The PVC programmed into the cardiac cycle is relatively late coupled with minimal fusion and yet preexcites the next atrial cycle, so it is clearly AVRT. Earliest atrial activation is still near the CS os as identified on the ABL atrial electrogram, but now the atrial activation in the coronary sinus has shifted (long arrow) from distal to proximal, although the far-field PCS EGM is relatively earlier (short arrow). One may speculate that there is a now a left pathway but the atrial activation at the CS os (ABL catheter) is still very early. Ablation at this site terminated tachycardia and this was no longer inducible. The initial ablation at the CS os region likely resulted in interatrial block over the CS interatrial connection. Although AVRT was still occurring over a posteroseptal accessory pathway, there was a change in atrial activation of the LA resulting in a distal to proximal CS activation in spite of the origin of preexcitation near the CS os. This is infrequently seen with minimal ablation in the CS os region but is an interpretative issue that has consequences for successful ablation.

The first observation is that there is some local activation after each pacing spike (asterisk) so that the spike is capturing the PV. The second is that the underlying rhythm is sinus (CL 890 milliseconds) and is dissociated from the paced activity inside the PV. The potentials in the pulmonary vein are “far field” coming from the left atrial appendage and this characteristically shows the biggest far-field potentials in the anterior part of the circumferential mapping catheter (i.e., 13–14, 11–12, 9–10, 7–8). Thus, “exit block” has been achieved. Entrance block is presumably present since sinus activity does not perturb the activity in the pulmonary vein but this is best assessed by noting activity inside the PV without the confounding effect of pacing within the vein.

There are interesting observations after the atrial extrastimulus (S2). In addition to the local activity right after the spike (asterisk), there is now near-field activity following this (long arrow) that is clearly not present without an extrastimulus (see first complex, short arrow). This is best explained by conduction delay within the pulmonary vein causing a double potential, although other explanations are conceivable. The observation does not impact on decisions for further ablation since there is still exit block and the activity is confined to the vein.

This is a posteroseptal pathway as evidenced by the early ventricular electrogram at the orifice of the coronary sinus. Although preexcitation disappears immediately with the onset of current, suggesting close proximity to the accessory pathway, there is a problem. Note that the P wave, which is upright in leads 1 and 2 during sinus rhythm (p), changes to “low to high” immediately with onset of ablation with a very short PR interval most evident on the surface ecg. This is an accelerated junctional rhythm (JT) and the loss of preexcitation does not reflect accessory pathway ablation. After a few more cycles of JT, the atrial component follows the ventricular component, making the diagnosis of JT even more apparent (asterisk).

Current was discontinued immediately with return of sinus rhythm and preexcitation and the catheter was repositioned. Continuation of current in such a case may result in JT with retrograde conduction over the intact accessory pathway with a false sense that the fast AV nodal pathway is not at risk. Inadvertent AV block in this young individual with WPW would have been very unfortunate and great vigilance is required to diagnose apparent loss of preexcitation related to accelerated junctional rhythm.

The QRS morphology during atrial pacing reflects a left lateral accessory pathway (asterisk). Note also that the earliest ventricular (V) activation on the intracardiac electrograms occurs in the distal coronary sinus (DCS; CS 3–4). Supraventricular tachycardia was induced with an atrial extrastimulus that blocked anterograde over the accessory pathway. However, the atrial activation sequence is septal with earliest atrial activation in the orifice (CS 9–10) of the coronary sinus. The retrograde limb of this tachycardia is clearly not over a left lateral accessory pathway and the tachycardia mechanism was proven to be AV node reentry with a relatively long VA interval. An expedited strategy of just ablating the obvious left lateral accessory pathway would not have prevented tachycardia in this patient, and would have been incorrect to do.

The sinus cycles at the right of the tracing are preexcited with earliest ventricular activation at the CS orifice (CS 9–10) of the available electrodes for review. Preexcitation is more marked during atrial pacing and the atrial extrastimulus blocks in the accessory pathway. Several nonstimulated cycles follow and this sequence was reproducible. The atrial activation is septal with earliest activation at the proximal CS and His electrograms. The possibilities for the repetitive atrial responses are atrial ectopy, AVRT echoes, or AV nodal echoes.

