The Effect of Spironolactone in Patients With Obesity at Risk for Heart Failure: Proteomic Insights from the HOMAGE Trial.


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:
05 2022
Historique:
received: 20 08 2021
revised: 03 12 2021
accepted: 04 12 2021
pubmed: 22 12 2021
medline: 18 5 2022
entrez: 21 12 2021
Statut: ppublish

Résumé

Adipose tissue influences the expression and degradation of circulating biomarkers. We aimed to identify the biomarker profile and biological meaning of biomarkers associated with obesity to assess the effect of spironolactone on the circulating biomarkers and to explore whether obesity might modify the effect of spironolactone. Protein biomarkers (n = 276) from the Olink Proseek-Multiplex cardiovascular and inflammation panels were measured in plasma collected at baseline, 1 month and 9 months from the HOMAGE randomized controlled trial participants. Of the 510 participants, 299 had obesity defined as an increased waist circumference (≥102 cm in men and ≥88 cm in women). Biomarkers at baseline reflected adipogenesis, increased vascularization, decreased fibrinolysis, and glucose intolerance in patients with obesity at baseline. Treatment with spironolactone had only minor effects on this proteomic profile. Obesity modified the effect of spironolactone on systolic blood pressure (P Among patients at risk for heart failure, those with obesity have a characteristic proteomic profile reflecting adipogenesis and glucose intolerance. Spironolactone had only minor effects on this obesity-related proteomic profile, but obesity significantly modified the effect of spironolactone on systolic blood pressure.

Sections du résumé

BACKGROUND
Adipose tissue influences the expression and degradation of circulating biomarkers. We aimed to identify the biomarker profile and biological meaning of biomarkers associated with obesity to assess the effect of spironolactone on the circulating biomarkers and to explore whether obesity might modify the effect of spironolactone.
METHODS AND RESULTS
Protein biomarkers (n = 276) from the Olink Proseek-Multiplex cardiovascular and inflammation panels were measured in plasma collected at baseline, 1 month and 9 months from the HOMAGE randomized controlled trial participants. Of the 510 participants, 299 had obesity defined as an increased waist circumference (≥102 cm in men and ≥88 cm in women). Biomarkers at baseline reflected adipogenesis, increased vascularization, decreased fibrinolysis, and glucose intolerance in patients with obesity at baseline. Treatment with spironolactone had only minor effects on this proteomic profile. Obesity modified the effect of spironolactone on systolic blood pressure (P
CONCLUSIONS
Among patients at risk for heart failure, those with obesity have a characteristic proteomic profile reflecting adipogenesis and glucose intolerance. Spironolactone had only minor effects on this obesity-related proteomic profile, but obesity significantly modified the effect of spironolactone on systolic blood pressure.

Identifiants

pubmed: 34933097
pii: S1071-9164(21)00501-7
doi: 10.1016/j.cardfail.2021.12.005
pii:
doi:

Substances chimiques

Biomarkers 0
Mineralocorticoid Receptor Antagonists 0
Spironolactone 27O7W4T232

Banques de données

ClinicalTrials.gov
['NCT02556450']

Types de publication

Journal Article Randomized Controlled Trial

Langues

eng

Sous-ensembles de citation

IM

Pagination

778-786

Commentaires et corrections

Type : CommentIn

Informations de copyright

Copyright © 2021 The Authors. Published by Elsevier Inc. All rights reserved.

Déclaration de conflit d'intérêts

Declaration of Competing Interest The authors have no relevant conflicts of interest to disclose with regards to the content of this article.

Auteurs

Job A J Verdonschot (JAJ)

Department of Clinical Genetics, Maastricht University Medical Center, Maastricht, the Netherlands.

JoÃo Pedro Ferreira (JP)

Universite de Lorraine, Inserm, Centre d'Investigation Clinique Plurithe´matique 1433, CHRU de Nancy, F-CRIN INI-CRCT, Nancy, France.

Anne Pizard (A)

Universite de Lorraine, Inserm, Centre d'Investigation Clinique Plurithe´matique 1433, CHRU de Nancy, F-CRIN INI-CRCT, Nancy, France.

Pierpaolo Pellicori (P)

Robertson Centre for Biostatistics, Institute of Health and Wellbeing, University of Glasgow, Glasgow Royal Infirmary, Glasgow, UK.

Hans-Peter Brunner La Rocca (HP)

Department of Cardiology, Maastricht University Medical Center, Maastricht, the Netherlands.

Andrew L Clark (AL)

Department of Cardiology, University of Hull, Castle Hill Hospital, Cottingham, East Riding of Yorkshire, UK.

Franco Cosmi (F)

Department of Cardiology, Cortona Hospital, Arezzo, Italy.

Joe Cuthbert (J)

Department of Cardiology, University of Hull, Castle Hill Hospital, Cottingham, East Riding of Yorkshire, UK.

Nicolas Girerd (N)

Universite de Lorraine, Inserm, Centre d'Investigation Clinique Plurithe´matique 1433, CHRU de Nancy, F-CRIN INI-CRCT, Nancy, France.

Olivia J Waring (OJ)

Department of Pathology, Maastricht University Medical Center, Maastricht, the Netherlands.

Michiel H T M Henkens (MHTM)

Department of Cardiology, Maastricht University Medical Center, Maastricht, the Netherlands.

Beatrice Mariottoni (B)

Department of Cardiology, Cortona Hospital, Arezzo, Italy.

Johannes Petutschnigg (J)

Department of Internal Medicine and Cardiology, Campus Virchow Klinikum, Charité University Medicine Berlin, Berlin Institute of Health (BIH), and German Centre for Cardiovascular research (DZHK), Berlin, Germany.

Patrick Rossignol (P)

Universite de Lorraine, Inserm, Centre d'Investigation Clinique Plurithe´matique 1433, CHRU de Nancy, F-CRIN INI-CRCT, Nancy, France.

Mark R Hazebroek (MR)

Department of Cardiology, Maastricht University Medical Center, Maastricht, the Netherlands.

John G F Cleland (JGF)

Robertson Centre for Biostatistics, Institute of Health and Wellbeing, University of Glasgow, Glasgow Royal Infirmary, Glasgow, UK.

Faiez Zannad (F)

Universite de Lorraine, Inserm, Centre d'Investigation Clinique Plurithe´matique 1433, CHRU de Nancy, F-CRIN INI-CRCT, Nancy, France.

Stephane R B Heymans (SRB)

Department of Cardiology, Maastricht University Medical Center, Maastricht, the Netherlands. Electronic address: s.heymans@maastrichtuniversity.nl.

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