The role of galectin-3 in lipid metabolism disorders in patients with chronic heart failure of ischemic origin and concomitant metabolic pathology

Abstract

Abstract: Chronic heart failure of ischaemic origin remains a leading cause of morbidity and mortality, and its course is significantly aggravated by concomitant metabolic pathology (type 2 diabetes mellitus and obesity). The role of galectin-3 in the mechanisms of direct participation in lipid metabolism disorders in this vulnerable cohort of patients remains insufficiently studied, which justifies the relevance of the study. The aim of the work was to study the role of galectin-3 as a potential diagnostic and prognostic marker of lipid metabolism disorders in patients with chronic heart failure of ischemic origin against the background of concomitant metabolic pathology. The study examined 225 patients with chronic heart failure with coronary artery disease, who were divided into four groups based on the presence of a combined course of diabetes mellitus and obesity (n=75), type 2 diabetes mellitus (n=50), obesity (n=50), isolated course of coronary artery disease (n=50), and 30 practically healthy individuals who were included in the control group. A biochemical study of lipid metabolism indicators was carried out, including total cholesterol, triglycerides, high-density lipoprotein cholesterol, low-density lipoprotein cholesterol, very low-density lipoprotein cholesterol and atherogenic index, as well as determination of serum galectin-3 levels by enzyme-linked immunosorbent assay. The results showed that the concentration of galectin-3 in the blood serum significantly increases in proportion to the degree of metabolic burden, reaching the highest values in patients with a combination of chronic heart failure, type 2 diabetes mellitus, and obesity, which was more than twice as high compared to patients without concomitant metabolic pathology (p<0.05). In the same group, the most pronounced deterioration of the lipid profile was found: low-density lipoprotein cholesterol increased by 99.2% compared to the group without metabolic pathology, and the atherogenic coefficient increased by 300.9% (p<0.001). At the same time, a significant decrease in antiatherogenic high-density lipoprotein cholesterol was recorded. Correlation analysis confirmed that serum galectin-3 has close links with dyslipidemic processes, and the strength of the correlation depends on the comorbid status. The strongest direct correlations with proatherogenic fractions, such as triglycerides and low-density lipoprotein cholesterol, were found in patients with comorbid obesity. These associations indicate that galectin-3 is actively involved in the mechanisms of dyslipidaemia and reflects a triglyceride-dependent aspect of the disorders, closely related to insulin resistance and chronic inflammation. The study also showed that even in patients without comorbid metabolic pathology, a statistically significant association of galectin-3 with total cholesterol and triglycerides persists, which emphasises its role as a marker of fundamental inflammation and fibrosis, independent of external metabolic factors. Thus, the results obtained expand the understanding of the role of galectin-3 as a key mediator integrating inflammatory, fibrotic, and dyslipidemic processes, providing a strong rationale for including galectin-3 in cardiometabolic risk stratification strategies and the search for new therapeutic targets in patients with chronic heart failure.