HEPATIC STEATOSIS INDEX IS INDEPENDENTLY RELATED TO HYPERTENSION MEDIATED ORGAN DAMAGE IN PATIENTS WITH FIRST DIAGNOSED AND NEVER TREATED ESSENTIAL HYPERTENSION AND SMOKING HABIT

Abstract

Objective: Non-alcoholic fatty liver disease (NAFLD) is closely related to the metabolic syndrome, 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 (I), already have an impaired CV risk profile estimated by increased blood pressure burden and accompanied by the presence of hypertension-mediated organ damage (HMOD). Design and method: We studied 254 non-diabetic, first diagnosed and never-treated young hypertensive patients, [mean age=51 + 11 years, 59% males, 31% smokers]. Ambulatory blood pressure monitoring (24 h 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). Results: The whole hypertensive population was divided regarding I median value=39.3 in Group A (high risk NAFLD group, n = 127, age = 50 + 10) and Group B (low risk NAFLD group, n = 127, age = 52 + 11). Group A had increased BMI (32 + 5 vs. 27 + 3, p < 0.001), systolic night-time ABPM (128 + 15 vs. 124 + 11, p = 0.04), Chol (217 + 40 vs. 206 + 35, p = 0.01) and Trigl (141 + 79 vs. 112 + 65, p = 0.002), E/Ea (7 + 2 vs. 6 + 2, p = 0.4) and LVMI (83 + 17 vs. 79 + 15, p = 0.03) compared to Group B while all other studied demographic/laboratory/ABPM/HMOD parameters (PWV, MAU, CFR and cIMT) were similar. I was related to BMI (p < 0.001) and office BP, systolic (p < 0.001) and diastolic (p = 0.01), in total population as well as to LVMI (r = 0.24, p = 0.03) in smokers. Finally, in multiple regression analysis, we noted that I was independently associated with LVMI (beta = 0.28, p = 0.05) only in male smokers. Conclusions: Our findings underscore the augmented CV risk (smoking, obesity, hyperlipidemia, BP burden and HMOD) in people with first diagnosed arterial hypertension who are at high risk for NAFLD. As successful antihypertensive treatment may lead to HMOD regression, 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