The initial four QRS complexes have an atypical right bundle branch block morphology suggesting either ventricular tachycardia (VT) or a preexcited tachycardia. There is 1:1 AV relationship with the earliest atrial electrogram in the septum. In such a situation, the differential diagnosis includes VT with 1:1 VA conduction, atrial tachycardia or AV node reentry with anterograde conduction over an accessory pathway (AP), and antidromic tachycardia with anterograde conduction over an AP and retrograde conduction over either a second septal AP or the normal VA conduction system.

An atrial stimulus (S2) introduced during tachycardia at the MCS electrode site terminates tachycardia without conduction to the ventricle. This eliminates VT as a diagnosis. Termination with a relatively late-coupled PAC also favors a macroreentrant tachycardia with close access of the PAC to the excitable gap, that is, antidromic reentry in this case. Additional pacing maneuvers during the study proved the mechanism to be antidromic tachycardia with retrograde conduction over the normal VA conduction system.

The last two QRS complexes show no evidence of anterograde AP conduction. In fact, there is not even local evidence of preexcitation on the coronary sinus leads as demonstrated by a long conduction time between the local A and V (arrow). In a patient with antidromic reciprocating tachycardia (ART) there is typically some evidence of anterograde AP activation during sinus rhythm. This was a very unusual AP that only became manifest with multiple premature atrial extrastimuli that resulted in block over the AV node and a very long conduction time over the AP.

The tachycardia exhibits an atypical left bundle branch block morphology that is less likely aberrancy and more consistent with either VT or preexcited tachycardia. If it is a preexcited tachycardia, it is conducting anterogradely over a right free wall AP. There appears to be a negative P wave before each QRS complex in ECG leads II, III, and aVF. If this is VT, 1:1 retrograde conduction is most likely over a slow AV nodal pathway. A preexcited tachycardia could be atrial tachycardia or AV node reentry with bystander conduction over the AP or ART.

The next figure demonstrates termination of tachycardia. Note the increase in the atrial cycle length from 536 to 624 milliseconds is followed by a similar increase in the ventricular cycle length, or, said another way, the change in A–A interval drives the change in V–V interval. This eliminates VT as the diagnosis. Initial atrial activation is in the septum, or concentric, which does not allow differentiation of septal atrial tachycardia, AV node reentry, and ART. Further maneuvers during the study confirmed the diagnosis of ART with anterograde conduction over a right free wall AP, and retrograde conduction over a slow AV node pathway. The latter was the cause of the long RP interval during tachycardia.

The atypical left bundle branch block pattern during tachycardia is consistent with either preexcitation or VT. The first two QRS complexes demonstrate retrograde VA conduction with a concentric atrial activation sequence. The third QRS complex has VA block and sinus rhythm persists for the rest of the tracing as noted by the change in atrial activation sequence. Regardless, the tachycardia persists for a few more beats with slowing from 508 to 548 milliseconds prior to termination. After termination there is a nonconducted sinus complex followed by conduction over the normal AV conduction system. Continuation of tachycardia with VA dissociation eliminates an AP-mediated tachycardia and this is clearly VT.

Why did VT terminate with adenosine? Some varieties of VT are sensitive to adenosine, especially those originating in the right and left ventricular outflow tracts. This patient obviously does not have an outflow tract VT. Some epicardial VTs and those around the epicardial veins can also terminate with adenosine. Initial mapping demonstrated early electrograms during VT near the posteroseptal area and the middle coronary vein. The exact site was never determined because the patient refused ablation.

A typical right bundle branch block is present during tachycardia. The tachycardia is regular and no clear P waves are identified. In essence, this could be any tachycardia that activates the ventricles with conduction over the left bundle branch. P waves are typically seen during atrial tachycardia, making this diagnosis much less likely. While a P wave is often discernible in the early ST segment in patients with AV reentry, this is not always the case, especially in the presence of a bundle branch block. Typical AV node reentry is the most likely diagnosis but junctional tachycardia is also a possibility. A fascicular VT originating in the proximal left bundle branch cannot be excluded but is highly unlikely.

