Elena-Mihaela Cordeanu1, Nicolas Duthil1, Francois Severac2, Hélène Lambach1, Jonathan Tousch1, Lucas Jambert3, Corina Mirea1, Alexandre Delatte4, Waël Younes5, Anne-Sophie Frantz1, Hamid Merdji6, Valérie Schini-Kerth7, Pascal Bilbault8, Patrick Ohlmann9, Emmanuel Andres10, Dominique Stephan1. 1. Department of Hypertension, Vascular Disease and Clinical Pharmacology, Strasbourg Regional University Hospital, 67091 Strasbourg, France. 2. Division of Public Health, Methodology and Biostatistics, University Hospitals of Strasbourg, 67091 Strasbourg, France. 3. Department of Vascular Medicine, Mulhouse Regional Hospital, 68100 Mulhouse, France. 4. Department of Cardiology, Haguenau Regional Hospital, 67500 Haguenau, France. 5. Department of Vascular Medicine, Colmar Regional Hospital, 68000 Colmar, France. 6. Intensive Care and Reanimation Department, Strasbourg Regional University Hospital, 67091 Strasbourg, France. 7. UMR 1260 INSERM Regenerative Nanomedecine, Faculty of Pharmacy, Strasbourg University, 67400 Illkirch, France. 8. Emergency Department, Strasbourg Regional University Hospital, 67091 Strasbourg, France. 9. Cardiology Department, Strasbourg Regional University Hospital, 67091 Strasbourg, France. 10. Internal Medicine Department, Strasbourg Regional University Hospital, 67091 Strasbourg, France.
Abstract
(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) 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 HumanCoronavirus 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-19patients 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.
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