Are high NT-proBNP levels more related to inflammation than to left ventricular systolic dysfunction in acute myocarditis?

Abstract

Type of funding sources: None.Plasma levels and N-terminal pro B-type natriuretic peptide (NT- proBNP), a cardiac neurohormone released in response to increased ventricular stress, represent an important predictor of clinical outcomes and left ventricular (LV) dysfunction; Although, its diagnostic and prognostic role in patients with acute myocarditis is not completely established; Our aim was to evaluate the relationship of BNP levels and LV ejection fraction (LVEF) in patients with myocarditis;Data from patients (pts) discharged with the diagnosis of myocarditis, from 2008 and 2018 were retrospectively analysed.62 pts were included. Mean age was 39.7 17 years and 89% (58 patients) were men. Plasma levels of NT-proBNP measured at admission ranged from 24 to 3110 pg/mL (median 514, IQR 947), and exceeded upper normal levels in 51 pts (82%). This values positively correlated with C- reactive protein (CRP) (p= 0.005, r = 0.36), leucocytes (p = 0.03, r= 0.37) and neutrophil-to-lymphocyte ratio (p= 0.05, r= 0.35), but not with left ventricular ejection fraction (LVEF) (p= 0.829). Higher levels of BNP were associated with higher troponin peak levels but not with increased mortality (p = 0.811), need of inotropic support (p= 0.059) or arrhythmic events (p= 0.130). Inflammatory parameters were significantly increased when BNP> 514 pg/mL vs BNP <514 pg/mL (CRP 7.2 vs 4 mg/dL, p= 0.008). This relationship was maintained at BNP > 900. LVEF was comparable in both groups (p = 0.938); In this population, the magnitude of recovery of the NT- proBNP values (variation between NT-proBNP at admission and discharge) strongly correlated with the magnitude of the inflammatory markers at admission (all p < 0,005)In patients with acute myocarditis, there is a significant relationship between NT-proBNP levels and inflammation (as measured by leucocytes, NLR or CRP), but not with LVEF; Despite the limitation of a small sample size, we could hypothesize that NTproBNP in this subset of patients appears to be regulated not only by hemodynamic changes but also by the underlying systemic inflammatory process and, therefore, it interpretation should take that into account;