Atrial Tachycardia Originating from the Aortomitral Junction
A 37-year-old woman with no relevant medical history was admitted to our center after 2 years of recurrent disabling episodes of palpitation and dizziness. She presented with abrupt onset and offset clinical tachycardia. The baseline electrocardiogram (ECG), chest radiograph, and echocardiogram were normal. The ECG recorded during an episode of palpitation revealed a narrow QRS complex tachycardia with a cycle length of 350 ms. The P-wave polarity was isoelectric in lead I and biphasic (initially negative with a late positive component) in leads V1 and V3. In addition, the P-wave polarity was positive in the inferior leads (II, III, and aVF) and negative in lead aVL ().\nAfter obtaining informed consent, we performed an electrophysiological study without sedation. Two quadripolar catheters were introduced into the right ventricle and His bundle region via the femoral vein. A 20-pole catheter with an interelectrode spacing of 2-5-2 mm was positioned at the lateral right atrium (RA), with its distal 10 electrodes in the coronary sinus. Ventriculoatrial conduction was absent at baseline and during isoproterenol infusion. Tachycardia was induced by burst pacing from the RA during isoproterenol infusion without a "jump-up" in the atrial-His (A-H) interval. The tachycardia was perpetuated regardless of the spontaneous AV block. The entrainment phenomenon was not observed during atrial pacing. An intravenous bolus injection of 2-mg adenosine 5'-triphosphate during tachycardia reproducibly terminated the tachycardia without any development of AV block. Ventricular overdrive pacing during tachycardia resulted in AV dissociation without tachycardia entrainment.\nActivation mapping in the RA during tachycardia revealed the earliest atrial activation at the His bundle region, which preceded the onset of the P wave by 30 ms on the surface ECG. Radiofrequency energy was delivered to the superoseptal RA, where the earliest RA activation was recorded, using a 7 F, 4-mm-tipped ablation catheter (Blazer II, Boston Scientific, Natick, MA, USA), with a maximal temperature of 55℃ and maximal power output of 35 W. The His bundle potential was not recorded from the ablation sites at the right superoseptum. The tachycardia was terminated with junctional beats. However, the tachycardia was still inducible and sustainable after the ablation at these sites. To find the other earliest atrial activation site, mapping was then performed around the left atrial septum. The activation at the left atrial septum close to the His-bundle region during the tachycardia was later than that at the right His-bundle region. Subsequently, detailed activation mapping was performed at the aortic sinus of Valsalva, using a transaortic approach, after the aortography. The local atrial electrogram inside the noncoronary aortic and left coronary sinuses preceded the onset of the surface P wave by 40 and 50 ms, respectively. Radiofrequency energy was delivered in the left coronary sinus. Although the tachycardia was terminated by the ablation, it was still inducible. Finally, the earliest site of atrial activation was found at the aortomitral junction where the local atrial electrogram preceded the onset of the surface P wave by 70 ms (). A single radiofrequency energy application at this site using the same ablation catheter with maximal temperature and power output of 50℃ and 30 W, respectively, terminated the tachycardia in 12 s. Thereafter, atrial tachycardia was no longer inducible regardless of isoproterenol infusion (). Neither junctional beats nor prolongation of the A-H interval occurred during or after the energy application. During a 12-month of postablation follow-up period, the patient has been free from recurrence of atrial tachycardia without any antiarrhythmic medications.