NT-proBNP in patients with severe COVID-19
BNP is synthesized as a prehormone (proBNP), upon release into the
bloodstream it is divided into equal proportions in biologically active
BNP and biologically inactive NT-proBNP.
Stress and myocardial damage are the main release stimuli for BNP and
NT-proBNP, studies have shown that increased cytokines and an
inflammatory state are important additional factors that induce hormone
secretion. (52) BNP is degraded by plasma through endopeptidase
Neprylisin (NEP), NT-proBNP is excreted mainly by renal excretion. BNP
and NT-proBNP are important biomarkers for the evaluation of cardiac
function. As described above, cardiac lesions are a common condition
among patients hospitalized with COVID-19. In fact, one study indicates
that 19.7% of patients out of a total of 416 cases with COVID-19
suffered cardiac damage with more unfavorable clinical outcomes than
those without cardiac damage (53). Another recent study showed that the
NT-proBNP marker increased significantly in more severe cases of
COVID-19 (54) suggesting a relationship between high plasma levels of
NT-proBNP, heart damage and risk of death in patients with severe
COVID-19. The explanation for the increase in NT-proBNP in severe
COVID-19 is probably due to cardiac complications resulting from
up-regulation of the sympathetic and angiotensin renin (RAS) system,
cytokinic cascade and systemic inflammation. In particular, cytokine
storm (55)(56) could probably play an important role in cardiac damage
(57). In addition, overactivation of RAS with reduced ACE-2
concentration, as evidenced in the more severe stages of COVID-19
infection, may lead to increased synthesis of Ang II with
pro-inflammatory and profibrotic effects (mediated by AT-1 receptors)
which facilitates the secretion of NT-proBNP (58)(59). Pending
well-structured and in-depth studies, to assess whether the NT-proBNP
marker can be a useful diagnostic test to assess the severity of
COVID-19 infection, all the considerations expressed suggest a
therapeutic drug solution with the action of increasing the
concentration of natriuretic peptides in circulation, decrease the
concentration of NT-proBNP, increase the RAS axis via ACE-2 with
increased synthesis of Ang 1-7 and Ang 1-9 with antifibrotic and
anti-inflammatory effects, and decrease the effects of Ang II on the
AT-1 receptor (60)(61)(62)
(63)