Tachycardia 1 had the earliest atrial activation in proximal CS and the
AH interval was longer than the HA interval. Attempt to entrain from the
RV apex, dissociated the ventricle without tachycardia termination.
However, after cessation of ventricular over-drive pacing (VOP) despite
changes in AH and HA intervals, the atrial activation pattern remained
the same with the earliest atrial EGM in the proximal CS - as shown in
tachycardia 2. The presence of AV dissociation ruled out orthodromic
Atrio- Ventricular Reentrant tachycardia (o-AVRT) leaving us with two
alternative diagnoses - (1) atrial tachycardia (AT) with origin near the
proximal CS with conduction via slow AV nodal pathway in tachycardia 1
and via fast AV nodal pathway in tachycardia 2, or (2) both the
tachycardias being various forms of atrioventricular nodal reentrant
tachycardia (AVNRT).1 Probably tachycardia 1 was a
slow/slow form and tachycardia 2 was a fast/slow form of AVNRT.
Differential atrial overdrive pacing showed “VA linking”, suggesting
tachycardia 1 was AVNRT.2 This manoeuvre could not be
done during tachycardia 2 due to repeated termination. However,
tachycardia 2 had identical atrial activation
to tachycardia 1 and was reproducibly induced with ventricular pacing,
making atrial tachycardia very unlikely. This implied that both the
tachycardias were likely different forms of atypical AVNRT.
In situations where a narrow complex tachycardia cannot be entrained by
VOP, besides demonstrating VA linking by differential site atrial
pacing, RA + RV pacing proposed by Saba et.al can be useful to
differentiate between AT and AVNRT.3 If the first
event after cessation of RA + RV pacing during narrow complex
tachycardia is a His electrogram it suggests AVNRT, while if atrial it
suggests AT. Although their study did not include atypical AVNRT,
“given the proximity of the His bundle to the tachycardia circuit they
suspected that the response to RA + RV pacing would be similar to that
of typical AVNRT.”3 Like the Roman God Janus who
looks simultaneously in opposite directions we were faced with
discordant responses to this manoeuvre.
The first event after RA+RV pacing in tachycardia 2 was always atrial
(Figure 2a). On most occasions during tachycardia 1, the first event
after RA+RV pacing was also an atrial electrogram (Figure 2b).
Interestingly, on cessation of pacing tachycardia 1 changed to
tachycardia 2 multiple times. Considering the evidence discussed above,
both tachycardias were likely to be different forms of AVNRT and in both
instances, with RA + RV pacing the His bundle was activated retrogradely
(AH during pacing was shorter than tachycardia, and the His morphology
was different). In tachycardia 2 (a fast-slow form of AVNRT with a
probable lower common pathway), during RA+RV pacing the likely site of a
collision between the two opposing wavefronts was in the lower common
pathway thereby leaving the tachycardia unaffected (Figure 3a).
Consequently, when the pacing was stopped, the tachycardia resumed, and
the first event was an atrial electrogram. In tachycardia 1 (a slow-slow
form of AVNRT), ventricular pacing likely reached the tachycardia
circuit and collision was probably above the lower turn-around point
(Figure 3b). On continued pacing, the antegrade conduction likely
changed from the slow pathway to the fast pathway due to retrograde
concealed conduction from the previous ventricular paced beat into the
slow pathway. This resulted in the transition of tachycardia 1 to
tachycardia 2 and explains the first event after pacing being the atrial
electrogram. (Figure 3b).
In our case, only on one occasion during tachycardia 1, the first event
after RA+RV pacing was a His electrogram (Figure 2c). However, on
careful analysis, it was observed that the His was activated
anterogradely during RA + RV pacing (similar AH interval and same His
morphology during tachycardia and pacing). Further evidence in favour of
antegrade His activation was the presence of His electrogram coinciding
with pacing spike artefact on His channel and ventricular fusion in
surface leads when compared to fully paced QRS complex in Figure 2b. The
2 paced wavefronts collided in the ventricle effectively leaving only
the atrial pacing wavefront to interact with the tachycardia circuit.
So, technically, this was only atrial pacing and not RA + RV pacing
(Figure 3c). The His response should be interpreted with caution as just
atrial pacing can result in a similar response in both AT and AVNRT.
Radiofrequency energy was delivered at the site of the right inferior
extension of the AV node below the level of the roof of the CS ostium.
There was accelerated junctional ectopy during the delivery of RF
energy. However, both the tachycardias were inducible after this. Then,
the earliest atrial activation was mapped to the roof of the proximal CS
during tachycardia 2, and ablation was performed at this location during
sinus rhythm. Post ablation there was no tachycardia inducible.
Even though the presence of a lower common pathway is refuted by many
electrophysiologists, we postulated the model employing a lower common
pathway for easy understanding. It may be a lower common pathway or
“longer refractory period below the circuit” as suggested by D.G.
Katritsis and
M.E. Josephson.1This case highlights that the first intracardiac electrical signal that
follows RA+ RV pacing for an atypical fast-slow form of AVNRT can be
atrial. Hence, this manoeuvre is unlikely to help distinguish atypical
forms of AVNRT from AT. Attention should also be paid to the activation
of the His bundle to make correct interpretations.