An Isoproterenol Dependent Broad QRS Tachycardia: What is the Mechanism?Weizhuo Liu MD1, Nanqing Xiong MD2*, Wentao Gu MD21. Department of Critical Care Medicine, Shanghai Chest Hospital, Shanghai Jiaotong University, 241 West Huaihai Road, Shanghai 200030, China2. Department of Cardiology, Huashan Hospital Fudan University, 12 Wulumuqizhong Road, Shanghai 200040, China*Corresponding author: Nanqing Xiong MD, Department of Cardiology, Huashan Hospital Fudan University, 12 Wulumuqizhong Road, Shanghai 200040, China. E-mail: [email protected] words: wide QRS complex tachycardia, intermittent preexcitation, Wolff-Parkinson-White syndrome, antidromic AV reentrant tachycardia, AV-nodal-refractory atrial extrastimulusThis research did not receive any specific grant from funding agencies in the public, commercial, or not-for-profit sectors.A 27-year-old female presenting with recurrent palpitation during exercise was referred for electrophysiology study. Electrocardiogram (ECG) during symptom was not documented. Her baseline ECG was sinus rhythm with normal PR interval. Ventricular pacing and programmed extrastimulus showed retrograde conduction via AV node. A-H interval was progressively prolonged during atrial extrastimuli without preexcitation (Figure 1). No tachycardia was inducible until isoproterenol infusion, after which a wide QRS tachycardia was initiated by ventricular burst pacing. Figure 2 showed 2 intracardiac recordings during tachycardia. What can be learned from the tracings?Figure 2A showed a wide QRS complex tachycardia with left bundle branch block morphology, left-inferior frontal axis and 1:1 VA relationship, the cycle length of which was about 365ms. There was no His electrogram preceding each QRS, instead, a putative retrograde His could be observed after local ventricular electrogram on His catheter with an H-A interval around 100ms. Differential diagnosis included ventricular tachycardia (VT) from right ventricular outflow tract and different types of preexcited tachycardia. A sensed atrial extrastimulus was delivered when AV node was refractory, indicated by the unchanged timing of atrial signal on His catheter, which advanced the next QRS with identical morphology to tachycardia. This phenomenon suggested the presence of an anterograde conducting accessory pathway. Measurement of A-A interval indicated the tachycardia was reset, providing the evidence that the AP was participating in the reentry [1]. VT can be ruled out by the unchanged QRS morphology during sensed atrial extrastimulus and entrainment from atrium, while preexcited AV nodal reentry and nodoventricular tachycardia was precluded by the resetting of tachycardia with AV-nodal-refractory atrial extrastimulus. The fact that atrial extrastimulus with earlier prematurity terminated the tachycardia without conduction to the ventricle (Supplemental Figure) also argued against AVNRT with innocent bypass tract, which in this setting would require the timing of the extrastimulus to exactly encounter the refractory period of the pathway when terminating AV nodal reentry. Furthermore, the tachycardia could also terminate spontaneously with an atrial signal, making preexcited atrial tachycardia highly unlikely (Figure 2B). Therefore, the diagnosis of antidromic atrioventricular reentrant tachycardia (AVRT) was made based on all the evidence above.But how could the patient have antidromic AVRT whose preexcitation was absent at baseline, during atrial extrastimuli, and pacing from both atria (not shown)? If we look into the sinus QRS configuration after tachycardia cessation in Figure 2B, prominent delta waves could be observed, which emerged only during isoproterenol infusion in this case. In Wolff-Parkinson-White syndrome, intermittent anterograde pathway conduction dependent on isoproterenol, although not common, has been reported [2]. The pathway conduction was unsustainable when isoproterenol was discontinued, proving the unidirectional conducting accessory pathway was highly isoproterenol-sensitive, which served as the anterograde limb of the antidromic AVRT. On the other hand, isoproterenol also facilitated the retrograde conduction of AV node, which played the role of the retrograde limb. The pathway was then ablated near 12 o’clock site of tricuspid annulus, after which no delta wave was present with isoproterenol infusion, and the tachycardia was therefore not inducible.

