Mechanisms of Posterior Fascicular Tachycardia
The Relationship Between High Frequency Potentials and the Ventricular Myocardium
A 17-year-old man presented with a history of palpitations and surface ECG demonstrating wide QRS tachycardia (QRS duration=140 ms) with a right bundle branch block pattern and left-axis deviation (Figure 1A). The 12-lead ECG was normal during sinus rhythm.
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During electrophysiology study, mapping was performed using a 20 pole multielectrode catheter (MEC) via a retrograde aortic approach (Figure 1C). The baseline A–H and H–V intervals were 57 and 55 ms, respectively (Figure 1B, left). A wide QRS tachycardia identical to the clinical tachycardia was observed with cycle length of 320 ms, H–V interval of −30 ms (Figure 1B, right). This was consistent with a diagnosis of fascicular ventricular tachycardia (FVT) with origin from the left posterior fascicle (LPF). Three distinct potentials could be recorded from the MEC during FVT: A) sharp inflection, high frequency potentials (P1) activated from midproximal to distal MEC; B) presystolic LPF potentials (P2) activated from distal to proximal MEC; and C) left-septal ventricular (V) potentials (Figure 1B, right).
Right ventricular programmed stimulation (S1S2, 400/300 ms) was used to induce FVT (Figure 2A). During S1 stimulation, P1 was recorded with a stable S1–P1 interval (S1–P1=255 ms) and the same conduction sequence as during tachycardia. With delivery of an extrastimulus, the S2–P1 interval increased to 320 ms, followed by P2 and V potentials, and induction of sustained FVT.
Additional pacing maneuvers were performed during tachycardia.
Delivery of Premature Ventricular Contraction
Premature ventricular contractions (PVCs) were introduced from the right midventricular septum beginning at 10 ms shorter than the tachycardia cycle length, until loss of ventricular capture or termination of tachycardia. A PVC advanced the immediate septal ventricle and His bundle via the right bundle brunch retrogradely, without advancing the immediate P1 and P2, however, advancing the subsequent P1 by 10 ms. The following P2 and QRS were also advanced sequentially. The P1 and P2 intervals during tachycardia were 315 ms before the PVC. However, the P1 and P2 intervals both shortened to 305 ms after the PVC (Figure 2B).
Atrial Overdrive Pacing
Atrial overdrive pacing was delivered from the proximal coronary sinus at 300 ms (Figure 2C and 2D). The tachycardia converted to a narrow QRS morphology with the His bundle conducting antegradely (noted by a longer A–H interval and antegrade P2 conduction). At the onset of atrial pacing, the proximal portion of P2 was activated antegradely, whereas the distal P2 was still activated retrogradely. The septal ventricular potentials (V*, beat 4) at the mid MEC were advanced by antegrade P2 conduction without a change in cycle length at the distal MEC, and the subsequent P1 (beat 5) was also advanced (Figure 2C). Timing of P1 was simultaneous with the antegrade His bundle activation after the last atrial stimulus (beat 7) without termination of tachycardia (Figure 2D).
Radiofrequency ablation targeted at the distal P1 potentials rendered tachycardia noninducible.
A 19-year-old man presented with a history of palpitations and surface ECG demonstrating wide QRS tachycardia (QRS duration=135 ms) with a right bundle branch block pattern and left-axis deviation. During sinus rhythm, the 12-lead ECG was normal.
During electrophysiology study, a 20 pole MEC was used via a retrograde aortic approach. The baseline A–H and H–V intervals were 58 ms and 60 ms, respectively (Figure 3A, left). A wide QRS tachycardia identical to the clinical tachycardia was observed with cycle length of 310 ms, H–V interval of −20 ms and 2:1 retrograde conduction (Figure 3A, right). Three distinct potentials P1, P2, and V potentials of the left septum were recorded at the MEC (Figure 3A, right). During tachycardia, PVCs were delivered from the right ventricular apex. A PVC advanced the immediate septal ventricle without advancing the immediate P1 and P2, however, advancing the subsequent P1, and the following P2 and QRS were also advanced sequentially (not shown).
Ablation of the P1 Potentials
A large curve deflectable sheath and a 4-mm saline-irrigated ablation catheter (SJM) were used to ablate via a trans-septal approach. Radiofrequency ablation was delivered at the location where the distal P1 fused with P2 and ventricular myocardium. After radiofrequency delivery, tachycardia was terminated with disconnection of the distal P1 potentials (Figure 3B). After cessation of ablation, P1 potentials were recorded during either sinus rhythm or ventricular pacing, and delayed conduction to P1 was observed (Figure 3C). Further attempts were then made to ablate the proximal P1 during sinus rhythm. During ablation, automaticity arising from the P2 or local ventricle was noted with elimination of the P1 potentials (Figure 3D). Tachycardia could not be induced after ablation.
