Cardiac Injury Patterns and Inpatient Outcomes Among Patients Admitted With COVID-19

Abstract

Although certain risk factors have been associated with increased morbidity and mortality in patients admitted with Coronavirus Disease 2019 (COVID-19), the impact of cardiac injury and high-sensitivity troponin-I (hs-cTnI) concentrations are not well described. In this large retrospective longitudinal cohort study, we analyzed the cases of 1,044 consecutively admitted patients with COVID-19 from March 9 until April 15. Cardiac injury was defined by hs-cTnI concentration >99th percentile. Patient characteristics, laboratory data, and outcomes were described in patients with cardiac injury and different hs-cTnI cutoffs. The primary outcome was mortality, and the secondary outcomes were length of stay, need for intensive care unit care or mechanical ventilation, and their different composites. The final analyzed cohort included 1,020 patients. The median age was 63 years, 511 (50% patients were female, and 403 (40% were white. 390 (38%) patients had cardiac injury on presentation. These patients were older (median age 70 years), had a higher cardiovascular disease burden, in addition to higher serum concentrations of inflammatory markers. They also exhibited an increased risk for our primary and secondary outcomes, with the risk increasing with higher hs-cTnI concentrations. Peak hs-cTnI concentrations continued to be significantly associated with mortality after a multivariate regression controlling for comorbid conditions, inflammatory markers, acute kidney injury, and acute respiratory distress syndrome. Within the same multivariate regression model, presenting hs-cTnI concentrations were not significantly associated with outcomes, and undetectable hs-cTnI concentrations on presentation did not completely rule out the risk for mechanical ventilation or death. In conclusion, cardiac injury was common in patients admitted with COVID-19. The extent of cardiac injury and peak hs-cTnI concentrations were associated with worse outcomes.

Using high sensitivity cardiac troponin values in patients with SARS-CoV-2 infection (COVID-19): The Padova experience

“…In patients in whom samples were obtained, 27% of patients had myocardial injury. Despite a highly sensitive assay, the percentage of those with increases was lower than previously described [8] , [12] , [21] . This percentage, however, refers to baseline hs-cTnI values, before complications of the disease occurred.…”

“…Similar to what has been previously reported in critically ill patients including in those with acute respiratory illness [5] , [6] , increases in cardiac troponin (cTn) are common in COVID-19 patients [7] , [8] , [9] . These increases are associated with the severity of the disease and prognosis [10] , [11] , [12] . The mechanisms for such elevations include increases due to underlying cardiac comorbidities, the severe acute respiratory illness that can ensue and complications associated with the disease process [13] , [14] .…”

Cardiac Troponin I Levels in Hospitalized COVID-19 Patients as a Predictor of Severity and Outcome: A Retrospective Cohort Study

“…This trend showed a propensity of COVID-19 virus disease in young patients in this part of the world. The mean BMI was (24.94 ± 4.81), which was lower than the BMI of patients in previous studies [7][8][9]. The lower BMI suggested that patients in Pakistan infected by the SARS-CoV-2 virus were leaner than those in other parts of the world.…”

Predictive Factor for COVID-19 Worsening: Insights for High-Sensitivity Troponin and D-Dimer and Correlation With Right Ventricular Afterload

“…Cardiac troponin is increased in the case of community-acquired pneumonia, in the context of myocardial oxygen supply-demand mismatch and supply (21), and seems to correlate with the severity of respiratory impairment. Yet, few data are currently available on troponin level at the time of COVID-19 diagnosis (20,(22)(23)(24). Mechanisms of myocardial and tissue injury as well as coagulopathy associated with COVID-19 could be linked to the cytokine storm (25).…”