The inflammatory markers sST2, HSP27 and hsCRP as a prognostic biomarker panel in chronic heart failure patients.


Journal

Clinica chimica acta; international journal of clinical chemistry
ISSN: 1873-3492
Titre abrégé: Clin Chim Acta
Pays: Netherlands
ID NLM: 1302422

Informations de publication

Date de publication:
Nov 2020
Historique:
received: 13 05 2020
revised: 22 07 2020
accepted: 26 07 2020
pubmed: 1 8 2020
medline: 22 6 2021
entrez: 1 8 2020
Statut: ppublish

Résumé

The inflammatory markers sST2, HSP27 and hsCRP have already been identified as prognostic markers in chronic heart failure (HF). Though individual biomarkers have proven their value in mortality risk prediction, the role of a multimarker strategy needs further evaluation. This is an exploratory reanalysis in chronic HF patients. Plasma HSP27, sST2 and hsCRP in outpatients with chronic HF were analysed. Patients were followed for a minimum of twelve months for the endpoint cardiovascular mortality and unplanned HF associated hospitalisation (=event). 15 year overall mortality was assessed retrospectively. The prognostic impact was assessed using a Cox proportional hazard model. 113 chronic HF patients were included. Median follow up time was 614 days and 37 patients (32.7%) experienced an event. A Kaplan-Meier analysis revealed that patients with increased sST2, HSP27 and hsCRP levels have significantly worse prognosis (p < 0.001). The use of a three-biomarker combination was superior in an independent risk prediction of an event (one high vs. two high: HR = 4.5, 95% CI: 1.3-15.5, p = 0.018; and one high vs. all high: HR = 9.8, 95% CI: 2.8-34.3, p < 0.001) as shown in a multivariable cox proportional hazard model. However, the biomarker panel did not predict 15 year overall mortality, in contrast to elevated HSP27 levels (p = 0.012). The combination of all three markers is an independent predictor of cardiovascular death and unplanned HF associated hospitalisation but not overall mortality. Our findings suggest that adding those markers in combination to well established risk assessment parameters may improve risk stratification.

Sections du résumé

BACKGROUND BACKGROUND
The inflammatory markers sST2, HSP27 and hsCRP have already been identified as prognostic markers in chronic heart failure (HF). Though individual biomarkers have proven their value in mortality risk prediction, the role of a multimarker strategy needs further evaluation.
MATERIALS AND METHODS METHODS
This is an exploratory reanalysis in chronic HF patients. Plasma HSP27, sST2 and hsCRP in outpatients with chronic HF were analysed. Patients were followed for a minimum of twelve months for the endpoint cardiovascular mortality and unplanned HF associated hospitalisation (=event). 15 year overall mortality was assessed retrospectively. The prognostic impact was assessed using a Cox proportional hazard model.
RESULTS RESULTS
113 chronic HF patients were included. Median follow up time was 614 days and 37 patients (32.7%) experienced an event. A Kaplan-Meier analysis revealed that patients with increased sST2, HSP27 and hsCRP levels have significantly worse prognosis (p < 0.001). The use of a three-biomarker combination was superior in an independent risk prediction of an event (one high vs. two high: HR = 4.5, 95% CI: 1.3-15.5, p = 0.018; and one high vs. all high: HR = 9.8, 95% CI: 2.8-34.3, p < 0.001) as shown in a multivariable cox proportional hazard model. However, the biomarker panel did not predict 15 year overall mortality, in contrast to elevated HSP27 levels (p = 0.012).
CONCLUSIONS CONCLUSIONS
The combination of all three markers is an independent predictor of cardiovascular death and unplanned HF associated hospitalisation but not overall mortality. Our findings suggest that adding those markers in combination to well established risk assessment parameters may improve risk stratification.

Identifiants

pubmed: 32735982
pii: S0009-8981(20)30374-0
doi: 10.1016/j.cca.2020.07.050
pii:
doi:

Substances chimiques

Biomarkers 0
CRP protein, human 0
HSP27 Heat-Shock Proteins 0
HSPB1 protein, human 0
Heat-Shock Proteins 0
IL1RL1 protein, human 0
Interleukin-1 Receptor-Like 1 Protein 0
Molecular Chaperones 0
Receptors, Immunologic 0
C-Reactive Protein 9007-41-4

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

507-514

Informations de copyright

Copyright © 2020 Elsevier B.V. All rights reserved.

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

Denise Traxler (D)

Division of Cardiology, Department of Internal Medicine II, Medical University of Vienna, Waehringer Guertel 18-20, 1090 Vienna, Austria; Laboratory for Cardiac and Thoracic Diagnosis, Regeneration and Applied Immunology, Waehringergürtel 18-20, 1090 Vienna, Austria; Division of Thoracic Surgery, Department of Surgery, Medical University of Vienna, Waehringer Guertel 18-20, 1090 Vienna, Austria.

Matthias Zimmermann (M)

Department of Oral and Maxillofacial Surgery, Medical University of Vienna, Waehringer Guertel 18-20, 1090 Vienna, Austria.

Elisabeth Simader (E)

Laboratory for Cardiac and Thoracic Diagnosis, Regeneration and Applied Immunology, Waehringergürtel 18-20, 1090 Vienna, Austria; Division of Thoracic Surgery, Department of Surgery, Medical University of Vienna, Waehringer Guertel 18-20, 1090 Vienna, Austria; Division of Rheumatology, Department of Internal Medicine III, Medical University of Vienna, Waehringer Guertel 18-20, 1090 Vienna, Austria.

Cecilia M Veraar (CM)

Division of Cardiothoracic and Vascular Anaesthesia and Intensive Care Medicine, Department of Anaesthesia, Intensive Care Medicine, and Pain Medicine, Medical University of Vienna, Waehringer Guertel 18-20, 1090, Vienna, Austria.

Bernhard Moser (B)

Division of Thoracic Surgery, Department of Surgery, Medical University of Vienna, Waehringer Guertel 18-20, 1090 Vienna, Austria.

Thomas Mueller (T)

Department of Clinical Pathology, Hospital of Bolzano, Lorenz Böhler Straße 5, 39100 Bolzano, Italy.

Michael Mildner (M)

Research Division of Biology and Pathobiology of the Skin, Department of Dermatology, Medical University of Vienna, Waehringer Guertel 18-20, 1090 Vienna, Austria.

Varius Dannenberg (V)

Division of Cardiology, Department of Internal Medicine II, Medical University of Vienna, Waehringer Guertel 18-20, 1090 Vienna, Austria.

Mitja Lainscak (M)

Division of Cardiology, General Hospital Murska Sobota, Ulica dr. Vrbnjaka 6, 9000 Murska Sobota, Slovenia; Faculty of Medicine, University of Ljubljana, Korytkova ulica 2, 1000 Ljubljana, Slovenia.

Borut Jug (B)

Department of Vascular Diseases, Division of Internal Medicine, University Clinical Center, Zaloška 7/VI, SI-1000 Ljubljana, Slovenia.

Hendrik J Ankersmit (HJ)

Division of Thoracic Surgery, Department of Surgery, Medical University of Vienna, Waehringer Guertel 18-20, 1090 Vienna, Austria. Electronic address: hendrik.ankersmit@meduniwien.ac.at.

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Classifications MeSH