FIB-4 stage of liver fibrosis is associated with incident heart failure with preserved, but not reduced, ejection fraction among people with and without HIV or hepatitis C.


Journal

Progress in cardiovascular diseases
ISSN: 1873-1740
Titre abrégé: Prog Cardiovasc Dis
Pays: United States
ID NLM: 0376442

Informations de publication

Date de publication:
Historique:
received: 12 02 2020
accepted: 12 02 2020
pubmed: 19 2 2020
medline: 23 6 2020
entrez: 19 2 2020
Statut: ppublish

Résumé

Liver fibrosis, is independently associated with incident heart failure (HF). Investigating the association between liver fibrosis and type of HF, specifically HF with reduced ejection fraction (EF; HFrEF) or HF with preserved ejection fraction (HFpEF), may provide mechanistic insight into this association. We sought to determine the association between liver fibrosis score (FIB-4) and type of HF, and to assess whether HIV or hepatitis C status modified this association. We included patients alive on or after 4/1/2003 from the Veterans Aging Cohort Study. We followed patients without prevalent cardiovascular disease until their first HF event, death, last clinic visit, or 9/30/2015. We defined liver fibrosis as: likely advanced fibrosis (FIB-4 > 3.25), indeterminate (FIB-4 range 1.45-3.25), unlikely advanced fibrosis (FIB-4 < 1.45). Primary outcomes were HFrEF and HFpEF (defined using ICD-9 diagnoses for HF, and EF extracted from electronic medical records using natural language processing). Cox proportional hazards models were adjusted for potential confounders and used to estimate hazard ratios (HR). Among 108,708 predominantly male (96%) participants mean age was 49 years. Likely advanced fibrosis was present in 4% at baseline and was associated with an increased risk of HFpEF [HR (95% confidence interval)] [1.70 (1.3-2.3)]; and non-significantly with HFrEF [1.20 (0.9-1.7)]. These associations were not modified by HIV or hepatitis C status. Likely advanced fibrosis was independently associated with incident HFpEF but not HFrEF. This suggests that risk factors and/or mechanisms for liver fibrosis may have greater overlap with those for HFpEF than HFrEF.

Sections du résumé

BACKGROUND
Liver fibrosis, is independently associated with incident heart failure (HF). Investigating the association between liver fibrosis and type of HF, specifically HF with reduced ejection fraction (EF; HFrEF) or HF with preserved ejection fraction (HFpEF), may provide mechanistic insight into this association. We sought to determine the association between liver fibrosis score (FIB-4) and type of HF, and to assess whether HIV or hepatitis C status modified this association.
METHODS
We included patients alive on or after 4/1/2003 from the Veterans Aging Cohort Study. We followed patients without prevalent cardiovascular disease until their first HF event, death, last clinic visit, or 9/30/2015. We defined liver fibrosis as: likely advanced fibrosis (FIB-4 > 3.25), indeterminate (FIB-4 range 1.45-3.25), unlikely advanced fibrosis (FIB-4 < 1.45). Primary outcomes were HFrEF and HFpEF (defined using ICD-9 diagnoses for HF, and EF extracted from electronic medical records using natural language processing). Cox proportional hazards models were adjusted for potential confounders and used to estimate hazard ratios (HR).
RESULTS
Among 108,708 predominantly male (96%) participants mean age was 49 years. Likely advanced fibrosis was present in 4% at baseline and was associated with an increased risk of HFpEF [HR (95% confidence interval)] [1.70 (1.3-2.3)]; and non-significantly with HFrEF [1.20 (0.9-1.7)]. These associations were not modified by HIV or hepatitis C status.
CONCLUSION
Likely advanced fibrosis was independently associated with incident HFpEF but not HFrEF. This suggests that risk factors and/or mechanisms for liver fibrosis may have greater overlap with those for HFpEF than HFrEF.

