Highlights. Patients with epicardial obesity develop myocardial fibrosis (the underlying mechanism of left ventricular diastolic dysfunction) the preclinical diagnosis of which is difficult to perform. In this regard, the search for non-invasive methods for diagnosing diastolic dysfunction at an early stage, including the methods of determining the serum level of biomarkers of heart failure and studying the parameters of left ventricular mechanics using speckle-tracking echocardiography, seems quite relevant.Background. Currently, the search for serum biomarkers and non-invasive methods for diagnosing diastolic dysfunction (DD) of the left ventricle (LV) at the preclinical stage in obese patients is relevant.Aim. To study the levels of heart failure biomarkers and their association with profibrotic factors and LV mechanics in patients depending on the presence of epicardial obesity (EO).Methods. Out of 143 men with general obesity, depending on the severity of EO, determined by the thickness of epicardial adipose tissue (tEАT), 2 groups of patients were identified: the EO (+) group with tEАT 7 mm or more (n = 70), and the EO (–) group with tEАT less than 7 mm (n = 40). The exclusion criteria from the study were: arterial hypertension, type 2 diabetes mellitus, coronary artery disease, and the presence of LVDD detected by echocardiography (echo). Levels of profibrotic factors (type I and type III collagen, procollagen type I C-terminal propeptide (PICP), matrix metalloproteinase-3 (MMP-3), transforming growth factor-β (TGF-β), vascular endothelial growth factor A (VEGF-A), sST2, and NT-proBNP were determined in all patients using enzyme immunoassay. With the help of speckle-tracking echocardiography, the mechanics of LV were analyzed.Results. The EO (+) group presented with increased sST2 level (22.11±7.36 ng/mL) compared to the EO (–) group (sST2 level 9.79±3.14 ng/mL (p<0.0001). In the EO (+) group, a significant influence of tEAT on sST2 level was identified (F = 8.57; p = 0.005). In the EO (+) group, an increase in the level of MMP-3, type I collagen, type III collagen, PICP, transforming growth factor-β, and VEGF-A was revealed. Moreover, in the EO (+) group, a statistically significant relationship between sST2 and type III collagen was revealed (p = 0.01). When comparing the parameters of speckle-tracking echo, the EO group (+) presented with increased LV untwisting rate of –128.31 (–142.0; –118.0) deg/s-1 (p = 0.002), and increased time to LV peak untwisting rate of – 476.44 (510.0; 411.0) msec compared with the EO group (–) (p = 0.03). Moreover, a significant association between LV untwisting rate and sST2 level was revealed in the EO (+) group (r = 0.35; p = 0.02).>˂0.0001). In the EO (+) group, a significant influence of tEAT on sST2 level was identified (F = 8.57; p = 0.005). In the EO (+) group, an increase in the level of MMP-3, type I collagen, type III collagen, PICP, transforming growth factor-β, and VEGF-A was revealed. Moreover, in the EO (+) group, a statistically significant relationship between sST2 and type III collagen was revealed (p = 0.01). When comparing the parameters of speckle-tracking echo, the EO group (+) presented with increased LV untwisting rate of –128.31 (–142.0; –118.0) deg/s-1 (p = 0.002), and increased time to LV peak untwisting rate of – 476.44 (510.0; 411.0) msec compared with the EO group (–) (p = 0.03). Moreover, a significant association between LV untwisting rate and sST2 level was revealed in the EO (+) group (r = 0.35; p = 0.02).Conclusion. The data obtained indicate that patients with EO have LVDD, which could not be detected using echo criteria for LVDD, and the determination of serum levels of the heart failure biomarker - sST2 can be used for the diagnosis of LVDD at the early stage.
