ecause of its refractoriness to medical therapy and the high mortality rate, 1,2 junctional ectopic tachycardia (JET) has been treated by ablation of the atrioventricular (AV) junction using either direct 1 or radiofrequency (RF) current. 3,4 However, these therapies may result in the need for permanent cardiac pacing. Recently, selective ablation of the JET focus while preserving normal AV conduction was reported, [5][6][7][8][9] suggesting that the junctional focus is usually perinodal and that ablative lesions created over the anterior, mid or posterior septum, avoiding the His bundle, may be effective. However, in the present patient we believed that the automatic focus of the JET existed at a site ajacent to the His bundle.
Case ReportThe patient was a 5-year-old boy with a tachyarrhythmia that had been present since birth and had been well controlled with propranolol and digoxin. For the 6 months prior to admission, he had recurrent episodes of tachycardia accompanied by signs of congestive heart failure, including vomiting, appetite loss, and cyanosis. Pharmacologic management with multiple antiarrhythmic drugs (excluding amiodarone) failed, and the patient was referred for catheter ablation. The 24-h Holter monitoring showed an incessant irregular narrow QRS tachycardia with a rate of 180 beats/min. Echocardiography showed a reduced left ventricular shortening fraction (22%).Two 5Fr quadripolar electrode catheters were introduced via the left femoral vein into the high right atrium and the right ventricle. A steerable 7Fr 20-pole catheter with a 2-mm interelectrode distance was placed across the tricuspid valve to record the AV junctional electrograms via a left femoral transvenous approach. A 6Fr 8-pole catheter was inserted from the right internal jugular vein into the coronary sinus. A baseline electrophysiologic study confirmed the diagnosis of JET based on the following observations: (1) during tachycardia, ventriculoatrial (VA) dissociation was present with a His potential always preceding the ventricular depolarization at an His-ventricular (HV) interval of 36 ms, (2) the earlier His potential recording was obtained by the more proximal electrode of the 20-pole catheter in the region expected to produce a His electrogram, (3) sinus beats that occasionally captured the ventricle caused a sudden shortening of the HH interval with subtle aberrancy in the QRS configuration, but the HV intervals were the same as those during tachycardia, (4) there was no evidence of retrograde atrial activation in the His bundle or the coronary sinus during tachycardia, (5) atrial overdrive pacing during tachycardia caused temporary suppression of the tachycardia, confirming normal AV nodal conduction, (6) with the termination of atrial overdrive pacing, the tachycardia immediately resumed with a warming-up of the HH interval and subtle changes in the QRS configuration (Fig 1), and (7) the tachycardia could not be terminated with either atrial or ventricular programmed pacing. A 7Fr ablation catheter (Medtronic CardioR...