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K E Y W O R D S : capture beat, double exit, fusion beat, multiple exits, wobble, wide QRS tachycardia 1 CASE A 63-year-old man suffering from ischemic ventricular tachycardias (VTs) with recurrent implantable cardioverter-defibrillator (ICD) shocks despite the use of amiodarone, underwent endocardial VT ablation. Using an activation map, an isthmus was located and targeted in the middle of the anteroseptal area of the left ventricle. Multiple simultaneous mid-diastolic potentials recorded on a multielectrode mapping catheter during tachycardia with alternating QRS morphologies (Figure 1). What are the possible mechanisms of the alternating QRS morphology and cycle length (CL)? DISCUSSIONMonomorphic VTs with alternating QRS morphologies have been observed to occur spontaneously and during programmed stimulation in human hearts. 1-3 The presence of fusion beats (QRS of intermediate duration between those during SR and during tachycardia) and capture beats (narrow QRS and equal to that during SR) may cause the different tachycardia morphologies. 4 However, two different reentry circuits may share the same exit with functional block changing the QRS morphology, may have the same "shared" isthmus with a different exit, or may have two different isthmuses in different areas of the same scar or different scar. [3][4][5][6][7] In the setting of the "fusion" and "capture" beats, measuring the P-P interval or P-QRS interval stay fairly constant before and after those "fusion" and "capture" beats; however, the "fusion beat" comes in early when measured the ventricular rate (R-R interval). Despite there was no atrial electrocardiogram in current tracing, we considered that the alternating VT morphologies in our patient were due to different exits of the same shared isthmus ( Figure 2) supported by the change in the QRS morphology precedes and predicts the next DP-DP interval ("wobble")( Figure 3). The septal origin VTs show narrower QRS complexes due to the early involvement of the His-Purkinje fibers and the simultaneous activation of both ventricles. As compatible with that, the exit of the narrower QRS cycles ("N" in Figure 3) was near the anteroseptal region but wider ones ("W" in Figure 3) were more anterior wall exit. Indeed, capture beats would be more random and also most unlikely to provide early ventricular activation in the close vicinity of the slow conduction zone immediately following a diastolic potential (DP) that would render that region refractory to a supraventricular impulse. Therefore, spontaneous changes in the measured intracardiac intervals during tachycardia (wobble) are useful in determining the mechanism of not only narrow QRS but also wide QRS tachycardias. 8

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A 33-year old woman presented with regular palpitations and documented a short RP narrow QRS complex tachycardia. A 12-lead surface electrocardiography during sinus rhythm showed no delta waves. At electrophysiological study, the retrograde conduction was decremental and concentric with the earliest activation site at the His bundle region. Para-Hisian pacing indicated retrograde conduction over the fast pathway of the atrioventricular (AV) node. No retrograde dual AV nodal physiology was observed, while programmed atrial extrastimuli exhibited an AH interval jump, demonstrating the presence of anterograde dual AV nodal pathways. No pre-excitation was inducible at any pacing site or atrial rate. After the AH interval jump, a narrow QRS tachycardia at a cycle length (CL) of 360 ms was reproducibly induced.A single late ventricular premature complex (VPC) applied from the right ventricular apex (RVA) during the tachycardia is shown in Figure 1. What is the mechanism of this tachycardia? DISCUSSIONThe differential diagnosis of a short RP supraventricular tachycardia with the earliest atrial activation in the His bundle region includes atrial tachycardia (AT) originating from near the AV node, orthodromic reciprocating tachycardia (ORT) using a septal accessory pathway, typical (slow-fast form) atrioventricular nodal reentrant tachycardia (AVNRT), junctional tachycardia (JT), and orthodromic nodofascicular (NF), or nodoventricular (NV) reentrant tachycardia (NFRT/NVRT). 1-6 The tachycardia with a short septal VA interval of <70 ms excludes ORT, although septal AT with a prolonged AV conduction is possible. 3 The His-refractory VPC stopped the tachycardia without changing the retrograde atrial activation sequence (RAAS) and AA interval, which excludes the diagnosis of AT and JT, leaving us the possibility of NFRT or AVNRT with bystander NF pathway. 4,7,8 Whereas a His-refractory VPC terminates the tachycardia without conducting to the atrium, it should not have any effect on the ongoing tachycardia during AVNRT. However, the presence of an NF or NV pathway connected to the nodal slow pathway may explain the paradoxical delay in His or termination of tachycardia by VPC maintaining the same RAAS (Figure 2). Although NF/NV connections are rare accessory pathways,their presence must be recognized because they can lead to diagnostic confusion, whether or not they participate in the tachycardia. 9-11 The para-Hisian pacing is generally not useful since an AV nodal response is not diagnostic of pure AV nodal conduction but can also be observed with a NF pathway. 12 The tachycardia induction with critical AH jump is also not discriminative evidence. Because the His bundle is not part of the AVNRT circuit, in theory it should be possible to dissociate the His-bundle potential from the tachycardia, 13 which favor AVNRT compared with NFRT. 14,15 Ho et al reported that the His-refractory VPC is the only maneuver to identify a concealed, bystander NFRT during atypical AVNRT. 12 It can terminate AVNRT in the presence of a concealed...

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