A 33-year-old man presented with a history of palpitations and surface ECG demonstrating wide QRS tachycardia (QRS duration=125 ms) with a right bundle branch block pattern and left-axis deviation (Figure 4A). During sinus rhythm, the 12-lead ECG was normal.
A 20 pole MEC was used via a retrograde aortic approach during electrophysiology study.
The baseline A–H and H–V intervals were 75 and 60 ms, respectively (Figure 4B, left). A wide QRS tachycardia identical to the clinical tachycardia was observed with cycle length of 330 ms, H–V interval of −5 ms and 1:1 retrograde conduction (Figure 4B, right). No manifest P1 potential could be recorded even with adjusting the MEC position along the septum. P2 potentials were observed along the MEC with earliest potentials seen at the midseptal left ventricle fluoroscopically.
Delivery of PVC
During tachycardia, PVCs were delivered from the midright ventricular septum. A PVC advanced the immediate proximal septal ventricle without advancing the immediate P2 and the septal ventricle from mid to distal; however, there was advancement of the subsequent P2 and QRS by 15 ms (Figure 4D).
Ventricular Overdrive Pacing
Ventricular overdrive pacing was delivered from the midright ventricular septum at different cycle lengths (Figure 4E). Entrainment of tachycardia and progressive fusion of QRS morphology were observed during decreasing pacing cycle length.
Atrial overdrive pacing failed to conduct through the His bundle antegradely. Radiofrequency ablation targeted at the earliest portion of P2 rendered tachycardia noninducible.
Left posterior FVT is the most common type of fascicular tachycardia involving the left ventricular conduction system and may have multiple underlying mechanisms. Nogami et al1 and Morishima et al2 suggested that P2 may be a bystander of the FVT, and the left ventricular myocardium and P1 may comprise the reentry circuit.
In the first 2 cases, 2 distinct sharp potentials (P1 and P2) were recorded during tachycardia with a negative H–V interval (H–V= −30 and −20 ms, respectively). Tachycardia demonstrated a negative H–V interval indicating activation of the P2 at the mid to low LPF where P1 inserted antegradely (Figure 1B, right; Figure 3A, right). In the third case, the H–V interval during tachycardia was less negative (−5 ms) suggestive of a more proximal initial activation of the LPF (Figure 4B, right).
During sinus rhythm in case 1, P2 conducted with an antegrade activation sequence was recorded preceding the onset of local V potential without recording of P1 (Figure 1B, left). Earliest local ventricular activation appeared to be at the middle portion of the MEC suggesting a connection of LPF to ventricular myocardium at the midseptal location. Right ventricular programmed stimulation was performed, and P1 was noted following the local V potential with antegrade conduction and a stable S1–P1 interval (S1–P1 = 255 ms). We also noted that P1 was not conducted antegradely to the distal MEC during ventricular stimulation suggestive of conduction block at the distal P1 or concealed retrograde conduction. With extrastimulus delivery, the S2–P1 interval increased by 65 ms (S2–P1=320 ms), and tachycardia was induced with retrograde P2 conduction from distal to proximal MEC after P1 conduction from proximal to distal MEC (Figure 2A).
During tachycardia, PVCs were introduced from the right midseptal ventricle. The local V potentials were advanced without advancement of the immediate P1 or P2, and the subsequent P1 and P2 were advanced by 10 ms (Figure 2B). These findings confirm the involvement of ventricular myocardium as part of the reentry circuit.
With atrial overdrive pacing from the coronary sinus during tachycardia, gradual antegrade activation of the His-Purkinje system was noted after the second paced beat (Figure 2C and 2D). The fourth beat demonstrates LPF (P2) activation from proximal to mid poles and slightly advanced local ventricular activation at the mid MEC poles. The distal retrograde activation of P2 and timing of ventricular activation at the distal MEC remained unaffected; however, the subsequent P1 (beat 5) was advanced. The proximal P1 must be activated by the mid portion of the LPF (P2) via ventricular myocardium and a slow conduction zone. After the last atrial stimulus, the timing of antegrade P1 (beat 7) was simultaneous with the His bundle potential which indicated that P1 was activated from the previous ventricular complex (beat 6). The antegrade activation of P2 (beat 7) from the last atrial stimulus conducts through ventricular myocardium that was connected to the subsequent P1 (beat 8) fiber with continuation of tachycardia. This suggests the involvement of 2 distinct reentry circuits in FVT. Both involve a slow conduction zone linked to the proximal P1 region. However, one circuit may include only the ventricular myocardium and the proximal P1 fiber with retrograde P2 conduction acting as a passive bystander. An alternative circuit utilizing retrograde LPF (P2) as part of the reentry circuit combines with the mid ventricular myocardium and proximal portion of P1. In this case, the successful ablation site was near the distal LPF, where the P1 transitioned to P2 activation.
