Distinct Pathological Pathways in Patients With Heart Failure and Diabetes.


Journal

JACC. Heart failure
ISSN: 2213-1787
Titre abrégé: JACC Heart Fail
Pays: United States
ID NLM: 101598241

Informations de publication

Date de publication:
03 2020
Historique:
received: 07 08 2019
revised: 05 11 2019
accepted: 06 11 2019
pubmed: 10 2 2020
medline: 4 3 2021
entrez: 10 2 2020
Statut: ppublish

Résumé

The aims of this study were to compare the characteristics of patients with and without diabetes and to use network analyses to compare biomarker profiles and associated pathways in patients with diabetes compared with those without diabetes, which might offer new avenues for potential therapeutic targets. Diabetes adversely affects clinical outcomes and complicates treatment in patients with heart failure (HF). A clear understanding of the pathophysiological processes associated with type 2 diabetes in HF is lacking. Network and pathway over-representation analyses were performed to identify unique pathological pathways in patients with and without diabetes using 92 biomarkers from different pathophysiological domains measured in plasma samples from 1,572 patients with HF (31% with diabetes) with reduced ejection fraction (left ventricular ejection fraction <40%). The results were validated in an independent cohort of 729 patients (30% with diabetes). Biomarker profiles were first compared between patients with HF with and without diabetes. Patients with diabetes showed higher levels of galectin-4, growth differentiation factor 15, and fatty acid binding protein 4 and lower levels of paraoxonase 3. Network analyses were then performed, revealing that epidermal growth factor receptor and galectin-3 were the most prominent connecting proteins. Translation of these networks to biologic pathways revealed that diabetes was associated with inflammatory response and neutrophil degranulation. Diabetes conferred worse outcomes after correction for an established risk model (hazard ratio: 1.20; 95% confidence interval: 1.01 to 1.42). Concomitant diabetes in patients with HF with reduced ejection fraction is associated with distinct pathophysiological pathways related to inflammation, protein phosphorylation, and neutrophil degranulation. These data support the evaluation of anti-inflammatory therapeutic approaches, epidermal growth factor receptor in particular, for patients with HF and diabetes.

Sections du résumé

OBJECTIVES
The aims of this study were to compare the characteristics of patients with and without diabetes and to use network analyses to compare biomarker profiles and associated pathways in patients with diabetes compared with those without diabetes, which might offer new avenues for potential therapeutic targets.
BACKGROUND
Diabetes adversely affects clinical outcomes and complicates treatment in patients with heart failure (HF). A clear understanding of the pathophysiological processes associated with type 2 diabetes in HF is lacking.
METHODS
Network and pathway over-representation analyses were performed to identify unique pathological pathways in patients with and without diabetes using 92 biomarkers from different pathophysiological domains measured in plasma samples from 1,572 patients with HF (31% with diabetes) with reduced ejection fraction (left ventricular ejection fraction <40%). The results were validated in an independent cohort of 729 patients (30% with diabetes).
RESULTS
Biomarker profiles were first compared between patients with HF with and without diabetes. Patients with diabetes showed higher levels of galectin-4, growth differentiation factor 15, and fatty acid binding protein 4 and lower levels of paraoxonase 3. Network analyses were then performed, revealing that epidermal growth factor receptor and galectin-3 were the most prominent connecting proteins. Translation of these networks to biologic pathways revealed that diabetes was associated with inflammatory response and neutrophil degranulation. Diabetes conferred worse outcomes after correction for an established risk model (hazard ratio: 1.20; 95% confidence interval: 1.01 to 1.42).
CONCLUSIONS
Concomitant diabetes in patients with HF with reduced ejection fraction is associated with distinct pathophysiological pathways related to inflammation, protein phosphorylation, and neutrophil degranulation. These data support the evaluation of anti-inflammatory therapeutic approaches, epidermal growth factor receptor in particular, for patients with HF and diabetes.

Identifiants

pubmed: 32035890
pii: S2213-1779(19)30868-6
doi: 10.1016/j.jchf.2019.11.005
pii:
doi:

Substances chimiques

Biomarkers 0

Types de publication

Journal Article Multicenter Study Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

234-242

Subventions

Organisme : Medical Research Council
ID : MR/T018186/1
Pays : United Kingdom

Informations de copyright

Copyright © 2020 American College of Cardiology Foundation. Published by Elsevier Inc. All rights reserved.

Auteurs

Jasper Tromp (J)

Department of Cardiology, University Medical Centre Groningen, University of Groningen, Groningen, the Netherlands; National Heart Centre Singapore, Singapore; Duke-NUS Medical School, Singapore.

Adriaan A Voors (AA)

Department of Cardiology, University Medical Centre Groningen, University of Groningen, Groningen, the Netherlands. Electronic address: a.a.voors@umcg.nl.

Abhinav Sharma (A)

Division of Cardiology, McGill University Health Centre, McGill University, Montreal, Quebec, Canada; Division of Cardiology, University of Alberta, Edmonton, Alberta, Canada; Division of Cardiology, Stanford University, Palo Alto, California.

João P Ferreira (JP)

Université de Lorraine, Inserm, Centre d'Investigations Cliniques-Plurithématique 1433, and Inserm U1116, CHRU, F-CRIN INI-CRCT (Cardiovascular and Renal Clinical Trialists), Nancy, France.

Wouter Ouwerkerk (W)

National Heart Centre Singapore, Singapore.

Hans L Hillege (HL)

Department of Cardiology, University Medical Centre Groningen, University of Groningen, Groningen, the Netherlands.

Karla A Gomez (KA)

Department of Cardiology, University Medical Centre Groningen, University of Groningen, Groningen, the Netherlands.

Kenneth Dickstein (K)

University of Bergen, Stavanger University Hospital, Stavanger, Norway.

Stefan D Anker (SD)

Division of Cardiology and Metabolism-Heart Failure, Cachexia & Sarcopenia, Department of Cardiology, Berlin-Brandenburg Center for Regenerative Therapies, Charité University Medicine, Berlin, Germany.

Marco Metra (M)

Institute of Cardiology, Department of Medical and Surgical Specialties, Radiological Sciences and Public Health, University of Brescia, Brescia, Italy.

Chim C Lang (CC)

Division of Molecular & Clinical Medicine, University of Dundee, Dundee, United Kingdom.

Leong L Ng (LL)

Department of Cardiovascular Sciences, Cardiovascular Research Centre, University of Leicester, Leicester, United Kingdom.

Pim van der Harst (P)

Department of Cardiology, University Medical Centre Groningen, University of Groningen, Groningen, the Netherlands.

Dirk J van Veldhuisen (DJ)

Department of Cardiology, University Medical Centre Groningen, University of Groningen, Groningen, the Netherlands.

Peter van der Meer (P)

Department of Cardiology, University Medical Centre Groningen, University of Groningen, Groningen, the Netherlands.

Carolyn S P Lam (CSP)

Department of Cardiology, University Medical Centre Groningen, University of Groningen, Groningen, the Netherlands; National Heart Centre Singapore, Singapore; Duke-NUS Medical School, Singapore; The George Institute for Global Health, Sydney, Australia.

Faiez Zannad (F)

Université de Lorraine, Inserm, Centre d'Investigations Cliniques-Plurithématique 1433, and Inserm U1116, CHRU, F-CRIN INI-CRCT (Cardiovascular and Renal Clinical Trialists), Nancy, France.

Iziah E Sama (IE)

Department of Cardiology, University Medical Centre Groningen, University of Groningen, Groningen, the Netherlands.

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