The liver-heart axis in patients with severe obesity: The association between liver fibrosis and chronic myocardial injury may be explained by shared risk factors of cardiovascular disease.

Background: Severe obesity is associated with increased risk of non-alcoholic fatty liver disease and cardiovascular disease. We hypothesized that liver fibrosis as quantified by the Enhanced Liver Fibrosis (ELF) test would be predictive of myocardial injury and fibrosis, expressed by higher concentrations of cardiac troponin T and I measured by high-sensitivity assays (hs-cTnT and hs-cTnI, respectively).
Material and Methods: We performed cross-sectional analyses of baseline data from 136 patients (mean age 45 years, 38 % male) with severe obesity participating in the non-randomized clinical trial Prevention of Coronary Heart Disease in Morbidly Obese Patients (ClinicalTrials.gov NCT00626964). Associations between ELF scores, hs-cTnT, and hs-cTnI concentrations were assessed using linear regression analysis.
Results: ELF scores were associated with hs-cTnT in the unadjusted model (B 0.381, 95 % Confidence Interval [CI] 0.247, 0.514), but the association was attenuated upon adjustment for potential confounders (B -0.031, 95 % CI -0.155, 0.093). Similarly, for hs-cTnI, an observed association with ELF scores in the unadjusted model was attenuated upon adjustment for potential confounders ((B 0.432, 95 % CI 0.179, 0.685) and (B 0.069, 95 % CI -0.230, 0.367), respectively). Age, sex, hypertension, and estimated glomerular filtration rate were amongst the shared predictors of ELF score, hs-cTnT, and hs-cTnI that provided the univariable models with the highest R-squared and lowest Akaike Information Criterion values.
Conclusions: Contrary to our hypothesis, ELF score did not predict myocardial injury and fibrosis, but we rather demonstrated an association between liver fibrosis and myocardial injury and fibrosis may be explained by shared risk factors of cardiovascular disease.
Competing Interests: Declaration of competing interest The authors declare the following financial interests/personal relationships which may be considered as potential competing interests: T.O. has received honoraria from Roche Diagnostics, Abbott Laboratories, Bayer and CardiNor not related to the current work, and nonfinancial support from Novartis, ChromaDexSomaLogic, Abbott Diagnostics, and Roche Diagnostics via institution. K.M.A. is an Associate Editor of Clinical Biochemistry and Chair of the International Federation of Clinical Chemistry Committee on Clinical Application of Cardiac Bio-Markers, she has served on advisory boards for Roche Diagnostics, Siemens Healthineers and SpinChip, and has received honorarium for consultancy from CardiNor, honorarium for lecturing from Siemens Healthineers and Snibe Diagnostics, and research grants from Siemens Healthineers and Roche Diagnostics. The remaining authors have no conflicts of interest to declare.
(Copyright © 2023 The Authors. Published by Elsevier Inc. All rights reserved.)