The degree of hepatic steatosis associates with impaired cardiac and autonomic function.


Journal

Journal of hepatology
ISSN: 1600-0641
Titre abrégé: J Hepatol
Pays: Netherlands
ID NLM: 8503886

Informations de publication

Date de publication:
06 2019
Historique:
received: 24 05 2018
revised: 05 12 2018
accepted: 22 01 2019
pubmed: 16 2 2019
medline: 2 12 2020
entrez: 16 2 2019
Statut: ppublish

Résumé

Cardiovascular disease is the principle cause of death in patients with elevated liver fat unrelated to alcohol consumption, more so than liver-related morbidity and mortality. The aim of this study was to evaluate the relationship between liver fat and cardiac and autonomic function, as well as to assess how impairment in cardiac and autonomic function is influenced by metabolic risk factors. Cardiovascular and autonomic function were assessed in 96 sedentary individuals: i) non-alcoholic fatty liver disease (NAFLD) (n = 46, hepatic steatosis >5% by magnetic resonance spectroscopy), ii) Hepatic steatosis and alcohol (dual aetiology fatty liver disease [DAFLD]) (n = 16, hepatic steatosis >5%, consuming >20 g/day of alcohol) and iii) CONTROL (n = 34, no cardiac, liver or metabolic disorders, <20 g/day of alcohol). Patients with NAFLD and DAFLD had significantly impaired cardiac and autonomic function when compared with controls. Diastolic variability and systolic variability (LF/HF-sBP [n/1]; 2.3 (1.7) and 2.3 (1.5) vs. 3.4 (1.5), p <0.01) were impaired in patients with NAFLD and DAFLD when compared to controls, with DAFLD individuals showing a decrease in diastolic variability relative to NAFLD patients. Hepatic steatosis and fasting glucose were negatively correlated with stroke volume index. Fibrosis stage was significantly negatively associated with mean blood pressure (r = -0.47, p = 0.02), diastolic variability (r = -0.58, p ≤0.01) and systolic variability (r = -0.42, p = 0.04). Hepatic steatosis was independently associated with cardiac function (p ≤0.01); TNF-α (p ≤0.05) and CK-18 (p ≤0.05) were independently associated with autonomic function. Cardiac and autonomic impairments appear to be dependent on level of liver fat, metabolic dysfunction, inflammation and fibrosis staging, and to a lesser extent alcohol intake. Interventions should be sought to moderate the excess cardiovascular risk in patients with NAFLD or DAFLD. Increased levels of fat in the liver impair the ability of the cardiovascular system to work properly. The amount of fat in the liver, metabolic control, inflammation and alcohol are all linked to the degree that the cardiovascular system is affected.

Sections du résumé

BACKGROUND & AIMS
Cardiovascular disease is the principle cause of death in patients with elevated liver fat unrelated to alcohol consumption, more so than liver-related morbidity and mortality. The aim of this study was to evaluate the relationship between liver fat and cardiac and autonomic function, as well as to assess how impairment in cardiac and autonomic function is influenced by metabolic risk factors.
METHODS
Cardiovascular and autonomic function were assessed in 96 sedentary individuals: i) non-alcoholic fatty liver disease (NAFLD) (n = 46, hepatic steatosis >5% by magnetic resonance spectroscopy), ii) Hepatic steatosis and alcohol (dual aetiology fatty liver disease [DAFLD]) (n = 16, hepatic steatosis >5%, consuming >20 g/day of alcohol) and iii) CONTROL (n = 34, no cardiac, liver or metabolic disorders, <20 g/day of alcohol).
RESULTS
Patients with NAFLD and DAFLD had significantly impaired cardiac and autonomic function when compared with controls. Diastolic variability and systolic variability (LF/HF-sBP [n/1]; 2.3 (1.7) and 2.3 (1.5) vs. 3.4 (1.5), p <0.01) were impaired in patients with NAFLD and DAFLD when compared to controls, with DAFLD individuals showing a decrease in diastolic variability relative to NAFLD patients. Hepatic steatosis and fasting glucose were negatively correlated with stroke volume index. Fibrosis stage was significantly negatively associated with mean blood pressure (r = -0.47, p = 0.02), diastolic variability (r = -0.58, p ≤0.01) and systolic variability (r = -0.42, p = 0.04). Hepatic steatosis was independently associated with cardiac function (p ≤0.01); TNF-α (p ≤0.05) and CK-18 (p ≤0.05) were independently associated with autonomic function.
CONCLUSION
Cardiac and autonomic impairments appear to be dependent on level of liver fat, metabolic dysfunction, inflammation and fibrosis staging, and to a lesser extent alcohol intake. Interventions should be sought to moderate the excess cardiovascular risk in patients with NAFLD or DAFLD.
LAY SUMMARY
Increased levels of fat in the liver impair the ability of the cardiovascular system to work properly. The amount of fat in the liver, metabolic control, inflammation and alcohol are all linked to the degree that the cardiovascular system is affected.

