Haemodynamic and Right Ventricular Mechanical Response to Exercise in Atrial Repaired Transposition of the Great Arteries

  • Miss Meera Ramani, Division of Cardiology, Department of Pediatrics, British Columbia Children's Hospital and The University of British Columbia, Canada
  • Dr George Sandor, Division of Cardiology, Department of Pediatrics, British Columbia Children's Hospital and The University of British Columbia, Canada
  • Miss Astrid De Souza, Division of Cardiology, Department of Pediatrics, British Columbia Children's Hospital and The University of British Columbia, Canada
  • Ms Mary Potts, Division of Cardiology, Department of Pediatrics, British Columbia Children's Hospital and The University of British Columbia, Canada
  • Mr Eustace De Souza, Division of Cardiology, Department of Pediatrics, British Columbia Children's Hospital and The University of British Columbia
  • Dr Michael Patterson, Division of Cardiology, Department of Pediatrics, British Columbia Children's Hospital and The University of British Columbia, Canada
  • Dr Marla Kiess, Division of Cardiology, Department of Medicine, St. Paul's Hospital and The University of British Columbia, Canada
  • Dr James Potts, Division of Cardiology, Department of Pediatrics, British Columbia Children's Hospital and The University of British Columbia, Canada

    • INTRODUCTION. Patients who have had atrial repair of Transposition of the Great Arteries (TGA) have decreased exercise tolerance. The mechanisms and factors for exercise intolerance are not clear. This study was performed to determine the different factors that may be involved in the impaired exercise response of TGA patients. METHODS. Patients exercised in 3 minute stages of 20-40 watts at 60-70 rpm on a semi-recumbent cycle ergometer until volitional fatigue. Echo-Doppler measurements were taken prior to, during, and after exercise. Segmental wall motion was assessed. Doppler velocities were measured. Right Ventricular (RV) dimensions and area change, time to peak contraction, and synchrony were expressed as ratios. RV strain was assessed using speckle tracking. There were 49 patients (female=17); mean age=24.2 years; 15 were post-intervention for SVC syndrome and 10 had pacemakers. RESULTS. Heart rate increased (70-160 bpm) while Stroke Volume Index (SVI) tended to fall (44- 41 mL/m2) with incremental exercise. The increase in Cardiac Index (3.0- 6.3 L/min/m2) was chronotropically-driven. Mean work was 870 J/kg, slightly lower than normal. Pacemakers had a negative effect on these variables, but previous SVC syndrome did not. Longitudinal and circumferential strain fell at peak exercise. Septal motion was biphasic and RV synchrony improved with exercise. CONCLUSION. Patients with atrial repair of TGA have decreased exercise capacity due to a number of factors including an inability to increase or sustain SVI, chronotropic dependence, decreased myocardial contractility, and ventricular dyssynchrony. Previous SVC obstruction did not influence exercise capacity.