Relationship of Nonalcoholic Fatty Liver Disease and Heart Failure With Preserved Ejection Fraction.
ALT, alanine aminotransferase
AST, aspartate aminotransferase
AV, arteriovenous
BCAA, branched-chain amino acid
GLP, glucagon-like peptide
HF, heart failure
HFpEF
HFpEF, heart failure with preserved ejection fraction
HFrEF, heart failure with reduced ejection fraction
IL, interleukin
LV, left ventricular
LVEF, left ventricular ejection fraction
NAFLD
NAFLD, nonalcoholic fatty liver disease
NASH, nonalcoholic steatohepatitis
NT-proBNP, N terminal pro–B-type natriuretic peptide
RAAS, renin-angiotensin aldosterone system
SGLT2, sodium-glucose cotransporter 2
SPSS, spontaneous portosystemic shunt(s)
TNF, tumor necrosis factor
cardiomyopathy
heart failure
liver
Journal
JACC. Basic to translational science
ISSN: 2452-302X
Titre abrégé: JACC Basic Transl Sci
Pays: United States
ID NLM: 101677259
Informations de publication
Date de publication:
Nov 2021
Nov 2021
Historique:
received:
28
06
2021
revised:
27
07
2021
accepted:
27
07
2021
entrez:
6
12
2021
pubmed:
7
12
2021
medline:
7
12
2021
Statut:
epublish
Résumé
Although there is an established bidirectional relationship between heart failure with reduced ejection fraction and liver disease, the association between heart failure with preserved ejection fraction (HFpEF) and liver diseases, such as nonalcoholic fatty liver disease (NAFLD), has not been well explored. In this paper, the authors provide an in-depth review of the relationship between HFpEF and NAFLD and propose 3 NAFLD-related HFpEF phenotypes (obstructive HFpEF, metabolic HFpEF, and advanced liver fibrosis HFpEF). The authors also discuss diagnostic challenges related to the concurrent presence of NAFLD and HFpEF and offer several treatment options for NAFLD-related HFpEF phenotypes. The authors propose that NAFLD-related HFpEF should be recognized as a distinct HFpEF phenotype.
Identifiants
pubmed: 34869957
doi: 10.1016/j.jacbts.2021.07.010
pii: S2452-302X(21)00260-6
pmc: PMC8617573
doi:
Types de publication
Journal Article
Review
Langues
eng
Pagination
918-932Informations de copyright
© 2021 The Authors.
Déclaration de conflit d'intérêts
Dr Rao is supported by a National Institutes of Health Training Grant (5T32HL069749-17). Dr Tedford has consulting relationships with Medtronic, Abbott, Aria CV, Acceleron, Itamar, Edwards Lifesciences, Eidos Therapeutics, Lexicon Pharmaceuticals, Gradient, and United Therapeutics; is a member of steering committees for Medtronic, Acceleron, and Abbott; is a research advisory board member for Abiomed; and does hemodynamic core laboratory work for Actelion and Merck. Dr Mentz has received research support and honoraria from Abbott, American Regent, Amgen, AstraZeneca, Bayer, Boehringer Ingelheim/Eli Lilly, Boston Scientific, Cytokinetics, Fast BioMedical, Gilead, Innolife, Medtronic, Merck, Novartis, Relypsa, Respicardia, Roche, Sanofi, Vifor, Windtree Therapeutics, and Zoll. Dr McGarrah is supported by National Institutes of Health award K08HL135275 and the Edna and Fred L. Mandel Jr Foundation. Dr Fudim was supported by National Heart, Lung, and Blood Institute grant K23HL151744, American Heart Association grant 20IPA35310955, the Mario Family Award, the Duke Chair’s Award, the Translating Duke Health Award, Bayer, and BTG Specialty Pharmaceuticals; and receives consulting fees from AxonTherapies, Bodyport, CVRx, Daxor, Edwards Lifesciences, Fire1, NXT Biomedical, Zoll, and Viscardia. All other authors have reported that they have no relationships relevant to the contents of this paper to disclose.
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