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.

Background Acute pulmonary vein reconnection via epicardial fibers can be found during observation period after PV isolation, the characteristics and related factors have not been fully studied. Objective To investigate the prevalence, locations, electrogram characteristics and ablation parameters related to acute epicardial pulmonary vein reconnection (AEPVR). Methods Acute PVR was monitored during observation period after PV isolation, from which AEPVRs were mapped and distinguished from endocardial conduction gaps. The clinical, electrophysiological characteristics and lesion set parameters were compared between patients with and without PVR. So were they compared among AEPVR, gap-related reconnection, and epicardial PVR in repeat procedures. Results 56.1% acute PVR were AEPVR, which required a longer waiting period ( P<0.001) than endocardial gap. The majority of AEPVR were connections from the posterior PV antrum to the left atrial posterior wall, followed by late manifestation of intercaval bundle conduction from the right anterior carina to right atrium. AEPVR was similar to epicardial PVR in redo procedures in distribution and electrogram characteristics. Smaller atrium ( P<0.001), lower impedance drop ( P=0.039) and ablation index ( P=0.028) on the posterior wall were independently associated with presence of AEPVR, while lower inter-lesion distance ( P=0.043) was the only predictor for AEPVR in acute PVR. An integrated model containing multiple lesion set parameters had the highest predictive ability for AEPVR in ROC analysis. Conclusions Epicardial reconduction accounted for the majority of acute PVR. AEPVR was associated with anatomic characteristics and multiple ablation-related parameters, which could be explained by nondurable transmural lesion or late manifestation of non-preferential conduction.

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.