Biomarkers and heart failure events in patients with atrial fibrillation in the ARISTOTLE trial evaluated by a multi-state model.


Journal

American heart journal
ISSN: 1097-6744
Titre abrégé: Am Heart J
Pays: United States
ID NLM: 0370465

Informations de publication

Date de publication:
09 2022
Historique:
received: 03 11 2021
revised: 04 03 2022
accepted: 04 03 2022
pubmed: 16 5 2022
medline: 8 7 2022
entrez: 15 5 2022
Statut: ppublish

Résumé

Atrial fibrillation (AF) and heart failure (HF) often coexist. We investigated the prognostic impact of biomarkers on the development of HF and death in patients with AF and different left ventricular systolic function considering the influence of competing events. The study included 11,818 patients with AF from the ARISTOTLE trial who at entry had information on history of HF, an estimate of left ventricular function and plasma samples for determination of biomarkers representing cardiorenal dysfunction (NT-proBNP, troponin T, cystatin C) and inflammation (GDF-15, IL-6, CRP). Patients were categorized into: (I) HF with reduced ejection fraction (HFrEF, n = 2,048), (II) HF with preserved ejection fraction (HFpEF, n = 2,520), and (III) No HF (n = 7,250). Biomarker associations with HF hospitalization and death were analyzed using a multi-state model accounting also for repeated events. Baseline levels of NT-proBNP, troponin T, cystatin C, GDF-15, IL-6, and CRP were highest in HFrEF and lowest in No HF. During median 1.9 years follow-up, 546 patients were hospitalized at least once for HF and 819 died. Higher levels of all investigated biomarkers were associated with both outcomes (all P< .0001), with highest event rates in HFrEF and lowest in No HF. The associations remained after adjustments and were more pronounced for first than for recurrent events. In anticoagulated patients with AF, biomarkers indicating cardiorenal dysfunction and inflammation improve the identification of patients at risk of developing HF or worsening of already existing HF. These biomarkers might be useful for targeting novel HF therapies in patients with AF.

Sections du résumé

BACKGROUND
Atrial fibrillation (AF) and heart failure (HF) often coexist. We investigated the prognostic impact of biomarkers on the development of HF and death in patients with AF and different left ventricular systolic function considering the influence of competing events.
METHODS
The study included 11,818 patients with AF from the ARISTOTLE trial who at entry had information on history of HF, an estimate of left ventricular function and plasma samples for determination of biomarkers representing cardiorenal dysfunction (NT-proBNP, troponin T, cystatin C) and inflammation (GDF-15, IL-6, CRP). Patients were categorized into: (I) HF with reduced ejection fraction (HFrEF, n = 2,048), (II) HF with preserved ejection fraction (HFpEF, n = 2,520), and (III) No HF (n = 7,250). Biomarker associations with HF hospitalization and death were analyzed using a multi-state model accounting also for repeated events.
RESULTS
Baseline levels of NT-proBNP, troponin T, cystatin C, GDF-15, IL-6, and CRP were highest in HFrEF and lowest in No HF. During median 1.9 years follow-up, 546 patients were hospitalized at least once for HF and 819 died. Higher levels of all investigated biomarkers were associated with both outcomes (all P< .0001), with highest event rates in HFrEF and lowest in No HF. The associations remained after adjustments and were more pronounced for first than for recurrent events.
CONCLUSIONS
In anticoagulated patients with AF, biomarkers indicating cardiorenal dysfunction and inflammation improve the identification of patients at risk of developing HF or worsening of already existing HF. These biomarkers might be useful for targeting novel HF therapies in patients with AF.

Identifiants

pubmed: 35569564
pii: S0002-8703(22)00091-6
doi: 10.1016/j.ahj.2022.03.009
pii:
doi:

Substances chimiques

Biomarkers 0
Cystatin C 0
Growth Differentiation Factor 15 0
Interleukin-6 0
Peptide Fragments 0
Troponin T 0
Natriuretic Peptide, Brain 114471-18-0

Types de publication

Clinical Trial Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

13-24

Informations de copyright

Copyright © 2022 The Authors. Published by Elsevier Inc. All rights reserved.

Auteurs

Julia Aulin (J)

Department of Medical Sciences, Cardiology, Uppsala University, Uppsala, Sweden; Uppsala Clinical Research Center, Uppsala University, Uppsala, Sweden. Electronic address: julia.aulin@ucr.uu.se.

Ziad Hijazi (Z)

Department of Medical Sciences, Cardiology, Uppsala University, Uppsala, Sweden; Uppsala Clinical Research Center, Uppsala University, Uppsala, Sweden.

Johan Lindbäck (J)

Uppsala Clinical Research Center, Uppsala University, Uppsala, Sweden.

John H Alexander (JH)

Duke Clinical Research Institute, Duke Health, Durham, NC.

Bernard J Gersh (BJ)

College of Medicine and Science, Mayo Clinic, Rochester, MN.

Christopher B Granger (CB)

Duke Clinical Research Institute, Duke Health, Durham, NC.

Michael Hanna (M)

Bristol-Myers Squibb, Princeton, NJ.

John Horowitz (J)

Basil Hetzel Institute, University of Adelaide, Adelaide, SA, Australia.

Renato D Lopes (RD)

Duke Clinical Research Institute, Duke Health, Durham, NC.

John J V McMurray (JJV)

BHF Cardiovascular Research Centre, University of Glasgow, Glasgow, Scotland, United Kingdom.

Jonas Oldgren (J)

Department of Medical Sciences, Cardiology, Uppsala University, Uppsala, Sweden; Uppsala Clinical Research Center, Uppsala University, Uppsala, Sweden.

Agneta Siegbahn (A)

Uppsala Clinical Research Center, Uppsala University, Uppsala, Sweden; Department of Medical Sciences, Clinical Chemistry, Uppsala University, Uppsala, Sweden.

Lars Wallentin (L)

Department of Medical Sciences, Cardiology, Uppsala University, Uppsala, Sweden; Uppsala Clinical Research Center, Uppsala University, Uppsala, Sweden.

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Classifications MeSH