Clinical significance of epicardial fat assessment in hypertensive patients with non-alcoholic fatty liver disease

Abstract

Objective. To study the relationship between the thickness of epicardial adipose tissue (EAT) and indicators of the structural and functional heart characteristics and cardiovascular risk in hypertensive patients with nonalcoholic fatty liver disease (NAFLD).Design and methods. A comparative cross-sectional study was conducted involved 120 patients, aged 45 to 65 years, with hypertension (HTN) of I–II stages, degrees 1–2, with NAFLD (Fatty Liver Index (FLI > 60)) and without NAFLD. A clinical examination was carried out: history, physical examination, measurement of “office” blood pressure and heart rate, anthropometric parameters (height, weight, body mass index). The indicators of carbohydrate and lipid metabolism, chronic low-intensity inflammation (C-reactive protein (CRP), tumor necrosis factor alpha (TNF-α)) were determined, insulin resistance indices were calculated. The structural and functional state of the liver and heart was assessed by ultrasound, and the thickness of the EAT was determined. The SCORE scale was used to assess the 10-year fatal risk.Results. Indicators characterizing chronic low-intensity systemic inflammation (CRP, TNF-α) and insulin resistance (HOMA-IR metabolic index (MI), triglycerides (TG) / high-density lipoproteins (HDL)) were higher in patients with HTN and NAFLD than in patients with isolated HTN. Echocardiography showed that patients with comorbid pathology had greater EAT thickness (p < 0,001) and more profound left ventricular myocardial hypertrophy (thickness of the left ventricular posterior wall (LVPW) (p = 0,019), interventricular septum (IVS) (p = 0,012), left ventricular myocardial mass (LVMM) (p = 0,029)). In the group of patients with HTN and NAFLD, the correlation analysis showed direct moderate-strong relationships between EAT thickness and TPWLV (r = 0,345, p < 0,001), IVS (r = 0,344, p < 0,001), LVMM (r = 0,372, p < 0,001), index LVMM (r = 0,221, p = 0,015), FLI (r = 0,722, p < 0,001), TNF-α (r = 0,495, p < 0,001), HOMA-IR (r = 0,38, p < 0,001), MI (r = 0,374, p < 0.001), TG/HDL (r = 0,354, p < 0,001), CRP (r = 0,30, p = 0,002), TG (r = 0,305, p = 0,001), very low density lipoprotein cholesterol (r = 0,306, p = 0,001) and medium strength inverse relationship with HDL (r = 0,30, p = 0,008). A multiple regression analysis was performed to assess the relationship between EAT thickness and the severity of chronic systemic inflammation and insulin resistance in patients with HTN and NAFLD: with an increase in TNF-α by 1 pg/ml and TG/HDL by 1, an increase in EAT thickness by 0,15 and 0,68 mm, respectively, should be expected. An increase in EAT thickness by 1 mm was accompanied by an increase in LVMM by 12,8 g. Logistic regression analysis showed a direct relation between EAT thickness and the probability of cardiovascular 10-year risk increase by 5,0% or more.Conclusions. This study showed that in patients with HTN and NAFLD, the EAT thickness was significantly higher, which strongly correlates with indicators of left ventricular hypertrophy, the severity of liver steatosis (FLI), chronic low-intensity systemic inflammation, and insulin resistance. With an increase in TNF-α and TG/HDL, an increase in the EAT thickness should be expected. EAT thickness was significantly associated with an increase in LVMM and increased chance of high and very high risk of cardiovascular complications in patients with HTN and NAFLD.