Abstract
Introduction: NT-proBNP is a widely available and frequently utilized laboratory marker in patients with congestive heart failure. Its availability and use as a surrogate marker for elevated ventricular filling pressures and ventricular strain that frequently manifests as shortness of breath makes it an attractive laboratory marker to triage patients with SARS-CoV-2 infection. Hypothesis: Elevated NT-proBNP is correlated with higher mortality and/or rate of major adverse cardiovascular events (MACE) in patients admitted with SARS-CoV-2 infection. Methods: A retrospective analysis was performed on 225 patients admitted for SARS-CoV-2 infection at a major metropolitan hospital located in the Southwestern United States from the period of March 2020 to May 2020. NT-proBNP levels were recorded in 117 patients (52.7%) on admission. Elevated NT-proBNP was defined as: above 450 pg/ml in patients less than 50 years old, above 900 pg/ml if 50 to 75 years old, and above 1,800 pg/ml if above 75 years old. The primary endpoint was a composite of MACE and mortality during hospitalization. MACE was defined as stroke, myocardial infarction, DVT or PE and shock requiring vasopressor support. Two-sample Wilcoxon rank-sum (Mann-Whitney) test, Pearson’s chi square test and Fisher’s exact test were utilized for data analysis. Results: Of the 117 SARS-CoV-2 positive patients that had admission NT-proBNP levels available for analysis, 23 (19.66%) met age-adjusted criteria for elevated NT-proBNP. There was no significant correlation between elevated NT-proBNP levels and MACE (p = 0.482) or mortality (p = 0.737) in patients with SARS-CoV-2 infections. There was no statistical difference in total length of stay (p-value = 0.6384) or ICU admission (p-value = 0.354) between those with elevated admission NT-proBNP and those without. Conclusions: An elevated NT-proBNP at time of admission does not significantly correlate with higher rates of MACE, hospital length of stay, ICU admission, and mortality in patients admitted with SARS-CoV-2 infection.
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