This is a relatively slow supraventricular tachycardia with a His electrogram preceding each QRS complex (HBED lead). The cycle length of tachycardia varied slightly from 726 to 735 milliseconds. The differential diagnosis includes an automatic junctional rhythm, slow–fast AV node reentry, or an atrial tachycardia with anterograde conduction over a slow pathway. The very short VA interval excludes AV reentry. A premature atrial complex is introduced at a time when the His bundle electrogram has already been activated and results in a shortening of the subsequent H–H interval to 657 milliseconds. There should be no change in the subsequent H–H interval if the mechanism is an automatic junctional rhythm because the junction would have already discharged and therefore the premature atrial complex could not have affected the subsequent cycle length. The shortening of the H–H interval is consistent with slow–fast AV node reentry in which the premature atrial complex engages a slow pathway earlier than anticipated and affects the next H–H interval. It could have also prolonged the next H–H interval and that would have still supported this diagnosis. Can one totally rule out an atrial tachycardia with conduction over a slow pathway? Note that the His to high rate interval remains constant even though the H–H interval changes, a finding consistent with AV node reentry but not atrial tachycardia. Indeed, this patient had relatively slow AV node reentry that was successfully ablated at a site around the coronary sinus ostium.

A single atrial premature stimulus is introduced at 340 milliseconds during an atrial paced cycle length of 500 milliseconds. The premature complex conducts over the AV node and induces a short VA interval tachycardia that is most consistent with AV node reentry. This mode of induction is referred to as a two-for-one response and seems to break the laws of initiation for a reentrant circuit. In other words, a single premature complex is conducted over both the fast and slow AV nodal pathways to initiate tachycardia.

Classical teaching of reentry proposes three requisites to form the circuit: two pathways of conduction, initial block in one pathway, and slowing of conduction in the second pathway to allow reexcitation of the initial blocked pathway and subsequent reentry. In this example, there is no block in either pathway since the premature atrial complex conducts anterogradely over both. This “breaking of the rules” is best explained by the inability of the initial fast pathway conduction to conceal retrogradely into the slow pathway, which thereby allows the slow pathway to conduct in an anterograde manner and start tachycardia. In all cases we have studied like this, slow–fast AV node reentry can always be induced during premature ventricular stimulation or incremental ventricular pacing, consistent with essentially minimal to no retrograde conduction into the slow pathway. This is shown with a premature ventricular complex initiating the same tachycardia in this patient at another point in this study. The successful ablation site was just anterior to the coronary sinus ostium and not substantively different from the usual site one selects for patients with AV node reentry.

As discussed in Chapter 1, it is always important to look for “wobble” or changes in intervals during tachycardia and these usually occur at the initiation or termination of tachycardia. This patient has some key observations that prove the mechanism of at least these two echo complexes. The accompanying figure shows an initial prolonged HV interval of 98 milliseconds followed by a shortening to 58 milliseconds. The HA interval on the first echo complex is 254 milliseconds and this shortens to 218 milliseconds as the HV interval shortens. The change in HV predicts the change in HA. The only supraventricular tachycardia that utilizes both the His–Purkinje system and ventricle in the circuit is AV reentry, and that is the diagnosis. Also note that termination of these echo complexes occurs with an atrial electrogram without conduction to the His bundle, which was a consistent finding and strongly suggests an AV node–dependent mechanism. Indeed, during isoproterenol infusion tachycardia persisted and ablation was successful.

This tracing demands careful measurement before coming to a conclusion. It also reminds us of the famous Shakespearean quote, “all that glitters is not gold.” At first glance it appears the patient may have 2:1 conduction over an accessory pathway. One of the hallmarks of an AV pathway, which is the typical accessory pathway, is a short PR interval that remains constant assuming there is no change of the site of origin of the P wave. Note that there is an apparent short PR interval associated with the wide QRS complexes. Importantly, the “PR interval” is not constant and this is clearly seen in the last two wide QRS complexes on this tracing. In essence, this is a “fooler” and is really a series of critically timed premature ventricular complexes that happen to be late in timing, in essence, “R on P waves.” The accompanying figure shows that these wide QRS complexes are PVCs. Indeed, this patient had PVCs and nonsustained VT that occurred in the presence of isoproterenol and no evidence of an accessory pathway.

