Published online Sep 26, 2023. doi: 10.4330/wjc.v15.i9.427
Peer-review started: April 21, 2023
First decision: June 19, 2023
Revised: July 12, 2023
Accepted: August 17, 2023
Article in press: August 17, 2023
Published online: September 26, 2023
Processing time: 152 Days and 16.4 Hours
Several studies have proposed that troponin elevation seen in coronavirus disease 2019 (COVID-19) patients is due to an interplay between viral myocarditis, demand ischemia and renin-angiotensin-aldosterone system pathway activation. This creates the hypothesis that the use of steroids, antivirals and angiotensin-converting enzyme inhibitors (ACEI) in patients with COVID-19 infection and troponin elevation would impact mortality outcomes.
The COVID-19 pandemic has had a monumental global impact and resulted in several deaths worldwide. The motivation of this study was to analyze if the use of the steroids, antivirals and ACEI would improve survival in patient with COVID-19 infection and troponin elevation.
Our main objective was to analyze any differences in mortality in our subjects, in the hopes of adding to existing knowledge and creating a standardized treatment protocol in patients with COVID-19 and troponin elevation.
Our study design was a retrospective observational study consisting of 1788 COVID-19 patients at seven hospitals across Southern California. To determine the predictors of mortality in our subjects, we did a backward selection cox multivariate regression analysis. Furthermore, to analyze survival in the subset of patients with troponin elevation we did a Kaplan Meier analysis comparing those that received treatment with steroids, remdesivir and ACEI and those that did not.
Though the beneficial role of steroids in the treatment of COVID-19 has been established, our study did not show any statistically significant difference in mortality in patients with elevated troponin who received steroids and those that did not. Therefore, the role of steroids in myocarditis caused by COVID-19 is still unclear and needs further investigation. On the other hand, our study showed improved survival in COVID-19 patients with elevated troponin that received remdesivir, although this was not statistically significant.
Although the mechanism of troponin elevation in COVID-19 patient has been linked to viral myocarditis and renin-angiotensin-aldosterone system activation, the novel treatments of these subsequent pathologies including steroids, remdesivir and ACEI showed no significant survival benefit in our study. This creates the theory that there are other mechanisms at play guiding this complex interaction.
Although our study did not show a statistically significant mortality benefit with the use of steroids and remdesivir, our sub-group analysis was limited by a small sample size, so further studies on the effect of remdesivir in the sub-set of COVID-19 patients with elevated troponin using a larger population will be beneficial.