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Neurohormonal activation and its relation to outcomes late after repair of tetralogy of Fallot
  1. Ee Ling Heng1,2,
  2. Aidan P Bolger3,
  3. Alexander Kempny1,
  4. Periklis A Davlouros4,
  5. Simon Davidson5,
  6. Lorna Swan1,
  7. Anselm Uebing1,
  8. Dudley J Pennell2,
  9. Michael A Gatzoulis1,2,
  10. Sonya V Babu-Narayan1,2
  1. 1Department of Adult Congenital Heart Disease, Royal Brompton Hospital, London, UK
  2. 2NIHR Cardiovascular Biomedical Research Unit, Royal Brompton & Harefield NHS Foundation Trust and Imperial College, London, UK
  3. 3East Midlands Congenital Heart Centre, Glenfield Hospital, University Hospitals of Leicester, Leicester, UK and Cardiovascular Biomedical Research Unit, University of Leicester
  4. 4Cardiology Department, Patras University Hospital, Patras, Greece
  5. 5Department of Haematology, Royal Brompton Hospital, London, UK
  1. Correspondence to Dr Sonya V Babu-Narayan, Department of Adult Congenital Heart Disease, National Heart and Lung Institute, Imperial College London, Royal Brompton Hospital, Sydney Street, London SW3 6NP, UK; s.babu-narayan{at}rbht.nhs.uk

Abstract

Background Brain natriuretic peptide (BNP) levels are elevated in patients with repaired Tetralogy of Fallot (rTOF), the clinical significance of which remains uncertain.

Methods and results Ninety consecutive adults (≥16 years) with rTOF (mean age 32.7±11.3 years, 64% men) were prospectively recruited from a single tertiary centre, together with 15 age-matched and gender-matched controls. Patients with rTOF had elevated BNP (8.9 (5.9–14.6) vs 5.4 (2.2–7.5) pmol/L; p<0.01), and BNP activation was common even in asymptomatic patients. Also, atrial natriuretic peptide (6.9 (4.0–9.9) vs 3.3 (1.0–4.0) pmol/L; p<0.01), endothelin-1 (1.14 (0.94–1.48) vs 0.75 (0.44–0.93) pmol/L; p<0.01) and renin (55.0 (45.5–66.5) vs 18.6 (12.0–22.7) pmol/L; p<0.01) were elevated at baseline compared with controls. Interactions between BNP with endothelin-1, cardiothoracic ratio and right atrial area were evident. Eight deaths occurred over a median follow-up of 10 years. On Cox regression analysis, BNP emerged as a strong predictor of death (HR 1.16 per 10 pmol/L, 95% CI 1.05 to 1.29; p<0.01). Survival receiver operating curve analysis revealed an optimum cut-off of BNP ≥15 pmol/L (=52 pg/mL), above which BNP was related to significantly increased mortality (HR 5.40, 95% CI 1.29 to 22.6; p<0.01); absolute mortality at 5 years 19% vs 3% in patients with BNP ≤15 pmol/L. BNP was also a predictor of sustained arrhythmia (HR 2.06 per 10 pmol/L, 95% CI 1.32 to 3.21; p<0.05).

Conclusions Neurohormonal activation is present in adults with rTOF including asymptomatic patients. BNP level ≥15 pmol/L is associated with a fivefold increased risk of death. These data suggest that BNP measurement in patients with rTOF should be incorporated in the periodic risk stratification assessment of these patients under lifelong follow-up.

  • CONGENITAL HEART DISEASE

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