The next figure demonstrates a short VA interval and a normal HV interval during tachycardia, which excludes AV reentry and VT. The diagnosis of AV node reentry was confirmed with pacing maneuvers and the patient underwent successful ablation.

Atrial fibrillation occurred during catheter manipulation at the start of the study. The high right atrial (HRA) tracing demonstrates a more organized pattern that is not infrequently seen in the right atrium during atrial fibrillation. The three QRS complexes on the left have a typical right bundle branch block morphology strongly favoring aberrancy. Ventricular activation during these cycles occurs near the onset of QRS at the HBE site (i.e., near the base of the heart), also consistent with aberrancy. After a pause, the three QRS complexes on the right have atypical left bundle branch block morphology consistent with VT or preexcitation.

The second figure highlights the normal HV interval in the first three complexes confirming aberrancy. However, the His is not visible in the last three beats and the mechanism remains unknown.

Tachycardia spontaneously terminated and the rest of the electrophysiology study was performed. The third figure shows atrial pacing (S1). The first three complexes conduct with the same morphology as noted on the right-hand portion of the initial figure and the His is not visible. This eliminates VT and establishes that conduction is over a left free wall AP. Note also in this figure that the fourth paced atrial complex blocks over the AP and conducts over the normal system with a normal HV interval. AV reentry was induced later in the study.

This complex tracing is best dealt with by breaking it up into components starting with a part that is manageable and that can form the basis for framing the problem.

The right part of the tracing shows a wide QRS tachycardia with a 1:1 AV relationship with a septal pattern of atrial activation. A rapid His deflection is evident right at the onset of the V electrogram at the HBE site. With this HV relationship, the tachycardia can only be VT or preexcited tachycardia. The RV apical EGM is very near the onset of the QRS, suggesting conduction over an atriofascicular AP. Note that the His recorded near the onset of the QRS in such a scenario is a retrograde His resulting from ventricular insertion of a decremental AP (i.e., the atriofascicular) into or near the RBB terminus. If we discount VT with the knowledge that atrial pacing reproduces this QRS morphology with a long AV interval, we can make conclusions about the mechanism of this preexcited tachycardia.

We then analyze the onset of tachycardia. The S2 captures the V and conducts to the A, the latter having a septal activation pattern identical to the tachycardia. The first QRS of tachycardia onsets 430 milliseconds after the A measured at the His site.

In essence, we can use the VES starting tachycardia in a fashion analogous to using ventricular entrainment from the RV apical region.

The first V of tachycardia at the pacing site is seen 602 milliseconds after the extrastimulus. We subtract 100 milliseconds from this to correct for the AV delay after the extrastimulus and we get a “corrected postpacing interval (PPI)” of 54 milliseconds (602 minus 448 minus 100). Thus, the “PPI” is “in.” Similarly, the St-A of 250 milliseconds minus the V-A of 180 of 70 milliseconds also supports the RV apical pacing site being “in” the circuit and supporting the diagnosis of antidromic reentry with anterograde conduction over an atriofascicular AP and returning via the normal AV conduction system. The results of “conventional” entrainment from the RV apex were identical to this. Note that we have not ruled out the very unlikely possibility of retrograde conduction over another septal AP.

The tracing shows a wide QRS tachycardia with a 1:1 AV relationship. The atrial activation is central with early activation at the His bundle electrogram. The QRS morphology is quite atypical for a bundle branch block pattern and there is no His deflection visible at the His channel where one was clearly visible in sinus rhythm. This leaves us with only two tenable diagnoses, namely, VT and preexcited tachycardia. A PAC is programmed into the cardiac cycle at the distal coronary sinus (S).

