Abstract

Abstract Introduction Non-alcoholic fatty liver disease (NAFLD) is the most common cause of liver disease, affecting approximately 25% of the population worldwide. In the majority of patients with NAFLD, other metabolic disorders, such as obesity, diabetes mellitus, dyslipidemia, and metabolic syndrome, are usually present. Purpose To study how NAFLD and steatosis are associated with left ventricular (LV) concentric remodeling and LV hypertrophy (LVH). Methods In this cross-sectional study we examined 1649 participants (997 women) of the Corinthia region, with a mean age of 64±12 years. Several demographic and clinical characteristics were recorded. Echocardiography was performed to all subjects. LV mass was calculated with the method of Devereux et al. LV mass was subsequently indexed for body surface area (BSA), and LVH was defined as left ventricular mass indexed for BSA ≥ 115 g/m2 in men and ≥ 95 g/m2 in women. Hepatic steatosis index (HSI) with the formula (8 × (ALT/AST) + BMI + (2, if diabetes mellitus) + (2, if female)) was used as a predictor of NAFLD. HSI values >36 was used to rule in steatosis. Results From the study population, 1353 were included in the steatosis category. Between the steatosis and non-steatosis group, there was a significant difference in age, gender, BMI and BSA and in several cardiovascular risk factors, including hypertension (Table 1). Interestingly, LV mass 155±38 gr vs. 142±31 gr, p<0.001) and LV mass index (82±17 gr/m2 vs. 79±14 gr/m2, p=0.01) were increased in the steatosis compared to non-steatosis group. LVH prevalence was higher in the steatosis compared to non-steatosis group (11% vs. 2%, p<0.001). Since significant confounders may interfere in the association of steatosis with LVH, we proceeded to a logistic regression analysis that confirmed the independent predictive value of steatosis to LVH (Table 2). Conclusion These findings highlight the interaction of cardiometabolic risks factors, liver steatosis and NAFLD with left ventricular remodeling and left ventricular hypertrophy independently of other known cardiovascular risk factors.

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