In the second case, a similar conduction sequence of P1 and P2 was observed during tachycardia (Figure 3A, right). However, we observed that there was a more distal connection between the LPF (P2) and ventricular myocardium during sinus rhythm (Figure 3A, left). Before ablation, P1 was retrogradely activated via the distal LPF, and P1 potentials were fused with V potentials at the MEC during sinus rhythm. After ablation at the site where distal P1 connected with P2 and ventricular myocardium, P1 was recorded during either sinus rhythm or right ventricular apex pacing, with significant delayed antegrade conduction following ventricular potentials (Figure 3C). After ablation of the proximal P1 region, total elimination of the proximal P1 activation from ventricular myocardium was observed (Figure 3D). This is evidence that P1 is critical to the reentry circuit and that ablation is feasible by either targeting the proximal or distal P1 region.
In contrast to the above 2 cases, during tachycardia, the third case had a slightly negative H–V interval (−5 ms), a relatively narrow QRS duration, and no manifest P1 could be recorded. The response to PVC delivery and the progressive fusion of QRS morphology noted during entrainment with decreasing pacing cycle length suggests a re-entrant mechanism of tachycardia with ventricular myocardium as part of the reentrant circuit, similar to those cases with a manifest recorded P1 and more negative H–V interval during tachycardia. The earliest LPF potentials were observed at the location of the midseptal left ventricle, and successful ablation was targeted at this area. We hypothesize a P1 fiber with a short length anatomically or nonparallel in orientation to the LPF and inserts into the LPF at the mid septum, with a slow conduction zone linked to the proximal P1 region. The potential reentrant circuit is shown as a schematic diagram (Figure 4D, right).
Catheter ablation guided by the relationship of P1 and P2 potentials recorded by the MEC may be useful for evaluation of the underlying substrate of FVT.
For the type of FVT with a more negative H–V interval and manifest recorded P1 during tachycardia, the successful ablation target should be the P1 potentials. However, the ideal level of P1 for ablation may be at a more distal site of P1 to avoid possible delayed conduction at the more proximal LPF.
For the other type of FVT with a slightly negative H–V interval and no manifest recorded P1 during tachycardia, the successful ablation target should be the earliest P2 potential. Theoretically, ablation targeting the distal or proximal LPF away from the optimal target may result in different changes in QRS morphology during tachycardia. The schematic diagram (Figure 4F) shows the potential mechanisms of these alterations. A narrow QRS morphology with positive H–V interval may be observed after ablating the distal part of the LPF away from the target, because the reentrant circuit may involve both the right bundle branch and the left anterior bundle branch after the ablation (Figure 4F, left). Contrarily, a wider QRS morphology with left-axis deviation and more negative H–V interval may emerge after ablating the proximal part of the LPF away from the target (Figure 4F, right).
It is possible that left posterior FVT may involve more than one form of reentrant circuit. We describe 2 types of FVT characterized by H–V interval. The first type has a more negative H–V interval with manifest recorded P1. The second type has a slightly negative H–V interval without recorded P1. Re-entry was the common mechanism of the 2 types of FVT. The reentrant circuit consists of ventricular myocardium, a Purkinje fiber (P1), a slow conduction zone exists at the proximal P1 region, and a part of LPF (P2) that connects distal P1 and ventricular myocardium. This unique slow conduction region may be part of ventricular myocardium, proximal P1, or other Purkinje fibers, which demonstrate delayed conduction properties and may represent a substrate for this arrhythmia. The successful ablation target should be the P1 potentials for the type of FVT with recorded P1, whereas the earliest P2 potential should be the successful target for the type of FVT without manifest recorded P1. Ablation at the different positions of P2 away from optimal target may change the reentrant circuit and the QRS morphology during tachycardia.
- Received August 26, 2015.
- Accepted February 1, 2016.
- © 2016 American Heart Association, Inc.
- Nogami A,
- Naito S,
- Tada H,
- Taniguchi K,
- Okamoto Y,
- Nishimura S,
- Yamauchi Y,
- Aonuma K,
- Goya M,
- Iesaka Y,
- Hiroe M