This is an extremely unusual variant of a much more common problem, slow–fast AV node reentry, which is rarely incessant. Typically, tachycardia starts with a premature atrial complex, infrequently with a PVC, and will terminate suddenly and not spontaneously reoccur. This patient typically showed Wenckebach conduction block over the fast AV nodal pathway until a critical AH interval occurred that allowed tachycardia to be initiated. Tachycardia would spontaneously terminate only to restart with another Wenckebach sequence. On occasion, as noted in the accompanying figure, during the Wenckebach sequence a PAC would occur, and here the AH interval increases from 168 to 270 milliseconds at which time reentry occurred with a relatively short HA interval. The tachycardia cycle length is 306 milliseconds and even though there are variable AH intervals at the start of tachycardia, the HA interval remains nearly constant, consistent with AV node dependence, ruling out atrial tachycardia as a mechanism. The VA interval is short but not short enough to eliminate conclusively AV reentry, which was excluded at electrophysiologic study.

As you prepare to ablate the slow pathway, you might wonder whether the patient will have repetitive sequences of Wenckebach block after elimination of slow pathway conduction. However, in such situations what usually happens is 1:1 conduction over the fast pathway after elimination of slow pathway conduction. The presumption is that electrotonic interaction occurs between the two AV nodal pathways and with elimination of the slow pathway the fast pathway can now maintain 1:1 conduction, which was what occurred in this patient.

The tracing starts with a narrow QRS tachycardia with a 1:1 AV relationship. The atrial activation is “eccentric,” that is, earliest in the distal coronary sinus. This can only be AVRT over a left lateral AP or an atrial tachycardia from the left atrium. The VA relationship stays constant in the few cycles seen, consistent with AVRT but not ruling out an AT, and AVRT was proved elsewhere in the study. A sudden change in atrial activation occurs after the asterisk, with prolongation of the AA interval and a total change in the atrial activation sequence to a central pattern. The subsequent QRS is also reset (CL 380 milliseconds from 370 milliseconds).

The differential diagnosis includes AVRT using a septal AP for retrograde conduction with a longer VA interval, AVNRT, and even AT. AVNRT was subsequently diagnosed. The pacing spikes are distracting but do not capture until the seventh cycle and even then the pacing is too slow to overtake the tachycardia.

It is interesting to speculate how this transition occurred. Why did the retrograde AV node pathway suddenly appear when the AP blocked, to start its own tachycardia? It is possible that the each QRS was resulting in both retrograde AP and retrograde AVN conduction but the AP was always “beating” the AVN to the atrium and the latter was not manifest. With block in the AP, the retrograde AVN pathway could now capture the atrium and drive its own tachycardia. One may think of this as the faster AVRT “entraining” the slightly slower potential AVNRT until block occurred in the AP, that is, analogous to termination of “overdrive pacing” from the atrial insertion of the left lateral AP.

It is also possible that onset of AVNRT was merely coincidental with the cessation of AVRT, although it is somewhat difficult to explain why there is immediate retrograde conduction over the AV node with the next cycle.

Earliest atrial activation is observed in the right atrium near the HB region. The coronary sinus is activated from proximal to distal.

The multipolar right atrial catheter and the coronary sinus cover a relatively large part of the atria and atrial electrograms cover a rather narrow band of the cardiac cycle (vertical lines). This is most compatible with a focal source rather than macroreentry during which the electrograms would fill more of the cardiac cycle.

The tachycardia terminates with a QRS complex. The last several complexes have a His recorded on the HIS d tracing and there is no preceding AH prolongation, which would usually be expected with termination of a junctional-dependent tachycardia, and slowing of the atrial cycle length precedes termination. Prolongation of conduction in a slowly conducting AV nodal or accessory retrograde pathway cannot be entirely excluded from this tracing alone.