In general, repetitive atrial responses are more closely coupled to the atrial extrastimulus and have an inconsistent relationship to the stimulated QRS.

If we consider atrial activation as retrograde, we are left with possible retrograde conduction over the AV node versus a septal or paraseptal accessory pathway. The retrograde Wenckebach sequence favors AV nodal conduction but the presence of an anterograde septal accessory pathway raises the possibility of an accessory pathway with decremental retrograde conduction. In this case, anterograde conduction over the accessory pathway was not decremental, making the latter less likely. Pacing maneuvers during tachycardia are problematic if sustained tachycardia is not induced.

In this instance, it is useful to determine if baseline retrograde conduction is occurring over the AV node or not. The next figure shows the atrial response to ventricular pacing from two sites, the right ventricle (RV) apex on the left and the RV posterobasal region on the right. Since the accessory pathway is closer to the RV base, the VA time here should be shorter than during pacing of the RV apex if a septal accessory pathway were present. The opposite holds true for AV nodal conduction since the RV apex is closer to the distal right bundle branch (RBB) where the normal AV conduction system activates the ventricles. This rationale is similar to that of the para-Hisian pacing technique. In this case, retrograde conduction is clearly over the AV node.

There is a caveat since the maneuver does not tell us what is happening during tachycardia, which is conceivably different. Repeating this differential pacing at multiple cycle lengths with similar results increases the confidence that the observation is relevant to the observed tachycardia. In this case, conduction over the accessory pathway was unidirectional (anterograde only). It would obviously be a mistake to map during ventricular pacing in this instance to ablate the accessory pathway since retrograde conduction is via the AV node.

One can begin with the tachycardia at the right of the tracing. The first observation is that the halo catheter in the right atrium has electrograms that span virtually the whole cardiac cycle. This is strongly supportive of right atrial macroreentry. The direction of activation is up the septum (starting from 19–20) and down the lateral wall (to 1–2), consistent with “counterclockwise” flutter. There is a relatively long “gap” between poles 11–12 and poles 9–10 of the halo catheter.

Poles 11–12 are paced slightly faster than the tachycardia and pacing is stopped. The tachycardia has been entrained or accelerated to the pacing cycle length with constant fusion. One identifies the last entrained electrograms (i.e., accelerated to 260 milliseconds) and notes the atrial cycle “entrained but not fused” indicated by the asterisk. The postpacing interval at MRA 11–12 is essentially equal to the tachycardia cycle length and this site is thus “in” the circuit.

Isthmus-dependent right atrial macroreentry is in fact the most common mechanism even in presence of atriotomy scar. In this instance, the isthmus was also “in” with entrainment, confirming the mechanism. Ablation here resulted in bidirectional block and failure to induce further tachycardia. The relative delay between electrode pair 11–12 and 9–10 was probably related to conduction delay around or through atriotomy scar.

The local ventricular electrogram on the ablation catheter during PVCs was complex with near-field activity noted 30 milliseconds prior to the onset of the QRS at the distal electrode of the catheter. This was the earliest that was obtainable after careful mapping of the region and injection of contrast showed that it was relatively distant from the orifice of the left coronary artery. Onset of energy (maximum 30 W) resulted in loss of ventricular ectopy within 10 seconds and no PVCs were seen during 1-hour waiting period with and without isoproterenol infusion.

The “optimal” site to ablate is generally relative and practically speaking is the best that can be obtained after careful mapping in the region of interest. In this case, the electrogram characteristics were reasonable but ectopy recurred 2 weeks later. At subsequent ablation, a site a few millimeters away from the initial ablation site resulted in a long-term cure.

