Circulating glypican-4 is a new predictor of all-cause mortality in patients with heart failure.


Journal

Clinical biochemistry
ISSN: 1873-2933
Titre abrégé: Clin Biochem
Pays: United States
ID NLM: 0133660

Informations de publication

Date de publication:
Nov 2023
Historique:
received: 28 06 2023
revised: 11 10 2023
accepted: 13 10 2023
medline: 4 12 2023
pubmed: 17 10 2023
entrez: 16 10 2023
Statut: ppublish

Résumé

Heart failure confers a high burden of morbidity and mortality. However, risk prediction in heart failure patients still is limited. Blood-based biomarkers hold promise to improve clinical risk assessment. Recently we have identified circulating glypican-4 (GPC4) as a significant predictor of mortality in coronary angiography patients and patients with peripheral artery disease. The impact of serum GPC4 on mortality in patients with heart failure is unknown and is addressed in this prospective cohort study. We prospectively recorded all-cause mortality in 288 patients with heart failure. GPC4 levels were measured using an enzyme-linked immunosorbent assay at baseline. During the 24-month follow-up period, 28.1% (n = 81) of the patients died. Serum GPC4 significantly predicted all-cause mortality (hazard ratio (HR) per doublingof GPC4 = 3.57 [2.31-5.53]; P < 0.001). Subgroup analysis showed that GPC4 was significantly associated with all-cause mortality in patients with reduced ejection fraction (HR per doubling = 3.25 [1.75-6.04]; P < 0.001) as well as in those with preserved ejection fraction (HR per doubling = 3.07 [1.22-7.70]; P = 0.017). The association between serum GPC4 and all-cause mortality remained significant in multivariable Cox regression analysis correcting for traditional risk factors (P = 0.035). Results from C-statistics indicated an additional prognostic value of GPC4 relative to NT-proBNP for the prediction of two-year all-cause mortality (P = 0.030). Circulating GPC4 independently predicts all-cause mortality in patients with heart failure.

Sections du résumé

BACKGROUND BACKGROUND
Heart failure confers a high burden of morbidity and mortality. However, risk prediction in heart failure patients still is limited. Blood-based biomarkers hold promise to improve clinical risk assessment. Recently we have identified circulating glypican-4 (GPC4) as a significant predictor of mortality in coronary angiography patients and patients with peripheral artery disease. The impact of serum GPC4 on mortality in patients with heart failure is unknown and is addressed in this prospective cohort study.
METHODS METHODS
We prospectively recorded all-cause mortality in 288 patients with heart failure. GPC4 levels were measured using an enzyme-linked immunosorbent assay at baseline.
RESULTS RESULTS
During the 24-month follow-up period, 28.1% (n = 81) of the patients died. Serum GPC4 significantly predicted all-cause mortality (hazard ratio (HR) per doublingof GPC4 = 3.57 [2.31-5.53]; P < 0.001). Subgroup analysis showed that GPC4 was significantly associated with all-cause mortality in patients with reduced ejection fraction (HR per doubling = 3.25 [1.75-6.04]; P < 0.001) as well as in those with preserved ejection fraction (HR per doubling = 3.07 [1.22-7.70]; P = 0.017). The association between serum GPC4 and all-cause mortality remained significant in multivariable Cox regression analysis correcting for traditional risk factors (P = 0.035). Results from C-statistics indicated an additional prognostic value of GPC4 relative to NT-proBNP for the prediction of two-year all-cause mortality (P = 0.030).
CONCLUSION CONCLUSIONS
Circulating GPC4 independently predicts all-cause mortality in patients with heart failure.

Identifiants

pubmed: 37844682
pii: S0009-9120(23)00203-5
doi: 10.1016/j.clinbiochem.2023.110675
pii:
doi:

Substances chimiques

Biomarkers 0
Glypicans 0
Natriuretic Peptide, Brain 114471-18-0
Peptide Fragments 0
GPC4 protein, human 0

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

110675

Informations de copyright

Copyright © 2023. Published by Elsevier Inc.

Déclaration de conflit d'intérêts

Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.

Auteurs

Axel Muendlein (A)

Vorarlberg Institute for Vascular Investigation and Treatment (VIVIT), Feldkirch, Austria. Electronic address: axel.muendlein@vivit.at.

Christine Heinzle (C)

Vorarlberg Institute for Vascular Investigation and Treatment (VIVIT), Feldkirch, Austria; Medical Central Laboratories, Feldkirch, Austria.

Andreas Leiherer (A)

Vorarlberg Institute for Vascular Investigation and Treatment (VIVIT), Feldkirch, Austria; Medical Central Laboratories, Feldkirch, Austria; Private University in the Principality of Liechtenstein, Triesen, Liechtenstein.

Eva Maria Brandtner (EM)

Vorarlberg Institute for Vascular Investigation and Treatment (VIVIT), Feldkirch, Austria.

Kathrin Geiger (K)

Vorarlberg Institute for Vascular Investigation and Treatment (VIVIT), Feldkirch, Austria; Medical Central Laboratories, Feldkirch, Austria.

Stella Gaenger (S)

Vorarlberg Institute for Vascular Investigation and Treatment (VIVIT), Feldkirch, Austria.

Peter Fraunberger (P)

Medical Central Laboratories, Feldkirch, Austria.

Arthur Mader (A)

Vorarlberg Institute for Vascular Investigation and Treatment (VIVIT), Feldkirch, Austria; Department of Internal Medicine I, Academic Teaching Hospital Feldkirch, Feldkirch, Austria.

Christoph H Saely (CH)

Vorarlberg Institute for Vascular Investigation and Treatment (VIVIT), Feldkirch, Austria; Private University in the Principality of Liechtenstein, Triesen, Liechtenstein; Department of Internal Medicine I, Academic Teaching Hospital Feldkirch, Feldkirch, Austria.

Heinz Drexel (H)

Vorarlberg Institute for Vascular Investigation and Treatment (VIVIT), Feldkirch, Austria; Private University in the Principality of Liechtenstein, Triesen, Liechtenstein; Vorarlberger Landeskrankenhausbetriebsgesellschaft, Feldkirch, Austria; Drexel University College of Medicine, Philadelphia, PA, USA.

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Classifications MeSH