Table 1
B-type natriuretic peptide (NT-pro-BNP) The system of natriuretic peptides (NP) counteracts the cardiovascular
and renal effects related to the activation of
renin–angiotensin–aldosterone system (RAAS)[18] and consists of
three structurally similar peptides with cardiorenal protective
properties: ANP, BNP, CNP[19].
In the case of HF, as the filling pressure of the LV increases, the
lengthening of the heart fibers causes the secretion of NP precursors
and one of their most recognized effects is vasodilation[20] , but
they also promote the excretion of water and sodium by inhibiting the
reabsorption of sodium in the proximal and distal tubule, also
preventing the reduction of glomerular filtration by regulating
tubule-glomerular feedback.
NPs, however, are predictors of an adverse outcome in acute myocardial
damage because their concentrations increase immediately after
myocardial damage, reducing only to clinical improvement[21].
A retrospective study conducted in China demonstrated that markedly
higher concentrations of CK, lactate dehydrogenase, TnT, and NT-pro-BNP
were seen in deceased patients than in recovered patients[9].
Also Caro-Codòn et al findings support the hypothesis that natriuretic
peptides are highly associated with prognosis in COVID‐19
patients[22]. A recent meta‐analysis including 13 observational
studies and 2248 patients (most of them also from the early COVID‐19
outbreak in China) also supported the idea that NT‐proBNP assessment may
improve the discrimination of high‐risk patients[23].
Yang et al retrospectovely analyzed 224 patients with confirmed
diagnosis of SARS-CoV-2 infection and definite outcomes (discharge or
death), consisting of 145 patients who recovered and 58 patients who
died. In their analysis, 53% of non-survivors had elevated
Nt-proBNP[10].
Finally, according to Gao et al[24], plasma NT-proBNP level and the
risk of in-hospital death in severe COVID-19 patients was directly
proportioned. Severe COVID-19 patients with high NT-proBNP levels tended
to be older with increased cardiac injury markers and higher levels of
systematic inflammation markers, and that with high NT-proBNP
(>88.64 pg/mL) level had lower cumulative survival rate.
After adjusting for potential cofounders in separate modes, NT-proBNP
presented as an independent risk factor of in-hospital death in patients
with severe COVID-19.
Also thanks to others Italian studies, it has been demonstrated
NT-pro-BNP levels were eight times higher at the time of hospitalization
in non survivors versus survivors[13], [14].
Therefore, despite cardiac injury is a common condition among
hospitalized patients with COVID-19, association with high level of
Nt-pro BNP was associated with higher risk of in-hospital mortality
(Table 2).