Oxidative stress plays a significant role in the pathogenesis of heart failure (HF). The aim of the study was to investigate the prognostic value of oxidation‐reduction (redox) markers in patients with HF due to ischemic and nonischemic cardiomyopathy. The study included 707 patients of HF allocated into two groups depending on ethology: ischemic cardiomyopathy (ICM) (n = 435) and nonischemic cardiomyopathy (nICM) (n = 272), who were followed up for one year. The endpoint occurrence (mortality or heart transplantation) in a 1‐year follow‐up was similar in the ICM and nICM group. The predictive value of endpoint occurrence of oxidative stress biomarkers such as the serum protein sulfhydryl groups (PSH), malondialdehyde (MDA), uric acid (UA), bilirubin, and MDA/PSH ratio and other clinical and laboratory data were assessed in both groups (ICM and nICM) separately using univariate and multivariate Cox regression analyses. In multivariate analysis, the higher concentrations of UA (p = 0.015, HR = 1.024, 95% CI (1.005‐1.044)) and MDA (p = 0.004, HR = 2.202, 95% CI (1.296‐3.741)) were significantly associated with adverse prognosis in patients with ICM. Contrastingly, in patients with nICM, we observed that higher bilirubin concentration (p = 0.026, HR = 1.034, 95% CI (1.004‐1.064)) and MDA/PSH ratio (p = 0.034, HR = 3.360, 95% CI (1.096‐10.302)) were significantly associated with increased risk of death or HT. The results showed the association of different oxidative biomarkers on the unfavorable course of heart failure depending on etiology.

Sodium-glucose co-transporter-2 (SGLT-2) inhibitors have become integral in treating both diabetes mellitus and heart failure, independent of left ventricular ejection fraction. Their pleiotropic effect influences multiple mechanisms, enhancing the function of various systems within the body. They exhibit nephroprotective and cardioprotective effects by improving cell metabolism, endothelial function, and slowing the fibrosis of the cardiac muscle, and they also have a beneficial impact on other organs. At the cellular level, they protect against the harmful effects of free radicals both by lowering glucose levels and by supporting the function of the antioxidant system. Moreover, SGLT-2 inhibitors can modify the metabolism of adipocytes by affecting the production of cytokines such as adiponectin—which increases insulin sensitivity, leading to weight loss and improved glycemic control.

Heart failure (HF) is a multifactorial clinical syndrome involving many complex processes. The causes may be related to abnormal heart structure and/or function. Changes in the renin-angiotensin-aldosterone system, the sympathetic nervous system, and the natriuretic peptide system are important in the pathophysiology of HF. Dysregulation or overexpression of these processes leads to changes in cardiac preload and afterload, changes in the vascular system, peripheral vascular dysfunction and remodeling, and endothelial dysfunction. One of the important factors responsible for the development of heart failure at the cellular level is oxidative stress. This condition leads to deleterious cellular effects as increased levels of free radicals gradually disrupt the state of equilibrium, and, as a consequence, the internal antioxidant defense system is damaged. This review focuses on pharmacotherapy for chronic heart failure with regard to oxidation–reduction metabolism, with special attention paid to the latest group of drugs, SGLT2 inhibitors—an integral part of HF treatment. These drugs have been shown to have beneficial effects by protecting the antioxidant system at the cellular level.