Abstract

Abstract Objective: Non-alcoholic fatty liver disease (NAFLD) is associated with an increased cardiovascular (CV) risk. However, it is still not clear whether NAFLD contributes independently to the development and progression of CV disease. This study aimed to assess the differences between NAFLD patients with or without hypertension (HT) and patients with HT but no NAFLD through markers of subclinical and clinical atherosclerosis, cardiac function and morphology and liver fibrosis. Design and method: Eighty-seven participants (51,9 ± 9y; males = 83,7%) were divided according to the presence of NAFLD and essential HT in three groups: only-NAFLD, only-HT and NAFLD + HT. Patients with BMI > 35 and type II diabetes were excluded. Blood pressure (BP) measurement, carotid ultrasonography, echocardiography and transient elastography were performed. Carotid intima–media thickness (cIMT), Carotid Distensibility (CD) and Carotid-femoral pulse wave velocity (cf-PWV) were measured as markers of subclinical atherosclerosis and arterial stiffness. Results: The prevalence of atherosclerotic plaques was significantly higher in NAFLD + HT group compared with only-NAFLD group (40% vs 5,7%; p < 0,001). Belonging to NAFLD + HT group, rather than other clinical variables, was independently associated with atherosclerotic plaques in stepwise multiple logistic regression analysis (beta ± SEM = 2.083 ± 0.958; p = 0,01). No differences in cIMT, CD, cf-PWV, echocardiographic parameters and liver stiffness were found among the three groups; nevertheless, a significant prevalence of concentric cardiac remodeling (RWT > 0,42) was detected in all groups (only-HT, NAFLD + HT and only-NAFLD group at 40,9%, 35,7% and 33,3%, respectively; p = not significant). Conclusions: Overt atherosclerosis, rather than subclinical atherosclerosis and arterial stiffness, was more evident in NAFLD + HT patients. A surprising finding was the high prevalence of concentric cardiac remodelling in all groups, including in the only-NAFLD one, suggesting a possible direct involvement of NAFLD in cardiac structural changes. Therefore, the impact of NAFLD on vascular and cardiac structure could be different and partially dependent on the presence of HT.

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