Responses to Ventricular Overdrive Pacing during Wide QRS Tachycardia: What is the Mechanism?Wentao Gu MD1, Xinping Luo MD1, Jian Li MD1, Jinjin Zhang MD1, Nanqing Xiong MD1*1. Department of Cardiology, Huashan Hospital Fudan University, 12 Wulumuqizhong Road, Jing’an District, Shanghai 200040, China*Corresponding author: Nanqing Xiong MD, Department of Cardiology, Huashan Hospital Fudan University, 12 Wulumuqizhong Road, Jing’an District, Shanghai 200040, China. E-mail: [email protected] words: wide QRS complex tachycardia, ventricular overdrive pacing, supraventricular tachycardia, AV reentrant tachycardia, orthodromic His activationFunding: (None)A 35-year-old female presenting with recurrent palpitation was referred for electrophysiology study. Short episodes of narrow QRS tachycardia could be recorded on ECG (Figure 1). During electrophysiology study, the tachycardia could be readily induced with atrial pacing or programmed atrial extrastimuli, but usually terminated in seconds, making it difficult to perform diagnostic maneuvers. When it spontaneously changed to a wide QRS tachycardia, a burst of ventricular overdrive pacing (VOD) was delivered which turned it back to the narrow complex one (Figure 2). What can be learned from the response?The first 4 beats in this tracing showed wide complex tachycardia (WCT) with right bundle branch block (RBBB) morphology and 1:1 ventriculo-atrial ratio. Candidates for diagnosis could be ventricular tachycardia, supraventricular tachycardia (SVT) with RBBB, bundle branch reentrant tachycardia and preexcited tachycardia. An H-V interval of 53ms approximating that during sinus rhythm excluded ventricular tachycardia from myocardium and preexcited tachycardia. The last 4 beats were clinical narrow complex tachycardia with the same cycle length, H-V interval and atrial activation sequence (earliest A at CS7-8) as the WCT, highly indicating that the WCT was SVT with functional RBBB caused by continuous concealed activation from left bundle branch before VOD peeled back the refractoriness of the right bundle branch in the following beats. In addition, A right-sided accessory pathway (AP) was unlikely given the same H-A interval (127ms, measured to CS7-8) with and without RBBB [1].The middle 4 beats demonstrated progressive change in QRS, from fusion to probable fully-paced morphology during VOD. The 3rdbeat advanced the subsequent A without atrial activation change, indicating the presence of a septal AP. However, post-pacing interval (PPI) was 125ms over tachycardia cycle length (TCL) with V-A-H-V response, which argued against AV reentrant tachycardia (AVRT) utilizing a septal AP. Note that His signal was found after the 3rd and the 4th stimulating artifact. Considering the extremely short interval between the 3rd artifact and the subsequent His (17ms), it could hardly be a retrograde His, but was activated in an orthodromic direction instead. A progressively increased A-H interval after the 2nd, 3rd and 4thpacing suggested decremental conduction in AV node before orthodromic His capture. When atrium was entrained, anterograde conduction to the His bundle during VOD supported the diagnosis of AVRT and excluded AV nodal reentry [2]. The long PPI was associated with the delay of the first return His-V following VOD-induced decremental AV nodal conduction. The corrected PPI-TCL was 78ms after subtracting the difference between the first return A-H and tachycardia A-H from PPI [3]. The AP was successfully ablated at left posterior septum, which rendered the tachycardia non-inducible.

Background Aberrant conduction during orthodromic reciprocating tachycardia (ORT) can prolong the ventriculo-atrial conduction time, which is found essential for the reentry in certain situations. Materials and Methods We searched for ORT cases relying on aberrancy from 220 cases in our center. Results 3 patients showed the phenomenon of aberrancy-dependent ORT. All accessory pathways were located at anterolateral regions of atrioventricular annulus. None of them had baseline bundle branch block. Creating functional bundle branch block was necessary to induce the tachycardias. In 2 cases, termination directly associated with resolution of aberration was observed. While in the other case, reentry required both interventricular block and slow pathway conduction. Conclusions We conclude that extra transseptal time caused by aberrancy can be an integral part of ORT, which can explain the infrequent or late onset and unsustainable episodes of ORT in certain patients and is useful in understanding the circuit and localizing the pathway.

A 27-year-old female presenting palpitation without ECG documentation underwent electrophysiology study. EP study revealed atrioventricular accessory pathway with poor and unidirectional pathway conduction, and a fasciculoventricular pathway. During isoproterenol infusion, delta wave promptly became prominent, after which an antidromic AV reentrant tachycardia was induced. When the pathway was mapped, widely split double pathway potentials were observed at 12 o'clock site of tricuspid annulus during mild preexcitation, demonstrating an example of intra-pathway conduction delay, which can be reversed by isoproterenol. Ablation at the site caused accelerated pathway rhythm and eliminated the pathway, rendering the tachycardia non-inducible.