Infectious biomarkers upon admission predict in-hospital mortality in COVID-19 patients with and without chronic heart failure.

BACKGROUND

Coronavirus disease 2019 (COVID-19), caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), can affect nearly every organ system in the human body and present with diverse clinical manifestations. However, its effects on cardiovascular outcomes remain discrepant.

AIM: The objective of this study was to determine whether blood inflammatory levels on admission were associated with in-hospital mortality risk in patients with congestive heart failure (CHF) and COVID-19.

METHODS

We performed a retrospective analysis of 4,711 inpatients with confirmed SARS-CoV-2 infection from the Dryad database. Among these individuals, 541 CHF patients with COVID-19 were compared with hospitalized non-CHF patients (n = 4,170). Admission variables including demographic characteristics, vital signs, preexisting comorbidities, and laboratory indicators were obtained as potential confounders for in-hospital mortality risk.

RESULTS

Univariate analysis with Kaplan-Meier curves suggested that higher inflammatory levels on admission-including white blood cell (WBC) count, interleukin-6 (IL-6), ferritin, procalcitonin, and C-reactive protein-were associated with a significantly higher risk of in-hospital mortality compared with lower levels. Consistently, multivariate Cox regression analysis showed that apart from ferritin [0.8 (0.7, 0.9), <0.001], the WBC [1.3 (1.1, 1.5), 0.013], IL-6 [1.4 (1.2, 1.7), <0.001], procalcitonin [1.2 (1.0, 1.3), 0.031] and C-reactive protein [1.2 (1.1, 1.4), 0.002] were independently associated with increased risk of in-hospital mortality in non-CHF patients in the adjusted II model. However, these independent relationships were not observed in CHF patients.

CONCLUSION

Elevated systemic inflammatory levels on admission were significantly associated with increased in-hospital mortality risk in non-CHF patients with COVID-19 but not in CHF patients. These findings may provide a clinical basis for risk stratification in CHF patients. Further studies are needed to support these results.