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Congenital heart disease
Original research article
Prognostic value of soluble ST2 in adults with congenital heart disease
  1. Laurie W Geenen1,
  2. Vivan J M Baggen1,
  3. Annemien E van den Bosch1,
  4. Jannet A Eindhoven1,
  5. Judith A A E Cuypers1,
  6. Maarten Witsenburg1,
  7. Eric Boersma1,2,
  8. Jolien W Roos-Hesselink1
  1. 1 Department of Cardiology, Erasmus MC, University Medical Centre Rotterdam, Rotterdam, The Netherlands
  2. 2 Department of Clinical Epidemiology, Erasmus MC, University Medical Centre Rotterdam, Rotterdam, The Netherlands
  1. Correspondence to Professor Jolien W Roos-Hesselink, Department of Cardiology, Erasmus MC, University Medical Centre Rotterdam, Rotterdam 3000 CA, The Netherlands; j.roos{at}erasmusmc.nl

Abstract

Objective Soluble suppression of tumourigenicity-2 (sST2) is upregulated as response to myocardial stress and may be a potential biomarker for risk stratification in patients with adult congenital heart disease (ACHD). This study aimed to investigate the release of sST2 and its association with cardiovascular events in ACHD.

Methods In this prospective cohort study, 602 consecutive patients with ACHD visiting the outpatient clinic were included (2011–2013). The association between sST2 and a primary composite endpoint of all-cause mortality, heart failure, hospitalisation, arrhythmia, thromboembolic events or cardiac interventions was investigated using multivariable Cox regression.

Results sST2 was measured in 590 (98%) patients (median age 33 [25–41] years, 42% women). After a median follow-up of 5.8 [IQR 5.1–6.2) years, 225 (38.5%) reached the primary endpoint. sST2 was significantly associated with the primary endpoint when adjusted for age, sex, creatinine and N  terminal pro-B type brain natriuretic peptide (NT-proBNP) (HR per twofold higher sST2: 1.28, 95% CI 1.03 to 1.58, p=0.025). This association negated when adjusted for clinical variables and NT-proBNP (HR per twofold higher sST2: 1.19, 95% CI 0.96 to 1.48, p=0.106). Stratified analysis in complex ACHD did show a significant association between sST2 and the primary endpoint when adjusted for clinical variables and NT-proBNP (HR per twofold higher sST2: 1.31, 95% CI 1.01 to 1.69, p=0.043). Sex-specific analysis showed an association between sST2 and the primary endpoint in women (HR per twofold higher sST2 1.80, 95% CI 1.30 to 2.49, p<0.001) but not in men (HR per twofold higher sST2 1.19, 95% CI 0.90 to 1.56, p=0.223).

Conclusions sST2 is a promising novel biomarker in patients with ACHD, specifically in complex ACHD and women. Future research is warranted to elucidate sex-specific and diagnosis-specific differences.

  • congenital heart disease

This is an open access article distributed in accordance with the Creative Commons Attribution 4.0 Unported (CC BY 4.0) license, which permits others to copy, redistribute, remix, transform and build upon this work for any purpose, provided the original work is properly cited, a link to the licence is given, and indication of whether changes were made. See: https://creativecommons.org/licenses/by/4.0/.

https://doi.org/10.1136/heartjnl-2018-314168

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    Footnotes

    • Contributors All of the authors contributed to one or more of the following: conception of design of the work (VJMB, AEvdB, JAE, JAAEC, MW, EB and JWR-H), data collection (LWG, VJMB, AEvdB, JAE, JAAEC, MW and JWR-H) , data analysis and interpretation (LWG, VJMB, EB and JWR-H), drafting the manuscript (LWG, VJMB, EB and JWR-H) and critical revision of the manuscript (all authors). All authors provided final approval of the manuscript. LWG and JWR-H are responsible for the overall content as guarantors.

    • Funding This work was supported by a grant from the Dutch Heart Foundation, The Hague, the Netherlands (grant number 2015T029) to VJMB.

    • Competing interests None declared.

    • Ethics approval The study protocol was approved by the local medical ethics committee.

    • Provenance and peer review Not commissioned; externally peer reviewed.

    • Correction notice This article has been corrected since it first published online. The open access licence type has been amended.

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