AI Article Synopsis

  • The study investigates if liver stiffness, indicated by the FIB-4 score, directly contributes to heart failure (HF) risk or if this is due to vascular damage.
  • In a cohort of over 3000 healthy Japanese subjects, researchers measured liver stiffness, serum NT-pro-BNP levels, and various vascular parameters over a 3-year period.
  • Results showed a significant relationship between FIB-4 scores and serum NT-pro-BNP levels, suggesting that liver stiffness is a direct risk factor for HF, independent of other vascular damages.

Article Abstract

Background: It remains to be clarified whether liver stiffness is a direct risk factor for heart failure (HF) or whether its association with HF is mediated by vascular damage. We conducted cross-sectional and prospective longitudinal studies to examine whether fibrosis 4 score (FIB-4 score) is directly associated with the serum NT-pro-BNP levels or the association is mediated by arterial stiffness and/or abnormal central hemodynamics.

Methods And Results: In 3040 health Japanese subjects with serum NT-pro-BNP levels < 125 pg/ml, the FIB-4 score was calculated, and the serum NT-pro-BNP levels, brachial-ankle pulse wave (baPWV) velocity and radial augmentation index (rAI) were measured. These parameters were measured again after a 3-year interval in 2135 subjects. Multivariate linear regression analysis demonstrated a significant cross-sectional association of the FIB-4 scores with the log-transformed the serum NT-pro-BNP levels (beta = 0.08,  < 0.01), but not with the baPWV or rAI. The change of serum NT-pro BNP levels during the study period was significantly higher in subjects with increase of the FIB-4 score during the study period (8.2 ± 22.5 pg/ml) than that in those with decrease/no change (5.4 ± 22.3 pg/ml) ( < 0.05).

Conclusion: Liver stiffness may have a significant direct association with the development of HF from the early stage, without the mediation of arterial stiffness and/or abnormal central hemodynamics. Therefore, the FIB-4 score appears to serve as a direct risk factor for HF from the early stage, and its association with HF may not be mediated by vascular damages.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6076211PMC
http://dx.doi.org/10.1016/j.ijcha.2018.07.001DOI Listing

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