title: Cardiac structure and function are altered in adults with non-alcoholic fatty liver disease.
abstract: OBJECTIVE
  Non-alcoholic fatty liver disease (NAFLD) is associated with a twofold greater risk of developing cardiovascular disease. Despite this, little is known about the effect of NAFLD upon cardiac function, limiting our ability to identify therapeutic strategies. This study aimed to address this by defining the effect of NAFLD on cardiac function, structure, and metabolism.
  
  
  METHODS
  Nineteen adults with NAFLD were age-, sex-, and BMI-matched to healthy controls without liver or metabolic disease. Cardiac structure and function were assessed using high-resolution cardiac MRI and tagging at 3.0 T. High-energy phosphate metabolism was assessed using (31)P-magnetic resonance spectroscopy to measure the PCr/ATP ratio.
  
  
  RESULTS
  Adults with NAFLD had significantly thicker left ventricular walls at systole (14 ± 3 vs. 12 ± 2 mm; p <0.01) and diastole (8 ± 1 vs. 7 ± 1 mm; p <0.01) than those without fatty liver and showed decreased longitudinal shortening (14 ± 3 vs. 17 ± 3%; p <0.01). The eccentricity ratio was significantly higher in the NAFLD group (1.1 ± 0.2 vs. 0.9 ± 0.2 g/ml; p <0.01) indicating concentric remodelling. Peak whole wall strain was higher in the NAFLD group (19 ± 2 vs. 17 ± 3%; p <0.01), as was peak endocardial strain (28 ± 4 vs. 22 ± 5%; p <0.01). Cardiac metabolism, measured by PCr/ATP ratio, was not altered in NAFLD (1.8 ± 0.3 vs. 1.9 ± 0.3; p=0.36).
  
  
  CONCLUSIONS
  Significant changes in cardiac structure and function are evident in adults with NAFLD in the apparent absence of metabolic changes or overt cardiac disease. Clinicians should continue to explore therapies to improve cardiac function as a means to modify the excess risk of cardiovascular disease associated with NAFLD.
authors.affiliation: Institute of Cellular Medicine, Newcastle University, Newcastle upon Tyne, UK.
authors.forename: Kate
authors.initials: K
authors.lastname: Hallsworth
authors.forename: Kieren G
authors.initials: KG
authors.lastname: Hollingsworth
authors.forename: Christian
authors.initials: C
authors.lastname: Thoma
authors.forename: Djordje
authors.initials: D
authors.lastname: Jakovljevic
authors.forename: Guy A
authors.initials: GA
authors.lastname: MacGowan
authors.forename: Quentin M
authors.initials: QM
authors.lastname: Anstee
authors.forename: Roy
authors.initials: R
authors.lastname: Taylor
authors.forename: Christopher P
authors.initials: CP
authors.lastname: Day
authors.forename: Michael I
authors.initials: MI
authors.lastname: Trenell
mesh_terms: D000328:Adult; D000368:Aged; D002318:Cardiovascular Diseases / Q000209:etiology / Q000473:pathology / Q000503:physiopathology; D016022:Case-Control Studies; D005234:Fatty Liver / Q000150:complications / Q000473:pathology* / Q000503:physiopathology*; D005260:Female; D006321:Heart / Q000503:physiopathology*; D006801:Humans; D017379:Hypertrophy, Left Ventricular / Q000209:etiology / Q000473:pathology; D008297:Male; D008875:Middle Aged; D009206:Myocardium / Q000473:pathology*; D065626:Non-alcoholic Fatty Liver Disease; D018487:Ventricular Dysfunction, Left / Q000209:etiology / Q000503:physiopathology; D020257:Ventricular Remodeling