Discussion:
The broad QRS tachycardia had LBBB morphology with retrograde His activation and VH interval of 10ms and morphology similar to Figure 1a – suggesting atriofascicular pathway as antegrade limb. The cycle length of the tachycardia was 310ms (Figure 3). Septal refractory APC advanced the next ventricular electrogram (V EGM) by 20ms, and this advanced the next His activation by 20ms (arrow in Figure 3). The atrial activation after the septal refractory APC is most likely a spontaneous APC. It could not have resulted from activation via a retrograde fast AV nodal pathway since it occurs before the His activation. This APC conducted decrementally down the atriofascicular pathway leading to delay in the next V and His EGM. Until this event, changes in the VV interval predicted changes in the HH interval. The next HA interval was 140ms which was shorter than the tachycardia HA interval of 160ms. This was followed by antegrade His activation with a HH interval of 250ms and a positive HV interval of 45ms. The ventricular activation that resulted after the antegrade His activation had a QRS with morphology as in Figure 1c suggestive of LBBB aberrancy. This was followed by a prolonged HA interval of 190ms and then the antidromic AVRT involving the atriofascicular pathway continued. The possible mechanisms to explain these findings are:
  1. Antidromic tachycardia with antegrade limb being atriofascicular pathway. Due to decremental conduction in the atriofascicular pathway, there was a prolongation of HH interval to 330ms. This HH prolongation facilitated rapid conduction in the retrograde direction through the AV node resulting in a short HA of 140msec. The impulse conducted back to the ventricle through another AV nodal slow pathway. Since the atriofascicular pathway was refractory this AV nodal slow pathway activated the His antegradely. The atrium was subsequently activated retrogradely through another slow AV nodal pathway with a prolonged HA interval of 190ms. The antidromic AVRT involving the atriofascicular pathway subsequently got reinitiated.
  2. Dual tachycardia – antidromic tachycardia involving atriofascicular pathway switching transiently to bundle branch reentrant ventricular tachycardia (BBRVT). However, this will still require the presence of dual AV node physiology to explain the antegrade His activation that occurred prior to resumption of the antidromic tachycardia. BBRVT with His dissociation has been described and presence of atriofascicular pathway makes deciphering the mechanism more complex.2
  3. Antidromic tachycardia involving atriofascicular pathway and bystander septal accessory pathway with decremental property which took the impulse retrogradely up for the beats where HA interval was 140ms and 190ms. However, there was no evidence of retrograde accessory pathway conduction by parahisian pacing and VA block was demonstrated with intravenous adenosine.
During the EP study, the tachycardia had two differing cycle lengths with AV, VH interval being constant and change in HA interval causing change in tachycardia cycle length. HA interval changed from 160ms to 210ms suggestive of dual AV nodal physiology. The atriofascicular pathway potential was mapped to lateral tricuspid annulus at 8 o clock position and was ablated with radiofrequency energy. Postablation of atriofascicular pathway, there was dual AV nodal physiology with AH jump. However, there was no tachycardia inducible even on isoprenaline and with aggressive atrial and ventricular pacing protocols. Hence, slow pathway modification with radiofrequency energy was not done.
In conclusion, a patient with an atriofascicular pathway and multiple AV nodal pathways can have a pseudo AVVA response due to intermittent shift from antidromic AVRT involving the atriofascicular pathway to pathways in the node.
Acknowledgements : None