Early reports from China suggest that cardiac troponin values > 99th percentile upper reference limit (99th% URL) are powerful predictors of poor outcomes in COVID-19 patients (1, 2) . Outcomes examined included intubation, ARDS, AKI and death. In one report the univariate odds ratio for death was 80:1 when cardiac troponin I (cTnI) was above the 99th% URL (1) . In fact, it was the strongest predictor of all biomarkers examined in 191 patients. In another study of 461 patients cTnI values above the 99th% URL had an increased odds ratio for death of 10:1 (2) . Furthermore, the odds ratios for intubation, ARDS and AKI were 5:1, 4:1 and 10:1, respectively. A recent preprint from a large hospital system in New York City examined cTnI as a marker of mortality amongst 2736 admitted COVID-19 patients (3) . It showed that patients with modest elevations of cTnI (0.03 -0.09 ng/mL) had an adjusted hazard ratio for mortality of 1.77 compared to those with undetectable cTnI while those with cTnI values > 0.09 ng/mL had a hazard ratio of 3.23 for mortality. While the exact causes of increased cTn in COVID-19 patients are unknown, these studies suggest it as a robust univariate marker for poor outcomes.
With IRB approval we performed a retrospective observational study of 182 consecutive SARS-2-COV PCR+ patients admitted and discharged at Barnes Jewish Hospital/Washington University Medical Center to determine if elevated cTnI was associated with poor outcomes at our institution. cTnI testing was performed in the Barnes-Jewish Hospital Laboratory using the contemporary cTnI assay on the Abbott Architect i2000. The 99 th % URL for this method is 0.028 ng/mL and the limit of quantification is 0.03 ng/mL. The reference interval is < 0.03 ng/mL. Outcomes were determined by review of the electronic health record (EPIC) and physician notes for: death, intubation, acute respiratory distress syndrome or acute hypoxic respiratory failure (ARDS/AHRF) and acute kidney injury (AKI). AKI was defined using RIFLE criteria of 2 fold increase in creatinine and urine output less than 5 mL/kg/hr. Both initial and peak cTnI values were examined as univariate markers at three concentration ranges; undetectable (< 0.03 ng/mL), moderate (0.03 -0.09 ng/mL) and elevated (> 0.09 ng/mL).
While we could not rule-in acute myocardial infarction, we also examined a subgroup of patients that exhibited a rise and/or fall of cTnI defined as a rise and/or fall of at least 0.2 ng/mL and a peak value > 0.2 ng/mL. Our findings confirm that in a Midwestern USA institution elevated cTnI concentrations are a powerful univariate marker for poor outcomes as seen in early studies (1) (2) (3) . However, there are limitations to this retrospective observational study. Pre-existing cardiovascular conditions are known to be a risk factor for poor outcomes in COVID-19 disease (4) and we
were not able to sufficiently determine the presence or absence of pre-existing cardiovascular comorbidities. Yet, in the New York study the presence of pre-existing cardiovascular disease/risk factors did not affect the hazard ratios for mortality amongst patients with elevated cTnI values (3) . The finding that having no cTnI ordered resulted in a reduced OR of ARDS suggests selection bias in our study which we minimized by using those with cTnI ordered but undetectable results as the reference population. It is also important to note that we cannot diagnose AMI in these patients as cTnI is a marker of cardiac injury and not myocardial infarction. Without evidence of thrombotic events or ischemic signs and symptoms we can only state the prevalence of cardiac injury. Nonetheless, it is becoming clear that cardiac troponin can be an ally in managing COVID-19 patients (5) . Combining troponin with other biomarkers may result in even better prognosis and future studies will be important to determine this (5). 