The relatively late-coupled PAC introduced at a time when the septal atrial electrogram has been already activated resets the tachycardia without a change in the QRS morphology, that is, advances the next QRS (345–320 milliseconds). This means that the PAC has excellent access to the circuit and makes a diagnosis of VT untenable. The A following the advanced QRS is also advanced and the VA relationship remains essentially the same. Since the preceding septal activation was not altered, advancement of this site cannot be caused by an atrial tachycardia. That is, the PAC results in fusion with “reset” of the subsequent A. In fact, the “PPI” at the distal CS pacing site is only a few milliseconds greater than the tachycardia cycle length (370 milliseconds vs. 350 milliseconds). That is, the distal CS region is “in” the circuit. This eliminates atrial tachycardia as the mechanism. Since the late PAC becomes essentially a late PVC, the fact that the last PVC preexcites the next atrial complex eliminates AVN reentry. Hence, we have a macroreentrant atrioventricular tachycardia with a left lateral AP as the anterograde limb and a retrograde limb that is either the normal VA conduction system (i.e., true antidromic atrioventricular reentry) or a second AP. This in fact was the former, a much more common tachycardia mechanism than the latter.

How would one prove that the retrograde limb is the normal AV conduction system? One might entrain from both the RV base and the RV apex and show that the RV apex is closer to the circuit (i.e., shorter PPI). This is because the RV base is closer to a potential posteroseptal accessory if that were part of the circuit. Alternately, one might just ablate the obvious AP first, which would make it much easier to discern the presence or absence of a septal AP. In fact, in our experience it is relatively rare for the retrograde limb to be a second AP.

If one assumes that this phenomenon is reproducible, one has an important clue to successful ablation. The VES has terminated the VT without apparent conduction to the ventricle as evidenced by absence of ventricular activation seen on the surface ECG. Since the electrical influence of the stimulating electrode at this site in the absence of generalized myocardial capture is very regional and local, it is probable that the electrode is well positioned near a critical component of a reentrant circuit and ablation is appropriate even in the absence of a visible electrogram suggesting that it is a good site.

A checklist of observations is useful to evaluate the effects of overdrive pacing and potential entrainment.

1. 
   

   The cycle length of the tachycardia has shortened from 420 milliseconds to the pacing cycle length of 390 milliseconds and is in a “steady state” when pacing is stopped.

   
   
2. 
   

   The QRS of the paced complex is identical to the QRS of the tachycardia. Although only 3 leads are shown here, this was verified for all 12 leads. This is termed “concealed” fusion because fusion is not apparent electrocardiographically and suggests that the pacing site is within the slow conduction zone of the circuit. (In this example, it may be “overtly” fused if one counts the RV apical electrogram slightly ahead of the pacing spike but this is a semantic issue.)

   
   
3. 
   

   The last cycle accelerated to the paced rate needs to be identified, that is, the last entrained QRS. This is identified in the figure by an asterisk before the following cycle ensues at the VT cycle length.

   
   
4. 
   

   Since the pacing ultimately drives the last entrained cycle, it is seen that the interval from the last stimulus to the QRS onset is relatively long (295 milliseconds), approximating the time required to get from the stimulus to the breakout point from the delayed conduction zone of the circuit. This is also reflected in the interval from the electrogram to the onset of the QRS (280 milliseconds), which is approximately the same. In general, the longer this interval, the more proximal in the delayed conduction zone it is hypothesized to be. In this case, it might be nearer the “entrance” than the “exit” of the slow zone of conduction. (The importance of step 3 now becomes obvious, that is, to identify which cycle is driven by the stimulus.)

   
   
5. 
   

   Finally, the PPI needs to be measured. The electrogram during pacing is quite noisy and the PPI here is approximated from the stimulus artifact to the return electrogram. It is approximately the cycle length of the tachycardia and is therefore “in” the circuit. It is a reasonable ablation site, although it may not for many reasons be the sole lesion required to “cure” the tachycardia.

The tachycardia on the right has a wide QRS with a 1:1 A and V relationship. The QRS morphology is atypical for a bundle branch block pattern. There is no obviously visible His deflection. The atrial activation sequence is “central.”

This tachycardia can only be preexcited SVT or VT. Overdrive pacing from the distal coronary sinus atrial electrogram results in entrainment of the tachycardia with identical QRS morphology ruling out VT.

