br Case A year old man

Case A 45-year-old man was referred for the management of sudden-onset tachycardia. He had experienced 3 episodes of palpitation attacks, lasting for a couple of hours each, during the last 6 months. A regular, wide QRS complex tachycardia (WCT) at 150beats/min with a prominent retrograde P wave on the surface electrocardiogram (ECG) was documented during the last attack, which was terminated by drip infusion of pilsicainide administered at another hospital. He did not experience loss of consciousness or dizziness during his palpitation attacks. The findings of other investigations, including physical examination, two-dimensional echocardiography, chest radiography, and laboratory tests, were unremarkable. During the EPS study, a WCT with a 1,3-PBIT dihydrobromide length of 330ms was induced by a ventricular extrastimulus. The morphology of the 12-lead ECG was consistent with that of the clinical tachycardia and showed the right bundle-branch block pattern and left axis deviation. Intracardiac ECG showed a 1:1 atrioventricular (A-V) relationship (Fig. 1). What is the cause of this tachycardia?
Commentary During EPS, the differential diagnosis of the WCT between the supraventricular and ventricular origin is not difficult if A-V dissociation is observed. However, a WCT with a 1:1 AV relationship necessitates careful observation and EP techniques to clarify the mechanism underlying the tachycardia. Several techniques have been described for determining the mechanism underlying tachycardia [1–3]. Shortening of the HV interval or a change of the His and RBB activation sequence will favor ventricular tachycardia (VT) or pre-excited supraventricular tachycardia (SVT). A shorter His-atrial (HA) interval during tachycardia than during RV pacing is consistent with AVNRT with aberration or bystander accessory pathway (AP) [1]. Abdelwahab et al. reported that atrial overdrive pacing during the tachycardia is useful for these differentiations [2]. They demonstrated that the presence of both a narrowing of the QRS complex during the atrial overdrive pacing and an AVVA response upon cessation of atrial overdrive pacing are suggestive of ventricular tachycardia as the mechanism of WCT. In this case, transient ventricular capture during overdrive atrial pacing resulted in marked narrowing of the QRS (Fig. 2). The AVVA response was also observed upon the termination of atrial pacing. Since these findings suggested a ventricular origin of tachycardia, we explored the left ventricular chamber through the transaortic approach.