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:
- 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.
- 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
- 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