This tracing is most compatible with an adenosine-sensitive atrial focus near the His bundle region and this is where it was ultimately mapped and ablated.

The figure shows onset of ventricular pacing during tachycardia. Ventricular capture is evident only after the fourth spike with the fourth QRS complex. This QRS obviously reflects fusion between the tachycardia QRS and the fully paced QRS. The subsequent atrial activation is advanced. This is the equivalent of the PVC programmed into the tachycardia cycle at a time when the His is refractory, that is, the “His refractory” PVC. It is not necessary to see the His deflection since the fused complex clearly derives in part from anterograde conduction over the His, which then must be refractory. Note also that the stimulus to A interval of the fused beat is almost the same as the VA interval of tachycardia, proving that the pacing stimulus is activating the atrium by the same route as during tachycardia, that is, the pacing catheter is “in” the circuit. This is analogous to comparing these two intervals after cessation of pacing with entrainment. Refer to Fig. 1–3 and consider how all this reflects good access of the pacing site to a sizable excitable gap.

This is a classical “entrainment” maneuver. The atrial activation sequence during tachycardia is central and might be an atrial tachycardia, AV node reentry, or AV reentry over a septal accessory pathway. At first glance, termination of pacing suggests a “V A A V” response diagnostic of an atrial tachycardia but this is not the case.

The maneuver is best interpreted with a checklist approach. Pacing should be done as close as possible to the tachycardia cycle length to minimize potential decremental conduction, which could confound the interpretation.

The first priority is to verify that the tachycardia has been accelerated to the pacing cycle length in a stable fashion. This is indeed the case here, that is, 340 milliseconds.

The second step is to identify the last entrained atrial electrogram. In this case it is indicated by the asterisk and it is the last atrial deflection at the paced CL. It is now apparent that the V during pacing does not conduct to the first but to the second atrial electrogram. This is then a “V A V” response. Another clue to relating the V to the correct A is that the VA during pacing should not be shorter than the VA during tachycardia and this alone would eliminate the shorter VA during pacing as the correct one.

At this point, one notes that the postpacing interval (PPI) at the RV apex is 165 milliseconds longer than the tachycardia cycle length and the change in VA between pacing and tachycardia is 180 milliseconds (i.e., 450–270). The usual published maximum PPI to be considered “in” the circuit for AV reentry over a septal AP is 115 milliseconds and the corresponding delta VA is 85 milliseconds; so one can consider that the pacing site is “out” of the circuit.

This is often loosely expressed as an “AV nodal” response but this can be misleading since other factors (free wall AP, decremental septal AP) can result in this type of response. It is more accurate to say that one has excluded a “conventional” or nondecremental septal accessory pathway as the retrograde limb of the circuit. In this case it was AVNRT.

The tachycardia is regular with a one to one AV relationship. The atrial activation shows earliest depolarization at CS 7,8, which is slightly in from the orifice of the CS. This is not an anterior septal pattern and is most likely either atrial tachycardia or atrioventricular reentry. AVNRT is technically possible with this pattern but would be more unusual.

A PAC with a different activation pattern is seen (asterisk) and delays the next cycle. This delayed cycle nonetheless has the same HA interval as the tachycardia (the A appears “linked” to the previous H) and this would be extremely fortuitous with an atrial tachycardia but expected with AVRT, which it was.

The differential diagnosis of a narrow QRS tachycardia is presented in Table 1–5. The tachycardia has a normal QRS, a cycle length of 320 milliseconds, and a 1:1 AV relationship. The atrial activation is central with earliest activation at the His (arrow) where atrial activation precedes ventricular activation. This excludes sinus node reentry. The short VA interval rules out AV reentry. Although atrial tachycardia is not excluded, the apparent requirement of AH prolongation at the onset of tachycardia makes AV node reentry most likely. Maneuvers to assess AV node participation in tachycardia such as carotid sinus massage will confirm the diagnosis.