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Optimized Analysis of In Vivo and In Vitro Hepatic Steatosis
Published on: March 11, 2017
The degree of hepatic steatosis associates with impaired cardiac and autonomic function
David Houghton1, Paweł Zalewski2, Kate Hallsworth1
1Institute of Cellular Medicine, Newcastle University, Newcastle upon Tyne, UK.
Insights
Elevated liver fat significantly impairs cardiac and autonomic function in patients with non-alcoholic fatty liver disease (NAFLD) and dual-etiology fatty liver disease (DAFLD). Interventions are needed to reduce cardiovascular risk in these populations.
Area of Science:
- Cardiology
- Hepatology
- Metabolic Syndrome
Background:
- Cardiovascular disease is the leading cause of death in individuals with elevated liver fat, surpassing liver-related mortality.
- Non-alcoholic fatty liver disease (NAFLD) and dual-etiology fatty liver disease (DAFLD) are associated with significant cardiovascular risk.
- Metabolic risk factors play a role in the cardiac and autonomic dysfunction observed in fatty liver disease.
Purpose of the Study:
- To investigate the relationship between liver fat accumulation and cardiac/autonomic function.
- To determine how metabolic risk factors influence cardiac and autonomic function impairment in fatty liver disease.
- To compare cardiac and autonomic function in individuals with NAFLD, DAFLD, and healthy controls.
Main Methods:
- Assessed cardiovascular and autonomic function in 96 sedentary individuals.
- Included groups with non-alcoholic fatty liver disease (NAFLD, n=46), dual-etiology fatty liver disease (DAFLD, n=16), and controls (n=34).
- Utilized magnetic resonance spectroscopy to quantify hepatic steatosis (>5%).
Main Results:
- NAFLD and DAFLD patients exhibited significantly impaired cardiac and autonomic function compared to controls.
- Diastolic and systolic variability were reduced in NAFLD and DAFLD groups, with DAFLD showing greater impairment.
- Hepatic steatosis, fasting glucose, and fibrosis stage were negatively correlated with cardiac function parameters; inflammatory markers (TNF-α, CK-18) were associated with autonomic function.
Conclusions:
- Cardiac and autonomic impairments in NAFLD/DAFLD are linked to liver fat levels, metabolic dysfunction, inflammation, and fibrosis.
- Alcohol intake has a lesser impact on these impairments compared to other factors.
- Targeted interventions are crucial to mitigate the elevated cardiovascular risk in patients with NAFLD or DAFLD.
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.
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