Identifiants

pubmed: 30769007
pii: S0168-8278(19)30112-6
doi: 10.1016/j.jhep.2019.01.035
pii:
doi:

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

1203-1213

Subventions

Organisme : Department of Health
ID : CAT CL-2013-04-010
Pays : United Kingdom
Organisme : Medical Research Council
ID : MR/L016354/1
Pays : United Kingdom
Organisme : Department of Health
ID : SRF-2011-04-017
Pays : United Kingdom

Informations de copyright

Copyright © 2019 The Authors. Published by Elsevier B.V. All rights reserved.

Auteurs

David Houghton (D)

Institute of Cellular Medicine, Newcastle University, Newcastle upon Tyne, UK.

Paweł Zalewski (P)

Department of Hygiene, Epidemiology and Ergonomics, Nicolaus Copernicus University in Torun, Ludwik Rydygier Collegium Medicum in Bydgoszcz, Faculty of Health Sciences, M. Sklodowskiej-Curie 9, 85-094 Bydgoszcz, Poland.

Kate Hallsworth (K)

Institute of Cellular Medicine, Newcastle University, Newcastle upon Tyne, UK.

Sophie Cassidy (S)

Institute of Cellular Medicine, Newcastle University, Newcastle upon Tyne, UK.

Christian Thoma (C)

Institute of Cellular Medicine, Newcastle University, Newcastle upon Tyne, UK.

Leah Avery (L)

Institute of Cellular Medicine, Newcastle University, Newcastle upon Tyne, UK.

Joanna Slomko (J)

Department of Hygiene, Epidemiology and Ergonomics, Nicolaus Copernicus University in Torun, Ludwik Rydygier Collegium Medicum in Bydgoszcz, Faculty of Health Sciences, M. Sklodowskiej-Curie 9, 85-094 Bydgoszcz, Poland.

Timothy Hardy (T)

Institute of Cellular Medicine, Newcastle University, Newcastle upon Tyne, UK; Liver Unit, Newcastle Upon Tyne Hospitals NHS Trust, Freeman Hospital, Newcastle upon Tyne, UK.

Alastair D Burt (AD)

Faculty of Health Sciences, The University of Adelaide, Level 2, Barr Smith South, North Terrace, Adelaide, SA 5005, Australia.

Dina Tiniakos (D)

Institute of Cellular Medicine, Newcastle University, Newcastle upon Tyne, UK; Dept of Pathology, Aretaieion Hospital, National & Kapodistrian University of Athens, Athens 11528, Greece.

Kieren G Hollingsworth (KG)

Institute of Cellular Medicine, Newcastle University, Newcastle upon Tyne, UK.

Roy Taylor (R)

Institute of Cellular Medicine, Newcastle University, Newcastle upon Tyne, UK.

Christopher P Day (CP)

Institute of Cellular Medicine, Newcastle University, Newcastle upon Tyne, UK; Liver Unit, Newcastle Upon Tyne Hospitals NHS Trust, Freeman Hospital, Newcastle upon Tyne, UK.

Steven Masson (S)

Institute of Cellular Medicine, Newcastle University, Newcastle upon Tyne, UK; Liver Unit, Newcastle Upon Tyne Hospitals NHS Trust, Freeman Hospital, Newcastle upon Tyne, UK.

Stuart McPherson (S)

Institute of Cellular Medicine, Newcastle University, Newcastle upon Tyne, UK; Liver Unit, Newcastle Upon Tyne Hospitals NHS Trust, Freeman Hospital, Newcastle upon Tyne, UK.

Quentin M Anstee (QM)

Institute of Cellular Medicine, Newcastle University, Newcastle upon Tyne, UK; Liver Unit, Newcastle Upon Tyne Hospitals NHS Trust, Freeman Hospital, Newcastle upon Tyne, UK.

Julia L Newton (JL)

Institute of Cellular Medicine, Newcastle University, Newcastle upon Tyne, UK; Liver Unit, Newcastle Upon Tyne Hospitals NHS Trust, Freeman Hospital, Newcastle upon Tyne, UK.

Michael I Trenell (MI)

Institute of Cellular Medicine, Newcastle University, Newcastle upon Tyne, UK. Electronic address: michael.trenell@ncl.ac.uk.

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Classifications MeSH