The first three atrial activation sequences are the same with the earliest activation on the DCS electrode. The fourth and fifth atrial activation sequence patterns change with earliest activation on the PCS electrode. However, note that there is no change in the H–H interval or in the atrial interval on the PCS electrode. This would be the case if the main AV circuit was over a second more septal pathway with the left lateral pathway providing another circuit simultaneously so that disruption of the left lateral pathway allows seamless continuity of AVRT over the more septal pathway. In other words, the atrial activation sequence over the first three cycles is a fusion of atrial activation over a more septal and left lateral accessory pathway. In this scenario, the more proximal pathway would have to branch off near the ablation site and slant toward the septum so that both branches would be ablated eventually as the lesion expands. Alternatively, block of lateral to medial conduction in the CS musculature with preserved conduction over the adjacent LA could also result in a change to proximal to distal CS activation times initially until the lesion expands to also incorporate the actual accessory pathway to LA muscle connection. If such were the case, one might expect “far-field” left atrial potentials going from distal to proximal to get to the septum via the LA prior to block to the A and such were not seen in the CS.

Tachycardia terminates without conduction to the atrium, and a PVC occurs on the last beat with normal retrograde septal activation sequence. There was no evidence of accessory pathway activation for the rest of the study and the patient has been arrhythmia free during follow-up.

This patient had relatively poor retrograde conduction during the diagnostic part of the study and required small doses of isoproterenol for induction of sustained AVN reentry. Regardless, excellent junctional runs with 1:1 VA conduction during RF energy delivery often occur even in the absence of isoproterenol in these patients. Typically, we start with no more than 15 W of energy and ramp up as needed with careful observation of retrograde conduction. As the energy was increased to 20 W retrograde block occurred.

There are several methods to troubleshoot this situation. The easiest may be to move the catheter to a more posterior position, but the resultant site may not yield any junctional beats at all. We prefer to pace the atrium during energy delivery and observe anterograde AV conduction, as is shown on the second tracing. Junctional beats commonly interrupt the drive train and that is fine as long as the subsequent atrial beats capture the AVN and conduct to the ventricle. Commonly, the atrial paced rate needs to increase during the ablation if more junctional complexes interrupt the drive train, and this maneuver requires the operator to keep a very close vigil on the paced AV or PR interval. Other strategies may be tried. Ablation during isoproterenol to allow better retrograde conduction may work but there is often more catheter movement during isoproterenol. Cryoablation with careful monitoring of AV conduction is also reasonable.

The best way to approach this complex tracing is to state what you know and then what maneuvers are needed to determine the rest. There is clear anterograde preexcitation over a left lateral AP during atrial pacing, and the premature stimulus (S2) causes prolongation of the AH interval with the His moving into the more preexcited QRS complex, characteristic physiology of an AV muscle connection. This is followed by an atrial complex with the initial activation at the PCS electrode, which was situated near the CS ostium. The differential for this beat is an atrial ectopic complex or retrograde activation over the AV node or a septal AP. More information is needed to determine this. The next atrial complex has a different activation pattern and the earliest activation is now on the DCS lead that is near the lateral margin of the mitral ring. This could be a left atrial tachycardia, but its location is consistent with the anterograde AP location, and, more importantly, there is slight wobble or irregularity in the AH intervals with constant VA intervals, confirming AV node involvement in the tachycardia. Another way of looking at this is that the V–V interval change precedes the A–A interval change during this cycle length irregularity and this is not compatible with atrial tachycardia. This is AV reentry and one ablation site will be at the left-sided AP.

What about the septal activation pattern? At another part of the study we were able to get sustained tachycardia with this activation pattern. Note on the next figure that a PVC introduced at the time of anterograde His activation terminates tachycardia without conducting to the atria. This confirms AV reentry with AP involvement in the circuit. This patient also had a concealed posteroseptal AP that required ablation, and this was done after the left-sided AP was ablated.

The key is to preserve the normal conduction system while trying to get a cure. If radio-frequency energy is used, you can start with very low energy levels, for example, 10 W, and go up very slowly with the hope that preexcitation will disappear before you increase the energy to levels that could result in damage to the AV node, typically more than 15 W. Alternatively, AV reentry can be induced and energy delivered during atrial pacing that has captured the circuit, and this will allow observation of the AV conduction during ablation and also prevent catheter movement after conduction over the pathway is gone. Another method is to pace the atrium until preexcitation disappears, if possible, and then introduce energy. The latter two techniques will allow careful observation of AV conduction during ablation, but the effect of the energy on AP conduction can only be determined after the energy delivery is done.