Commentary
The intracardiac electrograms (EGMs) during delivery of radiofrequency
energy reveal initially a RBBB-like morphology in lead V1, suggesting
ventricular pacing from the left ventricle. The QRS duration is 130 ms,
which is unusually short for left ventricular lateral wall pacing. Fused
ventricular and atrial EGMs can be appreciated in the bipolar signal
from the tip of the ablation catheter (RFD, Figure 3 left
panel ). Retrograde AP conduction is seen until the fifth QRS complex,
followed by ventriculo-atrial (VA) block; later there is variable VA
conduction via the AV node. Immediately after the VA block, there is an
abrupt vivid change in the QRS morphology with an increase in the QRS
width to 187ms.
In trying to understand the rationale behind the change in QRS
morphology, it is important to consider yet another important
observation in the intracardiac electrograms. The clue lies in the EGMs
on the His channel (HISD, Figure 3 left panel ). Clear sharp His
signals (H) are seen to precede the ventricular EGMs during LV pacing
until the retrograde VA block and change in QRS morphology. This
suggests antegrade activation of the His bundle, which can happen only
if LV pacing was being performed concomitant with the orthodromic
atrioventricular reentrant tachycardia. The relatively narrow QRS
complex is the result of fusion of ventricular activation from LV pacing
and the tachycardia wavefronts. This is further suggested by the short
HV interval of 20 ms (Figure 3 right panel) . This was actually
the case here, as the LV was being overdrive paced at 30 ms shorter than
the tachycardia cycle length, so as to maintain stability of the
ablation catheter during ablation, in case of termination of
tachycardia.
For a fusion to perpetuate between the orthodromic AVRT and ventricular
pacing, the following conditions are necessary: pacing close to the
insertion of the AP, pacing just shorter than the TCL, rapid AP
conduction, brisk antegrade AV nodal conduction and sluggish retrograde
AV nodal conduction. Basal pacing site near the pathway insertion leads
to more ventricular muscle activation by the orthodromic tachycardia
wavefront (1). Fusion can be identified by the presence of an
orthodromically captured His or right bundle potential.
In conclusion, a relatively narrow QRS during LV lateral wall pacing
along with evidence of antegrade activation of His bundle suggests
fusion between ventricular pacing and the ongoing orthodromic
tachycardia; here one would expect the QRS to change in morphology as
soon as the tachycardia terminates during the energy delivery. While one
concentrates on the atrial activation while ablating concealed accessory
pathways during ventricular pacing, the QRS complex can display valuable
evidence too!