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)