LAUSR

A 16-year-old female was referred to our evaluation for recurrent episodes of paroxysmal supraventricular tachycardia. Her basal ECG showed sinus rhythm without ventricular preexcitation and her echocardiogram did not reveal any abnormalities. Electrophysiological study was performed and diagnostic catheters were introduced via the femoral veins and positioned at the His bundle region and within the coronary sinus (CS). No accessory pathways were detected but there was evidence of bidirectional dual nodal physiology. During Isoproterenol infusion, burst atrial pacing induced supraventricular tachycardia with 2:1 AV rapport, mean atrial rate of 260ms, and concentric CS activation. At a first glance, 12-lead ECG during tachycardia revealed flutter-like P waves positive in V1 and negative in the inferior leads, compatible with typical counterclockwise atrial flutter (Figure 1A). Subsequently, 1:1 AV conduction was observed following mechanically induced premature ventricular beats without any significant change in atrial rate or activation. Earliest atrial activation was recorded at the CS ostium, while the AH and HA intervals were 110 and 150ms, respectively. Unexpectedly, atrial entrainment from the cavo-tricuspid isthmus (CTI) ruled out an isthmus-dependent atrial flutter and additional pacing manoeuvres were applied. Ventricular overdrive pacing at faster rates (e.g. 240ms) during Isoproterenol infusion was deemed potentially harmful and ventricular resetting was performed. While a single early premature ventricular extrastimulus had no significant effect on the ongoing tachycardia, double premature ventricular extrastimuli reproducibly produced a significant delay in next atriograms and preserving atrial activation sequence (Figure 1B). Moreover, intravenous adenosine resulted in tachycardia termination following minimal VA prolongation. While 2:1 AV block during the ongoing tachycardia ruled out orthodromic AV re-entry via an accessory AV pathway, the reproducible paradoxical delay in atrial activation by ventricular extrastimuli made atrial tachycardia unlikely as a mechanism. Based on these features, adenosine sensibility, and the presence of dual nodal physiology the most likely mechanism was atypical (fast-slow) AV nodal re-entrant tachycardia (AVNRT). Ventricular entrainment is another useful pacing manoeuvre to differentiate between AVNRT and orthodromic AV re-entry using a septal accessory pathway. During this manoeuvre, longer postpacing intervals (>115ms compared to tachycardia cycle length), and stimulus-atrium intervals (>85ms compared to tachycardia VA interval) favour the diagnosis of AVNRT. However, para-Hisian pacing manoeuvre performed in our patient at fast rates (280ms) during the basal study, showed a nodal response with the same retrograde atrial activation supporting the diagnosis of AVNRT (Figure 1C). Conventional radiofrequency ablation of the slow pathway at the inferior portion of Koch triangle produced prolonged junctional rhythm and rendered the tachycardia not inducible anymore. The patient remained asymptomatic and arrhythmia-free during the next 10months follow-up period. This case highlights that atypical AVNRT, particularly at fast rates, may mimic common atrial flutter. The fast atrial rate can produce physiological AV block while focal atrial activation propagating from the slow pathway region is extremely slow, or functionally blocked, at the CTI mimicking counterclockwise atrial flutter activation pattern and producing flutter-like P waves on the surface ECG. Pacing manoeuvres, particularly from the ventricle by applying multiple