Heart failure (HF) remains a major medical and social problem. The NT-pro-brain natriuretic peptide (NT-proBNP) and its active form, brain-type natriuretic peptide (BNP), in a simple blood test are the gold-standard biomarkers for HF diagnosis. However, even good biomarkers such as natriuretic peptides fail to predict all the risks associated with HF due to the diversity of the mechanisms involved. The pathophysiology of HF is determined by numerous factors, including oxidative stress, inflammation, neuroendocrine activation, pathological angiogenesis, changes in apoptotic pathways, fibrosis and vascular remodeling. High readmission and mortality rates prompt a search for new markers for the diagnosis, prognosis and treatment of HF. Oxidative-stress-mediated inflammation plays a crucial role in the development of subsequent changes in the failing heart and provides a new insight into this complex mechanism. Oxidative stress and inflammatory biomarkers appear to be a promising diagnostic and prognostic tool in patients with HF. This systematic review provides an overview of the current knowledge about oxidative stress and inflammation parameters as markers of HF.

Background: The coronavirus–caused disease (COVID-19), first identified in China in December 2019, has spread worldwide becoming a global pandemic. Although people infected with the SARS-CoV-2 virus presented mainly respiratory and gastrointestinal symptoms, an increase in cardiovascular incidents was observed in several scientific studies. SARS-CoV-2 virus has been shown to disrupt the normal immune response leading to a dysregulation of immune system function and massive production of inflammatory cytokines commonly known as “cytokine storm”. Methods: 57 patients eventually participated in the study, assigned to non–COVID (24 patients) and COVID (33 patients) groups. After signing consent to participate in the study, each patient was given a self–administered questionnaire to fill out prior to specimen collection, anthropometric measurements were taken and venous blood was collected for the following determinations: pro- and anti–inflammatory cytokines using a Bio–Plex 200 system, oxidative stress markers and basic hematological blood parameters. Results: showed statistically significant higher values of IL–1Ra and IL–1β in the COVID-19 group. Of the oxidative stress markers, only MDA levels were higher in the COVID-19 group. Conclusions: the results of our study provide evidence and support the occurrence of elevated levels of IL–1Ra, IL–1β and MDA in the COVID-19 group of patients, which are associated with a worse course and prognosis of COVID-19. A better understanding of the pathophysiology and dysregulation of the immune system associated with the cytokine storm is essential to select patients at risk and develop effective drugs and vaccines.

The aim of this study was to analyze the relationship between levels of sST2, NT-proBNP and oxidative stress markers in patients with reduced ejection fraction (HFrEF) due to non-ischemic cardiomyopathy. A total of 88 patients with HFrEF were divided into four groups based on left ventricular ejection fraction (≤25% and >25%) and NYHA functional class (group 1—LVEF > 25% and NYHA class I or II; group 2—LVEF > 25% and NYHA class III or IV; group III—LVEF ≤ 25% and NYHA class I or II; group IV—LVEF ≤ 25% and NYHA class III or IV). In 39 (44.32%) patients LVEF was reduced below 25%, and 22 of them (56.41%) were in NYHA functional class III/IV. Of the 49 (55.68%) patients with LVEF ≥ 25%, only 18.37% were in NYHA functional class III/IV (p < 0.001). Patients with LVEF ≥ 25% had lower levels of NT-proBNP, total oxidant status (TOS), total antioxidant capacity (TAC), and oxidative stress index (OSI). The levels of NT-proBNP but not sST-2 correlated positively with NYHA functional class (p < 0.001) and negatively with LVEF (p < 0.001). The levels of sST-2 were associated with increased TAC (p = 0.009) and uric acid (p = 0.040). These findings indicate that only NT-proBNP was related to the severity of heart failure, whereas sST2 correlated with total antioxidant capacity. Therefore, in stable patients with HFrEF due to dilated cardiomyopathy, sST2 may be an additional biomarker reflecting the redox status, but not the severity of heart failure.

Background: The COVID-19 outbreak began in December 2019 in China and quickly spread to other countries. Although most infected individuals experienced mild or moderate symptoms, 17% of patients were reported to have severe cases. Analysis of the available literature confirms the link between severe forms of COVID-19 and cyto-kine storm syndrome. Methods: A total of 57 patients participated in the study, divid-ed into a non-COVID group (24 people) and a COVID group (33 people). Each patient completed a questionnaire designed by the authors, followed by anthropometric measurements and venous blood sampling to determine cytokines, and pro- and an-ti-inflammatory chemokines using the Bio-Plex 200 system. Results: Showed statisti-cally significant higher values of IL-6, IL-13, TNF-α and the chemokines IP-10, MCP-1 (MCAF), MIP-1α, MIP-1β in the COVID-19 group. Conclusions: The results of our study support for the occurrence of elevated levels of IL-6, IL-13, TNF-α and selected chemokines in COVID-19 patients, which are associated with a worse course and prognosis of COVID-19. An in-depth understanding of the pathophysiology and im-mune dysfunction accompanying cyto-kine storm is crucial for identifying patients at increased risk, as well as for developing effective therapies and vaccines.