At baseline the patient exhibited

At baseline, the patient exhibited normal A–H (57ms) and H–V (44ms) intervals, with a sinus baicalein length of 784ms. Both antegrade and retrograde dual atrioventricular (AV) nodal physiologies were assessed by atrial and ventricular extrastimulus (Fig. 2), without inducible AV nodal reentrant tachycardia. The clinical tachycardia could be induced with reproducible results by single atrial extrastimulus (S1–S1: 600ms, S1–S2: 240–400ms) from the proximal CS (CS os). At this time, the tachycardia exhibited an inverse relationship between the S1 and the S2 interval and the first postpacing return cycle. The earliest site of atrial activation during tachycardia was recorded at the HIS. Although the earliest atrial activation during ventricular pacing was also observed at the HIS, the retrograde atrial activation sequence was different from that during tachycardia. The tachycardia could be induced with reproducible results by ventricular pacing with the V–A–A–V sequence on initiation (Fig. 3a). Rapid atrial pacing terminated the tachycardia, whereas ventricular pacing during tachycardia resulted in AV dissociation without affecting the atrial cycle length or perpetuation of the tachycardia (Fig. 3b). Intravenous administration of 5mg of adenosine 5′-triphosphate prolonged the tachycardia cycle length and terminated tachycardia prior to development of AV conduction block. At this time, the prolonged A–A intervals were reflected on the following V–V intervals, with the corresponding A–V intervals remaining constant, at 104ms (Fig. 3c). Induction and perpetuation of the tachycardia were independent of a jump-up of A–H interval and A–H block. During the tachycardia of a stable cycle length of 380ms, entrainment was demonstrated with reproducible results by rapid pacing from the CS os and the HIS (Fig. 4). When rapid pacing was performed from the CS os, P-wave morphology and atrial activation sequence were altered. The resultant P-wave morphology was slightly different from that formed by CS os pacing during sinus rhythm. We could confirm a small but obvious negative reflection in lead V2 during the entrainment from CS os (Fig. 1). At this time, the atrial activation sequence also showed a minute change (Fig. 5). No obvious changes were noted in P-wave morphology, and the atrial activation sequence when CS os pacing rates were increased (Figs. 4 and 5). During entrainment pacing from the HIS, the P-wave morphology became almost identical to that observed during tachycardia. However, minute differences were also evident in V1 and V2 (Fig. 1). When rapid pacing from the CS os and the HIS was terminated, the spontaneous tachycardia resumed promptly after the last captured atrial beat. The P-wave morphology of the last captured beat was similar to that of the spontaneous tachycardia beat (Figs. 1 and 4). An inverse relationship was found between the pacing cycle length (PCL) and the postpacing interval (PPI). PPI was shorter in the HIS than the CS os for each PCL (Fig. 4). Pacing with PCL shorter than 335ms terminated the tachycardia with reproducible results. On the basis of these electrophysiologic findings, the tachycardia was diagnosed as adenosine-sensitive focal reentrant AT near the His-bundle. We then performed precise mapping of the right atrium after replacing the electrode positioned in the RVA with a 7-French ablation catheter having a 4-mm-long electrode at its distal end, 2 mm interelectrode spacing, and a deflectable tip (Ablaze E, Japan Lifeline Co., Tokyo, Japan). The earliest atrial activation was found to be the right atrial anteroseptal region in the vicinity of the HIS (Fig. 6a). At this region, the local electrogram recorded from the distal electrodes of the ablation catheter during tachycardia preceded the discrete onset of the surface P-wave of V1 by 46ms, with an A/V ratio of 1.2 (Fig. 6b). Radiofrequency ablation for 180s (maximum power, 10W and maximum temperature, 50°C) applied at this region abruptly terminated the AT within 3.4s of the initiation of current delivery (Fig. 6c). Neither transient acceleration nor junctional beats were observed during the ablation. The AT could no longer be induced. The patient was discharged with no medication, except for 100mg oral aspirin for 4 weeks. She has had no recurrence of AT during the follow-up period of 26 months.