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J Thorac Cardiovasc Surg 2002;123:624-630
© 2002 The American Association for Thoracic Surgery

Surgery for Congenital Heart Disease (CHD)

Surgical substrates of postoperative junctional ectopic tachycardia in congenital heart defects

From the Cardiothoracic Unit, Great Ormond Street Hospital for Children National Health Service Trust, and the Institute of Child Health, London, United Kingdom.

Received for publication July 12, 2001. Revisions requested Aug 31, 2001; revisions received Oct 9, 2001. Accepted for publication Oct 12, 2001. Address for reprints: Marc R. de Leval, MD, Cardiothoracic Unit, Great Ormond Street Hospital for Children NHS Trust, Great Ormond St, London WC1N 3JH, United Kingdom (E-mail: DelevM{at}gosh.nhs.uk).

Background: Junctional ectopic tachycardia is a major cause of postoperative morbidity after surgery for congenital cardiac disease. To elucidate the mechanism of junctional ectopic tachycardia, surgical correlations were studied in four types of congenital heart defects involving closure of a ventricular septal defect, relief of right ventricular outflow tract obstruction, or both.
Methods: Between 1997 and 1999, a total of 343 consecutive patients underwent repair of tetralogy of Fallot (n = 114), common truncus arteriosus (n = 10), ventricular septal defect (n = 161), and atrioventricular septal defect (n = 58). Variables studied included demographic and bypass data, surgical approaches toward ventricular septal defect closure and relief of right ventricular outflow tract obstruction, and resection as opposed to division of muscle bundles.
Results: Junctional ectopic tachycardia occurred most frequently after repair of tetralogy of Fallot (n = 25; 21.9%), with no cases occurring after repair of common trunk, 6 occurring after repair of ventricular septal defect (3.7%), and 6 occurring after repair of atrioventricular septal defect (10.3%). Stepwise logistic regression revealed that resection of muscle bundles (P < .0001), higher bypass temperatures (P < .03), and relief of right ventricular outflow tract obstruction through the right atrium (P < .05) significantly and independently predicted postoperative junctional ectopic tachycardia.
Conclusions: Relief of right ventricular outflow tract obstruction appears to be more important in the causation of junctional ectopic tachycardia than does ventricular septal defect closure, which may explain the higher incidence of this complication after tetralogy of Fallot repair. Muscular resection seems to be more arrhythmogenic than is simple division. Increased traction through the right atrium for relief of right ventricular outflow tract obstruction would fit the hypothesis that enhanced automaticity of the His bundle, the morphologic substrate for junctional ectopic tachycardia, may result from direct trauma or infiltrative hemorrhage of the conduction system. When feasible, techniques avoiding both extensive muscle resection and excessive traction should be applied during resection of right ventricular outflow tract obstruction.

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