The relationship of epicardial obesity and levels of cardiac fibrosis markers

Lipotoxic myocardial damage with its fibrosis and subsequent formation of heart failure may develop due to epicardial obesity (EO). The possibility of early diagnosis of lipotoxic cardiac fibrosis is not well understood.Aim. To study the relationship of EO with the level of myocardial fibrosis markers.Material and methods. The study included 80 men aged 54,3±8,2 with grades I-III obesity. The level of metabolic factors, pro-inflammatory cytokines, adipokines (adiponectin, leptin), soluble leptin receptor and free fatty acids was determined for all patients; the presence of EO was determined by echocardiography with epicardial fat thickness (EFT) ≥7 mm. Coronary artery disease, arterial hypertension, type 2 diabetes mellitus, the presence of left ventricular diastolic dysfunction were the exclusion criteria of the study.Results. The patients were divided into 2 groups: group I with EO (n=49) and group II without EO (n=31). Group I showed a statistically significant increase in the levels of interleukin-6 (IL-6), C-reactive protein, tumor necrosis factor-α (TNF-α), leptin, a decrease in adiponectin, as well as an increase in all studied myocardial fibrosis markers. In addition, in the group with EO, a positive relationship between the EFT and TNF-α (r=0,29; p=0,041), IL-6 (r=0,28; p=0,049), leptin (r=0,41; p=0,004) and a negative relationship with the level of adiponectin (r=-0,29; p=0,042). We determine a significant effect of the degree of EO on the increase in the level of cardiac fibrosis markers (r=0,28, p=0,049), collagen (r=0,33, p=0,019), transforming growth factor-β (r=0,29, p=0,045).Conclusion. The results suggest that elevated levels of profibrotic factors in patients with EO may be signs of the presence of preclinical, and therefore, earlier lipotoxic myocardial fibrosis, which was not detected during echocardiographic research in the form of diastolic dysfunction