Abstract Background Non-alcoholic fatty liver disease (NAFLD) is closely related to the metabolic syndrome as well as to arterial hypertension and overall cardiovascular (CV) disease. We aimed to investigate if those first diagnosed and never treated patients with essential hypertension at high risk for NAFLD, measured by the Hepatic Steatosis Index (HSI), already have an impaired CV risk profile estimated by increased blood pressure burden and accompanied by the presence of hypertension-mediated organ damage (HMOD). Methods We studied 300 non-diabetic, first diagnosed and never-treated young hypertensive patients [mean age=51+11 years, 60% males, 32% smokers]. Ambulatory blood pressure monitoring (24h ABPM), CV risk factors [smoking, obesity (BMI), hyperlipidemia and HMOD [aortic stiffness (PWV), left ventricular diastolic dysfunction (EEa), cardiac hypertrophy (LVMI), coronary arteries microcirculation (CFR), carotid intima-media thickness (cIMT) and endothelial dysfunction (PBR5-25)] were estimated in each patient before treatment initiation. HIS was calculated as 8 times (ALT/AST ratio) +BMI (+2, if female; +2, if diabetes mellitus). Increased HIS levels predispose for augmented risk for NAFLD. Results The whole hypertensive population was divided regarding HSI median value=39.5 in two groups, Group A (higher risk for NAFLD group, n=150, age=50+10, 59% males, 33% smokers) and Group B (lower risk for NAFLD group, n=150, age=51+11, 60% males, 31% smokers). Group A patients had increased BMI (32+5 vs. 27+3, p<0.001), systolic night-time ABPM (127+15 vs. 124+11, p=0.05), office systolic (152+19 vs. 145+17 mmHg, p=0.004) and diastolic BP (94+11 vs. 90+11 mmHg, p=0.002), central systolic BP (146+20 vs. 137+15, p=0.006), Chol (216+39 vs. 206+35, p=0.02), LDL (138+35 vs.130=33 mg/dl, p=0.04) and Trigl (139+75 vs. 112+63, p=0.001), E/Ea (7+2 vs. 6+2, p=0.01) and LVMI (83+18 vs. 79+17, p=0.03) compared to Group B. All other studied demographic, laboratory, ABPM and HMOD parameters (PWV, MAU, CFR and cIMT) were similar between groups. HSI was related to BMI (p<0.001) and office BP, both systolic (p=0.001) and diastolic (p=0.008) in total population as well as to LVMI (r=0.17, p=0.02) in males. Finally, in multiple regression analysis, we found that HSI was independently associated with LVMI (beta=0.14, p=0.05) only in male hypertensives. Conclusions Patients first diagnosed arterial hypertension and augmented CV risk (smoking, obesity, hyperlipidemia, BP burden and HMOD) are also at high risk for NAFLD. As successful antihypertensive treatment may lead to HMOD regression, probably there is still time for those patients to be treated for hypertension disease and hyperlipidemia and quit smoking, in order to reduce future CV risk.LVMI and HSI in male hypertensives
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