Diastolic dysfunction of left ventricle as a consequence of lipotoxic myocardial damage in epicardial obesity

Abstract

Abstract Funding Acknowledgements Type of funding sources: None. Visceral obesity results in lipotoxic myocardial damage and myocardial fibrosis with impaired diastolic function (DD) of left ventricle (LV), followed by progression to heart failure. However, there are no markers for early diagnosis DD of LV. Objective to study the relationship between levels of serum markers of lipotoxic myocardial damage and echocardiographic (ECG) parameters DD of LV in patients with epicardial obesity (EO). Materials and methods The study included 110 men with general obesity. According to the results of ECG, patients were divided into 2 groups: EO (+) with epicardial fat thickness (tEAT) ≥7 mm (n = 70); EO (-) with tEAT <7 mm (n = 40) without DD according to the results of ECG. All patients were assessed for the level of free fatty acids (FFA), as early markers of lipotoxic myocardial damage, markers of myocardial fibrosis in the blood serum (MMP-3, collagen I, collagen III, TGF – β, VEGFA, PICP) using enzyme immunoassay. ECG was used to determine such parameters DD of LV as the velocity of the lateral part of the mitral valve fibrous ring (e"); the ratio of the velocity E of the transmitral diastolic flow to the average velocity of the mitral ring E/e"; the left atrial volume index; the maximum speed of tricuspid regurgitation. Using speckle-tracking ECG, the mechanics of LV were studied (twist LV, peak twist ratio LV, time to peak twist of LV, peak untwist ratio LV, time to peak untwist of LV). Results The level of serum markers of myocardial fibrosis a statistically significant increase all 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 (0.82 ± 0.02 mmol/l and 0.35 ± 0.01 mmol/l, respectively). According to the results of speckle-tracking ECG in the EO (+) group, an increase peak untwist ratio LV to -128.31 (-142.0; -118.0) deg/s-1 (p = 0.002) and an increase time to peak untwist of LV of 476.44 (510.0; 411.0) msec was determined (p = 0.03). There were no statistically significant differences in the study DD of LV parameters in the study groups. Weak statistically significant relationship between the level of FFA and peak untwist ratio LV was revealed (r = 0.26; p = 0.04) in the EO (+) group. Relationships between the level of FFA and the parameters of ECG (e"; E/e"; left atrial volume index; maximum tricuspid regurgitation rate) was not found in both groups. Conclusion In EO, as a result of neurohumoral disorders, lipotoxic myocardial damage develops and progresses, leading DD to LV, the detection of which is probably possible with the help of the rate of LV untwist.