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

Επιστημονική δημοσίευση - Άρθρο Περιοδικού uoadl:3105990 28 Αναγνώσεις

Μονάδα:
Ερευνητικό υλικό ΕΚΠΑ
Τίτλος:
The degree of hepatic steatosis associates with impaired cardiac and autonomic function
Γλώσσες Τεκμηρίου:
Αγγλικά
Περίληψη:
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. © 2019 The Authors
Έτος δημοσίευσης:
2019
Συγγραφείς:
Houghton, D.
Zalewski, P.
Hallsworth, K.
Cassidy, S.
Thoma, C.
Avery, L.
Slomko, J.
Hardy, T.
Burt, A.D.
Tiniakos, D.
Hollingsworth, K.G.
Taylor, R.
Day, C.P.
Masson, S.
McPherson, S.
Anstee, Q.M.
Newton, J.L.
Trenell, M.I.
Περιοδικό:
WORLD JOURNAL OF HEPATOLOGY
Εκδότης:
Elsevier B.V.
Τόμος:
70
Αριθμός / τεύχος:
6
Σελίδες:
1203-1213
Λέξεις-κλειδιά:
glucose, abdominal fat; adult; alcohol consumption; Article; autonomic dysfunction; cardiac patient; cardiovascular disease; cardiovascular risk; cohort analysis; comparative study; controlled study; diastolic blood pressure; disease association; fasting; female; heart output; heart rate variability; heart stroke volume; human; human tissue; liver biopsy; liver histology; major clinical study; male; mean arterial pressure; medical history; nonalcoholic fatty liver; Nonalcoholic Fatty Liver Disease Activity Score; nuclear magnetic resonance spectroscopy; physical examination; priority journal; risk factor; screening test; sedentary lifestyle; systolic blood pressure; aged; autonomic nervous system; cardiovascular disease; complication; fatty liver; heart; hemodynamics; middle aged; nonalcoholic fatty liver; pathophysiology; physiology, Adult; Aged; Autonomic Nervous System; Cardiovascular Diseases; Fatty Liver; Female; Heart; Hemodynamics; Humans; Male; Middle Aged; Non-alcoholic Fatty Liver Disease
Επίσημο URL (Εκδότης):
DOI:
10.1016/j.jhep.2019.01.035
Το ψηφιακό υλικό του τεκμηρίου δεν είναι διαθέσιμο.