Is hepatic steatosis associated with left ventricular mass index increase in the general population?

Katharina Piontek; Carsten O Schmidt; Sebastian E Baumeister; Markus M Lerch; Julia Mayerle; Marcus Dörr; Stephan B Felix; Henry Völzke

doi:10.4254/wjh.v9.i19.857

Is hepatic steatosis associated with left ventricular mass index increase in the general population?

World J Hepatol. 2017 Jul 8;9(19):857-866. doi: 10.4254/wjh.v9.i19.857.

Authors

Katharina Piontek¹, Carsten O Schmidt¹, Sebastian E Baumeister¹, Markus M Lerch¹, Julia Mayerle¹, Marcus Dörr¹, Stephan B Felix¹, Henry Völzke¹

Affiliation

¹ Katharina Piontek, Institute for Medical Psychology, University Medicine Greifswald, 17489 Greifswald, Germany.

Abstract

Aim: To investigate the association between hepatic steatosis and change in left ventricular mass index (LVMI) over five years, and examine whether systolic and diastolic blood pressures are mediators of the association between hepatic steatosis and LVMI using a general population sample.

Methods: We analyzed data from the Study of Health in Pomerania. The study population comprised 1298 individuals aged 45 to 81 years. Hepatic steatosis was defined as the presence of a hyperechogenic pattern of the liver together with elevated serum alanine transferase levels. Left ventricular mass was determined echocardiographically and indexed to height^2.7. Path analyses were conducted to differentiate direct and indirect paths from hepatic steatosis to LVMI encompassing systolic and diastolic blood pressure as potential mediating variables.

Results: Hepatic steatosis was a significant predictor for all measured echocardiographic characteristics at baseline. Path analyses revealed that the association of hepatic steatosis with LVMI change after five years was negligibly small (β = -0.12, s.e. = 0.21, P = 0.55). Systolic blood pressure at baseline was inversely associated with LVMI change (β = -0.09, s.e. = 0.03, P < 0.01), while no association between diastolic blood pressure at baseline and LVMI change was evident (β = 0.03, s.e. = 0.05, P = 0.56). The effect of the indirect path from hepatic steatosis to LVMI via systolic baseline blood pressure was small (β = -0.20, s.e. = 0.10, P = 0.07). No indirect effect was observed for the path via diastolic baseline blood pressure (β = 0.03, s.e. = 0.06, P = 0.60). Similar associations were observed in the subgroup of individuals not receiving beta-blockers, calcium channel blockers, or drugs acting on the renin-angiotensin system.

Conclusion: Baseline associations between hepatic steatosis and LVMI do not extend to associations with LVMI change after five years. More studies are needed to study the longitudinal effects of hepatic steatosis on LVMI.

Keywords: Blood pressure; General Population; Hepatic steatosis; Left ventricular mass index; Study of Health in Pomerania.