Features of changes in the level of fibrosis markers in lipotoxic myocardial damage in patients with epicardial obesity

Abstract

Abstract In visceral obesity, lipotoxic myocardial damage develops, which leads to the formation of myocardial fibrosis with impaired diastolic function and the development of heart failure (HF). Currently, the search for markers of early diagnosis of left ventricular (LV) diastolic dysfunction (DD) is relevant. Objective To study the features of changes in the level of fibrosis markers in lipotoxic myocardial damage in patients with epicardial obesity (EO). Materials and methods The study included 125 men with general obesity (BMI average 33.24±3.65 kg / sq. m.). All patients underwent transthoracic echocardiography (ECG) to assess the thickness of epicardial adipose tissue (tEAT) as the equivalent of visceral obesity, as well as to diagnose DD LV. According to the results of echocardiography, the patients were divided into 2 groups: EO(+) with epicardial fat thickness (tEAT) ≥7 mm (n=78); EO(−) with tEAT <7 mm (n=40). DD LV was detected in 7 patients, who were subsequently excluded from the analysis. All patients were assessed for profibrotic markers in the blood serum (MMP-3, collagen I, collagen III, TGF – β, VEGFA, PICP) using enzyme immunoassay. The level of free fatty acids (FFA), as early markers of lipotoxic myocardial damage, was also determined in all patients using enzymelinked immunosorbent assay. The peak untwist ratio LV was studied using speckle-tracking ECG. The exclusive criteria were the presence of coronary pathology, arterial hypertension, type 2 diabetes mellitus, as possible causes of lipotoxic myocardial damage. Results When studying the features of changes in the level of serum markers of myocardial fibrosis, a statistically significant increase in the level of all the studied markers was revealed in the EO(+) group compared to the EO(−) group, and a statistically significant increase in the level of FFA in the EO(+) group compared to the EO(−) group (0.84±0.02 mmol/l and 0.35±0.01 mmol/L, respectively, p=0.02). A statistically significant relationship was found between the levels of FFA and collagen III (r=0.32, p=0.03) and TGF – β (r=0.30, p=0.04). According to the results of speckle-tracking ECG in the EO(+) group, an increase in the rate of LV untwist to −125.56 (−141.0; −117.0) deg/s (p=0.003) was determined. When studying the effect of FFA as a marker of lipotoxic effect on the myocardium, a weak statistically significant relationship was revealed between the level of FFA and the rate of LV untwist (r=0.27; p=0.03) in the EO(+) group, while no such effect was found in the EO(−) group. Conclusion In EO, as a result of neurohumoral disorders, lipotoxic myocardial damage develops and progresses, leading to LV DD, the detection of which is probably possible with the help of the LV unwinding rate. Funding Acknowledgement Type of funding sources: None.