas, Mirea Corina, Delatte Alexandre, Younes Waël, Frantz Anne-Sophie, Merdji Hamid, Schini-Kerth Valérie, Bilbault Pascal, Ohlmann Patrick, Andres Emmanuel, Stephan Dominique
Department of Hypertension, Vascular Disease and Clinical Pharmacology, Strasbourg Regional University Hospital, 67091 Strasbourg, France.
Division of Public Health, Methodology and Biostatistics, University Hospitals of Strasbourg, 67091 Strasbourg, France.
J Clin Med. 2020 Dec 17;9(12):4078. doi: 10.3390/jcm9124078.
(1) Background: Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) penetrates the respiratory epithelium through angiotensin-converting enzyme-2 (ACE2) binding. Myocardial and endothelial expression of ACE2 could account for the growing body of reported evidence of myocardial injury in severe forms of Human Coronavirus Disease 2019 (COVID-19). We aimed to provide insight into the impact of troponin (hsTnI) elevation on SARS-CoV-2 outcomes in patients hospitalized for COVID-19. (2) Methods: This was a retrospective analysis of hospitalized adult patients with the SARS-CoV-2 infection admitted to a university hospital in France. The observation period ended at hospital discharge. (3) Results: During the study period, 772 adult, symptomatic COVID-19 patients were hospitalized for more than 24 h in our institution, of whom 375 had a hsTnI measurement and were included in this analysis. The median age was 66 (55-74) years, and there were 67% of men. Overall, 205 (55%) patients were placed under mechanical ventilation and 90 (24%) died. A rise in hsTnI was noted in 34% of the cohort, whereas only three patients had acute coronary syndrome (ACS) and one case of myocarditis. Death occurred more frequently in patients with hsTnI elevation (HR 3.95, 95% CI 2.69-5.71). In the multivariate regression model, a rise in hsTnI was independently associated with mortality (OR 3.12, 95% CI 1.49-6.65) as well as age ≥ 65 years old (OR 3.17, 95% CI 1.45-7.18) and CRP ≥ 100 mg/L (OR 3.62, 95% CI 1.12-13.98). After performing a sensitivity analysis for the missing values of hsTnI, troponin elevation remained independently and significantly associated with death (OR 3.84, 95% CI 1.78-8.28). (4) Conclusion: Our study showed a four-fold increased risk of death in the case of a rise in hsTnI, underlining the prognostic value of troponin assessment in the COVID-19 context.
(1) 背景：严重急性呼吸综合征冠状病毒2（SARS-CoV-2）通过与血管紧张素转换酶2（ACE2）结合穿透呼吸道上皮。ACE2在心肌和内皮中的表达可能解释了越来越多关于严重新型冠状病毒肺炎（COVID-19）患者心肌损伤的报道证据。我们旨在深入了解肌钙蛋白（hsTnI）升高对因COVID-19住院患者SARS-CoV-2预后的影响。(2) 方法：这是一项对法国一家大学医院收治的成年SARS-CoV-2感染住院患者的回顾性分析。观察期至出院时结束。(3) 结果：在研究期间，772名有症状的成年COVID-19患者在我们机构住院超过24小时，其中375人进行了hsTnI检测并纳入本分析。中位年龄为66（55 - 74）岁，男性占67%。总体而言，205（55%）名患者接受了机械通气，90（24%）人死亡。队列中34%的患者hsTnI升高，而只有3例患者患有急性冠状动脉综合征（ACS），1例心肌炎。hsTnI升高的患者死亡更频繁（风险比3.95，95%置信区间2.69 - 5.71）。在多变量回归模型中，hsTnI升高与死亡率（比值比3.12，95%置信区间1.49 - 6.6）以及年龄≥65岁（比值比3.17，95%置信区间1.45 - 7.18）和C反应蛋白≥100mg/L（比值比3.62，95%置信区间1.12 - 13.98）独立相关。在对hsTnI缺失值进行敏感性分析后，肌钙蛋白升高仍与死亡独立且显著相关（比值比3.84，95%置信区间1.78 - 8.28）。(4) 结论：我们的研究表明，hsTnI升高时死亡风险增加四倍，突出了在COVID-19背景下肌钙蛋白评估的预后价值。
