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Original article
Fibroblast growth factor 23 as novel biomarker for early risk stratification after ST-elevation myocardial infarction
  1. Martin Reindl1,
  2. Sebastian Johannes Reinstadler1,
  3. Hans-Josef Feistritzer1,
  4. Lukas Mueller1,
  5. Constantin Koch1,
  6. Agnes Mayr2,
  7. Markus Theurl1,
  8. Rudolf Kirchmair1,
  9. Gert Klug1,
  10. Bernhard Metzler1
  1. 1University Clinic of Internal Medicine III, Cardiology and Angiology, Medical University of Innsbruck, Innsbruck, Austria
  2. 2University Clinic of Radiology, Medical University of Innsbruck, Innsbruck, Austria
  1. Correspondence to Dr Bernhard Metzler, University Clinic of Internal Medicine III, Cardiology and Angiology, Medical University of Innsbruck, Anichstrasse 35, Innsbruck A-6020, Austria; Bernhard.Metzler{at}tirol-kliniken.at

Abstract

Objective Adverse left ventricular (LV) remodelling is the major determinant of heart failure and mortality in survivors of ST-elevation myocardial infarction (STEMI). The role of fibroblast growth factor 23 (FGF-23) for LV remodelling prediction after STEMI is unknown. We therefore aimed to investigate the relation between circulating FGF-23 and LV remodelling following revascularised STEMI.

Methods In this prospective observational study, we included 88 consecutive patients with STEMI treated by primary percutaneous coronary intervention. FGF-23 concentrations were measured 2 (IQR: 2–2) days after symptom onset. Cardiac magnetic resonance was performed 2 (IQR: 1–3) days as well as 4 (IQR: 4–5) months after infarction to evaluate LV remodelling, defined as ≥20% increase in LV end-diastolic volume.

Results Levels of FGF-23 were significantly higher in patients who developed LV remodelling (n=11, 13%) as compared with those without LV remodelling (152.6 (102.5–241.3) vs 75.8 (58.6–105.4) relative units per millilitre, p=0.002). The association between FGF-23 and LV remodelling remained significant (OR: 14.1, 95% CI 2.8 to 70.9; p=0.001) after adjustment for biomarkers reflecting myocardial necrosis (high-sensitivity cardiac troponin T (hs-cTnT)), myocardial stress (N-terminal pro B-type natriuretic peptide (NT-proBNP)) and inflammatory state (high-sensitivity C reactive protein (hs-CRP)). Moreover, a multimarker approach adding FGF-23 to the established LV remodelling-predictive biomarkers (hs-cTnT, NT-proBNP and hs-CRP) led to a net reclassification improvement of 0.92 (95% CI 0.44 to 1.41, p<0.001) and to an integrated discrimination improvement of 0.16 (95% CI 0.08 to 0.24, p<0.001).

Conclusions Circulating FGF-23 is independently associated with LV remodelling after reperfused STEMI. A comprehensive multimarker strategy that includes FGF-23 provides incremental prognostic value for prediction of LV remodelling.

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Footnotes

  • Contributors MR: designed the study; analysis and interpretation of data; drafting of the manuscript. SJR: designed the study, interpretation of the data; drafting of the manuscript and revising critically for important intellectual content. H-JF and GK: analysis and interpretation of the data; revising critically for important intellectual content. LM, CK, MT and RK: analysis of the data; revising critically for important intellectual content. AM: image analysis; revising critically for important intellectual content. BM (corresponding author): designed the study; analysis and interpretation of data; drafting of the manuscript; revising critically for important intellectual content.

  • Funding This study was supported by grants from the ‘Austrian Society of Cardiology’, by an intramural funding programme of the Medical University Innsbruck for young scientists MUI-START, Project 2015-06-013, and by a research grant from the ‘Hans and Blanca-Moser Stiftung’.

  • Competing interests None declared.

  • Patient consent Obtained.

  • Ethics approval Local Research Ethics Committee.

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

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