Identifiants

pubmed: 32068085
pii: S0033-0620(20)30050-5
doi: 10.1016/j.pcad.2020.02.010
pmc: PMC7278895
mid: NIHMS1587068
pii:
doi:

Substances chimiques

Anti-HIV Agents 0

Types de publication

Comparative Study Journal Article Research Support, N.I.H., Extramural Review

Langues

eng

Sous-ensembles de citation

IM

Pagination

184-191

Subventions

Organisme : NIAID NIH HHS
ID : P30 AI050409
Pays : United States
Organisme : NCATS NIH HHS
ID : UL1 TR001863
Pays : United States
Organisme : NHLBI NIH HHS
ID : K01 HL134147
Pays : United States
Organisme : NHLBI NIH HHS
ID : R01 HL146588
Pays : United States
Organisme : NIDDK NIH HHS
ID : K23 DK113252
Pays : United States

Informations de copyright

Copyright © 2020. Published by Elsevier Inc.

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Auteurs

Kaku A So-Armah (KA)

Boston University School of Medicine, Boston, MA, USA. Electronic address: kaku@bu.edu.

Joseph K Lim (JK)

Yale University School of Medicine, New Haven, CT, USA. Electronic address: joseph.lim@yale.edu.

Vincent Lo Re (V)

Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA, USA. Electronic address: vincentl@pennmedicine.upenn.edu.

Janet P Tate (JP)

Yale University School of Medicine, New Haven, CT, USA; VA Connecticut Healthcare System, West Haven, CT, USA. Electronic address: Janet.Tate2@va.gov.

Chung-Chou H Chang (CH)

University of Pittsburgh Schools of Medicine and Public Health, Pittsburgh, PA, USA. Electronic address: changjh@upmc.edu.

Adeel A Butt (AA)

Weill Cornell Medical College, NY, USA; VA Pittsburgh Healthcare System, PA, USA; Hamad Healthcare Quality Institute, Hamad Medical Corporation, Doha, Qatar. Electronic address: aab2005@qatar-med.cornell.edu.

Cynthia L Gibert (CL)

VA Medical Center & George Washington University School of Medicine and Public Health, Washington, DC, USA. Electronic address: Cynthia.Gibert@va.gov.

David Rimland (D)

Atlanta VA Medical Center & Emory University School of Medicine, Atlanta, GA, USA.

Vincent C Marconi (VC)

Atlanta VA Medical Center; Emory University School of Medicine and Rollins School of Public Health, Atlanta, GA, USA. Electronic address: vcmarco@emory.edu.

Matthew Bidwell Goetz (MB)

VA Greater Los Angeles Healthcare System and the David Geffen School of Medicine at the University of California, Los Angeles, CA, USA. Electronic address: Matthew.Goetz@va.gov.

Vasan Ramachandran (V)

Boston University School of Medicine, Boston, MA, USA. Electronic address: vasan@bu.edu.

Evan Brittain (E)

Vanderbilt University School of Medicine, Nashville, TN, USA. Electronic address: evan.brittain@vumc.org.

Michelle Long (M)

Boston University School of Medicine, Boston, MA, USA. Electronic address: mtlong@bu.edu.

Kim-Lien Nguyen (KL)

David Geffen School of Medicine at the University of California, Los Angeles, CA, USA. Electronic address: kimliennguyen@mednet.ucla.edu.

Maria C Rodriguez-Barradas (MC)

Michael E. DeBakey VA Medical Center and Baylor College of Medicine, Houston, TX, USA. Electronic address: Maria.Rodriguez-Barradas2@va.gov.

Matthew J Budoff (MJ)

Harbor-UCLA Medical Center and Los Angeles Biomedical Research Institute, Los Angeles, CA, USA. Electronic address: mbudoff@labiomed.org.

Hilary A Tindle (HA)

Vanderbilt University School of Medicine, Nashville, TN, USA. Electronic address: hilary.tindle@vanderbilt.edu.

Jeffrey H Samet (JH)

Boston University Schools of Medicine and Public Health, Boston Medical Center, Boston, MA, USA. Electronic address: jsamet@bu.edu.

Amy C Justice (AC)

VA Connecticut Healthcare System, West Haven, CT, USA; Yale University Schools of Medicine and Public Health, New Haven, CT, USA. Electronic address: Amy.Justice2@va.gov.

Matthew S Freiberg (MS)

Vanderbilt University School of Medicine, Nashville, TN, USA; Nashville Veterans Affairs Medical Center, Tennessee Valley Healthcare System, Nashville, TN, USA. Electronic address: matthew.s.freiberg@vanderbilt.edu.

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