Interleukin-6 and Outcomes in Acute Heart Failure: An ASCEND-HF Substudy.


Journal

Journal of cardiac failure
ISSN: 1532-8414
Titre abrégé: J Card Fail
Pays: United States
ID NLM: 9442138

Informations de publication

Date de publication:
06 2021
Historique:
received: 02 10 2020
revised: 21 12 2020
accepted: 07 01 2021
pubmed: 27 1 2021
medline: 21 10 2021
entrez: 26 1 2021
Statut: ppublish

Résumé

The inflammatory cytokine IL-6 has been previously implicated in the pathophysiology of acute decompensated heart failure (HF). Prior observations in acute HF patients have suggested that IL-6 may be associated with outcomes and modulated by nesiritide. We aimed to evaluate the associations between serial IL-6 measurements, mortality and rehospitalization in acute HF. We analyzed the associations between IL-6 in acute HF, readmission, and mortality (30 and 180 days) using a cohort of 883 hospitalized patients from the ASCEND-HF trial (nesiritide vs placebo). Plasma IL-6 was measured at randomization (baseline), 48-72 hours, and 30 days. The median IL-6 was highest at baseline (14.1 pg/mL) and decreased at subsequent time points (7.6 pg/mL at 30 days). In a univariable Cox regression analysis, the baseline IL-6 was associated with 30- and 180-day mortality (hazard ratio per log 1.74, 95% confidence interval 1.09-2.78, P = .021; hazard ratio 3.23, confidence interval 1.18-8.86, P = .022, respectively). However, there was no association after multivariable adjustment. IL-6 at 48-72 hours was found to be independently associated with 30-day mortality (hazard ratio 8.2, confidence interval 1.2-57.5, P= .03), but not 180-day mortality in multivariable analysis that included the ASCEND-HF risk model and amino terminal pro-B-type natriuretic peptide as covariates. In comparison with placebo, nesiritide therapy was not associated with differences in serial IL-6 levels. Although elevated IL-6 levels were associated with higher all-cause mortality in acute HF, no independent association with this outcome was identified at baseline or 30-day measurements. In contrast with prior reports, we did not observe any impact of nesiritide over placebo on serial IL-6 levels.

Sections du résumé

BACKGROUND
The inflammatory cytokine IL-6 has been previously implicated in the pathophysiology of acute decompensated heart failure (HF). Prior observations in acute HF patients have suggested that IL-6 may be associated with outcomes and modulated by nesiritide. We aimed to evaluate the associations between serial IL-6 measurements, mortality and rehospitalization in acute HF.
METHODS AND RESULTS
We analyzed the associations between IL-6 in acute HF, readmission, and mortality (30 and 180 days) using a cohort of 883 hospitalized patients from the ASCEND-HF trial (nesiritide vs placebo). Plasma IL-6 was measured at randomization (baseline), 48-72 hours, and 30 days. The median IL-6 was highest at baseline (14.1 pg/mL) and decreased at subsequent time points (7.6 pg/mL at 30 days). In a univariable Cox regression analysis, the baseline IL-6 was associated with 30- and 180-day mortality (hazard ratio per log 1.74, 95% confidence interval 1.09-2.78, P = .021; hazard ratio 3.23, confidence interval 1.18-8.86, P = .022, respectively). However, there was no association after multivariable adjustment. IL-6 at 48-72 hours was found to be independently associated with 30-day mortality (hazard ratio 8.2, confidence interval 1.2-57.5, P= .03), but not 180-day mortality in multivariable analysis that included the ASCEND-HF risk model and amino terminal pro-B-type natriuretic peptide as covariates. In comparison with placebo, nesiritide therapy was not associated with differences in serial IL-6 levels.
CONCLUSIONS
Although elevated IL-6 levels were associated with higher all-cause mortality in acute HF, no independent association with this outcome was identified at baseline or 30-day measurements. In contrast with prior reports, we did not observe any impact of nesiritide over placebo on serial IL-6 levels.

Identifiants

pubmed: 33497809
pii: S1071-9164(21)00009-9
doi: 10.1016/j.cardfail.2021.01.006
pii:
doi:

Substances chimiques

Interleukin-6 0
Natriuretic Agents 0
Natriuretic Peptide, Brain 114471-18-0

Types de publication

Journal Article Randomized Controlled Trial

Langues

eng

Sous-ensembles de citation

IM

Pagination

670-676

Informations de copyright

Copyright © 2021 Elsevier Inc. All rights reserved.

Auteurs

Antonio L Perez (AL)

Kaufman Center for Heart Failure Treatment and Recovery, Heart, Vascular and Thoracic Institute, Cleveland Clinic, Cleveland, Ohio.

Justin L Grodin (JL)

Division of Cardiology, Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas, Texas.

Thanat Chaikijurajai (T)

Kaufman Center for Heart Failure Treatment and Recovery, Heart, Vascular and Thoracic Institute, Cleveland Clinic, Cleveland, Ohio.

Yuping Wu (Y)

Department of Mathematics & Statistics, Cleveland State University, Cleveland, Ohio.

Adrian F Hernandez (AF)

Duke University Medical Center, Durham, North Carolina.

Javed Butler (J)

Department of Medicine, University of Mississippi Medical Center, Jackson, Mississippi.

Marco Metra (M)

Department of Cardiology, University of Brescia, Brescia, Italy.

G Michael Felker (GM)

Duke University Medical Center, Durham, North Carolina.

Adriaan A Voors (AA)

University of Groningen, University Medical Center Groningen, Groningen, the Netherlands.

John J McMurray (JJ)

University of Glasgow, Glasgow, UK.

Paul W Armstrong (PW)

Department of Cardiology, University of Alberta, Edmonton, Canada.

Christopher O'Connor (C)

Inova Heart & Vascular Institute, Falls Church, Virginia.

Randall C Starling (RC)

Kaufman Center for Heart Failure Treatment and Recovery, Heart, Vascular and Thoracic Institute, Cleveland Clinic, Cleveland, Ohio.

W H Wilson Tang (WHW)

Kaufman Center for Heart Failure Treatment and Recovery, Heart, Vascular and Thoracic Institute, Cleveland Clinic, Cleveland, Ohio. Electronic address: tangw@ccf.org.

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