The role of epicardial obesity in the development of left ventricular diastolic dysfunction

AIM: To study the effect of epicardial adipose tissue on risk of left ventricular (LV) diastolic dysfunction (DD) in patients with visceral obesity. MATERIAL AND METHODS: Obesity leads to the development of LV DD and is a major cause of heart failure with preserved LV ejection fraction (HFpEF). However, the contribution of epicardial adipose tissue to DD is understudied. This study included 101 men with general obesity (body weight index, 32.9±3.6 kg /m2). Based on severity of epicardial obesity (EO), two groups were formed: group 1, patients with an epicardial adipose tissue thickness (EATt) >7 mm (n=70), and group 2, patients with EATt <7 mm (n=31). Arterial hypertension, diabetes mellitus, coronary atherosclerosis, and disorders of LV diastolic function according to echocardiography (EchoCG) were the exclusion criteria. Diastolic function and LV mechanics were evaluated by speckle-tracking EchoCG for all patients at the start of the study and again at 4.7±0.3 years. RESULTS: At baseline, none of the patients of either group had significant differences in EchoCG characteristics of LV diastolic function (left atrial volume index, LV early diastolic longitudinal lengthening velocity, peak tricuspid regurgitation velocity, and the ratio of diastolic transmitral flow velocity to mean mitral annular velocity (E / e'). However, there were significant increases in the LV untwisting velocity to -122.11 [-142.0; -116.0 degrees /s -1] degrees/s and the time to LV peak untwisting velocity to 472.3 ms. Repeated EchoCG showed an increase in left atrial volume index in group 1 to 35.04 [33.0; 39.7] ml /m2. Repeated evaluation of the LV mechanics revealed increases in the times to LV peak untwisting and twisting and decreases in the LV twisting and untwisting velocities. The logistic regression analysis showed that EATt was a risk factor for LV DD in obesity. Furthermore, the ROC analysis determined the optimal EATt cut-off threshold of ≥9 mm as a predictor for LV DD development. CONCLUSION: EO facilitates the development of LV DD and, thus, represents a major cause for HFpEF. An EATt value of ≥9 mm can be considered as a risk factor for LV DD development in patients with EO.