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.
Highlights
Human Coronavirus Disease 2019 (COVID-19), resulting from a newly described respiratory viral infection with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), was originally identified in December 2019 in Wuhan, China, before becoming a global pandemic
All patients aged more than 18 years old were selected on the basis of laboratory-confirmed COVID-19 infection by positive reverse-transcriptase polymerase chain reaction (RT-PCR) on a nasopharyngeal swab
A total of 943 COVID-19 patients were admitted to the University Hospital of Strasbourg from 25 February 2020 to 1 April 2020, of whom 375 (67% of males, mean age of 66 ± 14.4 ranging from 21 to 93 years) were included in this analysis after exclusion of patients hospitalized for less than 24 h (n = 145), minors (n = 14), patients hospitalized for other medical reasons and incidentally found positive for SARS-CoV-2 PCR (n = 12), and patients without a high-sensitivity troponin I (hsTnI) test (n = 397) (Figure 1)
Summary
Human Coronavirus Disease 2019 (COVID-19), resulting from a newly described respiratory viral infection with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), was originally identified in December 2019 in Wuhan, China, before becoming a global pandemic. Endothelial and myocardial expression of ACE2 could account for myocardial injury, defined by a rise in troponin (Tn) associated with some severe forms of COVID-19 [5,6]. Recent publications have associated an elevation in cardiac and inflammatory biomarkers with infection severity and worse prognosis [13,14]. Whether cardiac biomarkers such as Tn could have a prognostic value in SARS-CoV-2 is still under debate, and Tn measurement is not systematically performed in infected patients. We report a retrospective analysis of hospitalized adult patients, in whom a high-sensitivity troponin I (hsTnI) test was performed, from a university hospital in Eastern France, one of the most affected areas in Europe during the first wave of the COVID-19 pandemic
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