Article Text

Download PDFPDF
Original research
Exercise capacity in patients with repaired Tetralogy of Fallot aged 6 to 63 years
  1. Graziella Eshuis1,
  2. Julia Hock2,
  3. Gideon Marchie du Sarvaas1,
  4. Hiske van Duinen3,
  5. Rhoia Neidenbach2,
  6. Freek van den Heuvel1,
  7. Hans Hillege4,
  8. Rolf MF Berger1,
  9. Alfred Hager2
  1. 1 Center of Congenital Heart Disease, Department of Paediatric Cardiology, Beatrix Children’s Hospital, University of Groningen, University Medical Centre Groningen, Groningen, The Netherlands
  2. 2 Department of Paediatric Cardiology and Congenital Heart Disease, Technical University Munich, German Heart Centre Munich, München, Germany
  3. 3 Department of Biomedical Sciences of Cells & Systems, Section of Anatomy & Medical Physiology, University of Groningen, University Medical Centre Groningen, Groningen, The Netherlands
  4. 4 Center for Congenital Heart Disease, Department of Epidemiology, University of Groningen, University Medical Centre Groningen, Groningen, The Netherlands
  1. Correspondence to Graziella Eshuis, Center of Congenital Heart Disease, Department of Paediatric Cardiology, Beatrix Children’s Hospital, University of Groningen, University Medical Centre Groningen, Groningen, The Netherlands; g.eshuis01{at}umcg.nl

Abstract

Objectives This study aimed to provide a perspective for the interpretation of exercise capacity (peakVO2) in patients with repaired Tetralogy of Fallot (patients with rTOF) by describing the course of peakVO2 from patients aged 6–63 years.

Methods A retrospective study was performed between September 2001 and December 2016 in the German Heart Centre Munich, Germany, and in the University Medical Centre Groningen, the Netherlands. A total of 1175 cardiopulmonary exercise tests (CPETs) were collected from 586 patients with rTOF, 46% female. Maximal exertion was verified using a respiratory exchange ratio ≥1.00. PeakVO2 was modelled using time-dependent multilevel models for repeated measurements (n=889 in 300 patients), and compared with subject-specific reference values calculated by the models of Bongers et al and Mylius et al.

Results The peakVO2 of patients with rTOF was reduced at all ages. At the age of 6, the peakVO2 was 614 mL/min (70% of predicted (95% CI 67 to 73)). The reduced increase in peakVO2 during adolescence resulted in a significant lower maximum peakVO2 of 1209 mL/min at 25 years (65% predicted, p<0.001). A linear decline after 25 years was observed in patients and references, although patients showed an accelerated decline, with a -0.24% point of predicted (95% CI 0.11 to 0.38) per year without differences between sexes (p=0.263).

Conclusions This study provides a context for peakVO2 across ages in patients with rTOF under contemporary treatment strategies. It showed that the reduction in peakVO2 originates from childhood and declines over time. Sex differences in patients with rTOF were similar to natural existing sex differences.

  • heart defects
  • congenital
  • tetralogy of Fallot
  • epidemiology

Data availability statement

Data are available on reasonable request. Please contact the corresponding author for questions about the availability of the data.

Statistics from Altmetric.com

Request Permissions

If you wish to reuse any or all of this article please use the link below which will take you to the Copyright Clearance Center’s RightsLink service. You will be able to get a quick price and instant permission to reuse the content in many different ways.

Data availability statement

Data are available on reasonable request. Please contact the corresponding author for questions about the availability of the data.

View Full Text

Footnotes

  • Twitter @Graziel36647415

  • Contributors All authors contributed to the manuscript. GE and RMFB are responsible for the overall content as guarantors in addition to planning, conduct and reporting of the work. JH, RN and FvdH: conduct. GMdS: reporting of the work. HvD: reporting of the work. HH: reporting of the work. AH: conduct and report of the work.

  • Funding GE received a student grant for the research abroad from the Dutch Heart Foundation (td/dekker/2755).

  • Competing interests None declared.

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

  • Supplemental material This content has been supplied by the author(s). It has not been vetted by BMJ Publishing Group Limited (BMJ) and may not have been peer-reviewed. Any opinions or recommendations discussed are solely those of the author(s) and are not endorsed by BMJ. BMJ disclaims all liability and responsibility arising from any reliance placed on the content. Where the content includes any translated material, BMJ does not warrant the accuracy and reliability of the translations (including but not limited to local regulations, clinical guidelines, terminology, drug names and drug dosages), and is not responsible for any error and/or omissions arising from translation and adaptation or otherwise.