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!