Abstract

Epicardial obesity (EO) can lead to lipotoxic myocardial damage with the development of myocardial fibrosis, which underlie the impairment of left ventricular (LV) diastolic function. The identification of markers of lipotoxic myocardial damage is important at an early preclinical stage for preventive measures. Objective. To study the relationship of plasma levels of markers of insulin resistance and lipotoxic fibrosis with the parameters of LV mechanics in patients with EO. We hypothesized that there are significant differences in plasma levels of markers of insulin resistance and myocardial fibrosis and that they are associated with the parameters of LV mechanics in EO. Design and methods. The study included 143 men. Inclusion criteria: general obesity I–III degree. Exclusion criteria: type 2 diabetes mellitus, hypertension, LV diastolic dysfunction based on echocardiography (Echo). Patients were divided into 2 groups: EO (+) with epicardial fat thickness (tEAT) ≥ 7 mm (n = 70); EO (–) with tEAT < 7 mm (n = 31). All patients were assessed for glucose, blood insulin, profibrotic factors and free fatty acids (FFA) using enzyme-linked immunosorbent assay. HOMA-IR insulin sensitivity index was calculated as (insulin × glucose)/22,5. With the help of speckle-tracking Echo, the mechanics of LV were studied (LV twisting, LV twisting ratio, time to LV twisting peak, LV untwisting ratio, time to LV untwisting peak). Results. The patients with EO (+) showed a statistically significant increase in the level of FFA up to 0,82 (0,39; 1,30) mmol/L (< 0,0001) and HOMA-IR index up to 3,89 (2,02; 5,76) (< 0,0001) in comparison with the group EO (–). There was a statistically significant effect of tEAT on the level of FFA (F = 7,90; p = 0,006) and on the development of insulin resistance (F = 14,85; p < 0,001). The correlation analysis in the EO (+) group showed the relationship between FFA and type III collagen (r = 0,29, p = 0,01) and procollagen type I carboxy-terminal propeptide (PICP) (r = 0,26, p = 0,03), as well as between HOMA-IR and MMP-3 (r = 0,30, p = 0,01). In the EO (–) group, the relationship of profibrotic factors with the level of FFA and HOMA-IR was not found. There was also a significant relationship between LV untwisting ratio and level of FFA (r = 0,24, p = 0,04) in the group EO (+). Conclusions. Thus, an increase in the level of FFA in patients with EO may be accompanied by an increase in the level of some profibrotic factors and a LV untwisting violation determined by speckle-tracking Echo. Our data supports the need for assessing the FFA level and speckle-tracking Echo for the early diagnosis of LV diastolic dysfunction in patients with EO.

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