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Cardiac troponin I release after transcatheter atrial septal defect closure depends on occluder size but not on patient’s age
  1. A Tárnok1,
  2. J Bocsi1,
  3. P Osmancik2,
  4. H-J Häusler3,
  5. P Schneider3,
  6. I Dähnert3
  1. 1Research Laboratory, Department of Paediatric Cardiology, Heart Centre, University Hospital, Leipzig, Germany
  2. 2Cardiac Centre, Department of Paediatric Cardiology, University Hospital Kralovske Vinogrady, Prague, Czech Republic
  3. 3Department of Paediatric Cardiology, Heart Centre, University Hospital, Leipzig, Germany
  1. Correspondence to:
    Dr Attila Tárnok
    Department of Paediatric Cardiology, Heart Centre, University of Leipzig, Strümpellstrasse 39, 04289 Leipzig, Germany;


Objective: To examine whether transcatheter closure of secundum atrial septal defect (ASD) with the Amplatzer septal occluder leads to more myocardial injury in children than in adults.

Design: In a prospective study with children and adults cardiac troponin I (cTnI) serum concentrations were determined by immunoassay (AxSYM, Abbott Laboratories) before, during, and up to 20 months after surgical or transcatheter ASD closure.

Patients: Four groups of patients were studied: transcatheter ASD closure (group 1: 22 children, age range 3.26–14.7 years; group 2: 22 adults, 18.0–67.3 years), surgical ASD closure (group 3: 18 children, 3.12–13.5 years), and diagnostic catheterisation (group 4: 12 children, 2.68–15.0 years).

Results: cTnI concentrations were significantly increased after occluder implantation with higher serum concentrations in children than in adults (immediately after implantation: group 1, 3.2 (4.4) μg/l; group 2, 1.1 (4.2) μg/l; four hours after implantation: group 1, 4.8 (5.0) μg/l; group 2, 1.7 (2.3) μg/l; both p < 0.01, group 1 v group 2; one day after implantation: group 1, 3.0 (5.7) μg/l; group 2, 2.2 (5.2) μg/l) but were less than 20% of those after surgical ASD closure (group 3; p < 0.001) where the highest cTnI concentration was found (37.1 (26.3) μg/l). Diagnostic catheterisation (group 4) was not associated with detectable cTnI increase. From the cTnI concentrations the total amount of cTnI released after ASD closure was estimated for each patient. This was dependent on the size of the occluder (p < 0.05) but not on the patient’s age or procedural duration.

Conclusion: In regard to interventional ASD closure our data do not provide evidence that the child’s myocardium is more vulnerable. Transcatheter ASD closure induces minor myocardial lesion, the extent of which depends on the size of the Amplatzer septal occluder but is irrespective of the patient’s age.

  • ASD, atrial septal defect
  • AUC, area under the curve
  • cTnI, cardiac troponin I
  • atrial septal defect
  • paediatric cardiology
  • Amplatzer septal occluder
  • myocardial damage

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