The question is now to determine the mechanism of the preexcited tachycardia, namely, AT, AVNRT with bystander AP, or AVRT (antidromic). Statistically, antidromic tachycardia would be the leading candidate by prevalence alone.

One notes that the PPI at the distal CS is virtually identical to the tachycardia cycle length, that is, it is “in.” This clearly rules out AVNRT with a bystander, as the PPI would be considerably longer. The only viable possibilities for this tachycardia now remain atrial tachycardia fortuitously at the pacing site in the presence of an AP at that site or antidromic reentry over an AP at that site. Clearly the former would constitute a very rare happening indeed but the maintenance of a constant VA relation in the cycle immediately after entrainment essentially rules out AT.

We now have preexcited AVRT with a left lateral AP as the anterograde limb of the circuit. The retrograde limb is in all likelihood the normal AV conducting system. How might one prove that? That is, from where might one entrain?

This figure demonstrates tachycardia with a CS lead in place, which was omitted in Fig. 5–11A. Note that there is eccentric atrial activation with earliest atrial activation at the distal CS electrode. The HV interval is normal. Thus, this is either a left atrial tachycardia or AV reentry utilizing a left-sided AP (Table 1–7). Analysis of Fig. 5–11A demonstrates preexcitation of the atrium with a PVC introduced at a time when the His bundle is refractory. Thus, a left-sided AP is present and in this patient was involved in the tachycardia circuit. This observation alone does not absolutely exclude a coexisting atrial tachycardia.

The preexcitation index (PI) is a helpful adjunct to locate the site of the AP. It is determined by introducing progressively more premature right ventricular extrastimuli during tachycardia. The PI is calculated by subtracting the longest premature interval (V₁V₂) that preexcites the atrium from the tachycardia cycle length (V₁V₁). During a narrow QRS complex tachycardia, a relatively late-coupled V₁V₂ that preexcites the atrium (short PI) is typical for a right-sided or septal AP, and a PI <45 milliseconds essentially excludes a left-sided AP. The PI of slow/fast AV node reentry is almost always >90 milliseconds.

In Fig. 5–11A, the PI is 24 milliseconds (332–308 milliseconds). Note that this patient has LBBB aberrancy. In this situation the ventricle is activated anterogradely over the right bundle branch, which exits near the moderator band in the right ventricular apex. The PVC has a morphology consistent with right ventricular apical pacing. Thus, the right ventricular catheter is near the tachycardia circuit, which now incorporates the right ventricular endocardium. During narrow QRS complex tachycardias, the premature ventricular complex conducts transseptally to enter the tachycardia circuit in a patient with a left-sided AP, and the PI is much longer.

In summary, a diagnosis of AV reentry was reasonable from Fig. 5–11A, but the location of the AP could not be determined from just this figure.

Figure 5–12A is a RBBB tachycardia without evidence of VA dissociation. The differential diagnosis is VT, SVT with aberrancy, and a preexcited tachycardia (Table 1–4). The RBBB is “atypical,” and less likely to represent aberrancy. The presumptive diagnosis should be VT until proven otherwise. After tachycardia was terminated a simultaneous 12-lead ECG rhythm strip was obtained (Fig. 5–12B). Note that this patient has intermittent wide QRS complexes during sinus rhythm, but more than one wide QRS morphology is present. Complexes 2 and 6 are nearly identical to the QRS complexes noted in Fig. 5–12A. This strongly suggests that a preexcited tachycardia was present in Fig. 5–12A since the PR intervals of the wide complexes are constant. An alternative diagnosis that must be excluded is coupled PVCs giving the illusion of a constant PR interval. The presence of an AP can be confirmed at EP study. The preexcited QRS morphology suggests a left posterior AP location. In contrast, QRS complexes 4, 8, and 10 demonstrate a different wide QRS morphology, and the PR intervals are constant. This likely represents a second preexcited QRS morphology, and the 12-lead ECG is consistent with a posteroseptal AP position. In patients with more than one AP, a common combination is posteroseptal and left free wall. VT is always part of the differential diagnosis.