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).