Left atrial voltage, circulating biomarkers of fibrosis, and atrial fibrillation ablation. A prospective cohort study

PLoS One. 2018 Jan 2;13(1):e0189936. doi: 10.1371/journal.pone.0189936. eCollection 2018.

Abstract

Aims: To test the ability of four circulating biomarkers of fibrosis, and of low left atrial voltage, to predict recurrence of atrial fibrillation after catheter ablation.

Background: Circulating biomarkers potentially may be used to improve patient selection for atrial fibrillation ablation. Low voltage areas in the left atrium predict arrhythmia recurrence when mapped in sinus rhythm. This study tested type III procollagen N terminal peptide (PIIINP), galectin-3 (gal-3), fibroblast growth factor 23 (FGF-23), and type I collagen C terminal telopeptide (ICTP), and whether low voltage areas in the left atrium predicted atrial fibrillation recurrence, irrespective of the rhythm during mapping.

Methods: 92 atrial fibrillation ablation patients were studied. Biomarker levels in peripheral and intra-cardiac blood were measured with enzyme-linked immunosorbent assay. Low voltage (<0.5mV) was expressed as a proportion of the mapped left atrial surface area. Follow-up was one year. The primary endpoint was recurrence of arrhythmia. The secondary endpoint was a composite of recurrence despite two procedures, or after one procedure if no second procedure was undertaken.

Results: The biomarkers were not predictive of either endpoint. After multivariate Cox regression analysis, high proportion of low voltage area in the left atrium was found to predict the primary endpoint in sinus rhythm mapping (hazard ratio 4.323, 95% confidence interval 1.337-13.982, p = 0.014) and atrial fibrillation mapping (hazard ratio 5.195, 95% confidence interval 1.032-26.141, p = 0.046). This effect was also apparent for the secondary endpoint.

Conclusion: The studied biomarkers do not predict arrhythmia recurrence after catheter ablation. Left atrial voltage is an independent predictor of recurrence, whether the left atrium is mapped in atrial fibrillation or sinus rhythm.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adult
  • Aged
  • Atrial Fibrillation / physiopathology
  • Atrial Fibrillation / surgery*
  • Biomarkers / blood*
  • Blood Proteins
  • Catheter Ablation / methods*
  • Collagen Type I / blood
  • Female
  • Fibroblast Growth Factor-23
  • Fibroblast Growth Factors / blood
  • Fibrosis
  • Galectin 3 / blood
  • Galectins
  • Heart Atria / physiopathology*
  • Humans
  • Male
  • Middle Aged
  • Peptide Fragments / blood
  • Peptides / blood
  • Procollagen / blood
  • Prospective Studies

Substances

  • Biomarkers
  • Blood Proteins
  • Collagen Type I
  • FGF23 protein, human
  • Galectin 3
  • Galectins
  • LGALS3 protein, human
  • Peptide Fragments
  • Peptides
  • Procollagen
  • collagen type I trimeric cross-linked peptide
  • procollagen Type III-N-terminal peptide
  • Fibroblast Growth Factors
  • Fibroblast Growth Factor-23

Grants and funding

The study was supported by the National Institute for Health Research, Leeds Cardiovascular Clinical Research Facility. Rashed Karim was supported by the National Institute for Health Research Biomedical Research Centre at Guy’s and St. Thomas’ NHS Foundation Trust and King’s College London. Sven Plein is funded by British Heart Foundation fellowships (FS/1062/28409). The work of Tobias Oesterlein is funded by the German Research Foundation under grant DO637/14-1. St. Jude Medical supports Gordon Begg’s research fellowship. Additional funding was provided by the Leeds General Infirmary cardiac electrophysiology research fund. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript. The specific roles of these authors are articulated in the ‘author contributions’ section.