Fascicular Ventricular Arrhythmias

Fascicular Ventricular Arrhythmias

82 Fascicular Ventricular Arrhythmias Akiko Ueda and Kyoko Soejima CHAPTER OUTLINE Verapamil-Sensitive Fascicular Ventricular Tachycardia 793 Focal ...

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82

Fascicular Ventricular Arrhythmias Akiko Ueda and Kyoko Soejima

CHAPTER OUTLINE Verapamil-Sensitive Fascicular Ventricular Tachycardia 793 Focal Ventricular Tachycardia and Ventricular Premature Contraction Originating From the Purkinje System 796 Ventricular Premature Contractions and Ventricular Fibrillation Triggered From the Purkinje System

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Bundle Branch Reentry and Interfascicular Reentry

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Conclusions 797

Various types of ventricular tachycardia (VT) are known to arise from the His-Purkinje network in patients with or without structural heart diseases (SHDs). In this chapter, we describe the clinical manifestation, mechanism, diagnosis, and therapeutic option for each VT. We first focus on the basic concept of the most common reentrant fascicular VT, which is known as verapamil-sensitive fascicular VT. Recent findings on the VT circuit and characteristics of the rare form are also addressed. We then describe focal Purkinje VT and ventricular premature contractions (VPCs) arising from the Purkinje system that could trigger ventricular fibrillation (VF). We also briefly describe bundle branch reentrant VT (BBRVT) and interfascicular reentrant VT (IFVT).

Verapamil-Sensitive Fascicular Ventricular Tachycardia Clinical Manifestation Although most VTs are related to SHDs, 10% are identified in patients with no apparent structural abnormalities. Following right ventricular (RV) outflow tract VTs, left ventricular (LV) fascicular VT is the second most common form, comprising 7% to 12% of such “idiopathic” VTs.1,2 In 1979, Zipes and colleagues first described the diagnostic characteristics of this type of VT, which included (1) induction by atrial pacing, (2) VT configuration of the right bundle branch block (RBBB) and left axis, and (3) manifestation in patients with no apparent SHD.3 Belhassen and associates reported verapamil sensitivity of this VT in 1981,4 currently known as the fourth feature. This VT typically presents in young adulthood, and there is a slight male predominance. 

Classification Following the initial report by Zipes,3 two additional QRS morphologies have been reported.5,6 At present, idiopathic verapamilsensitive fascicular VT is classified into three forms according to the QRS morphologies: (1) RBBB pattern with left axis deviation (common form, left posterior fascicular [LPF] VT, 90%), (2) RBBB pattern with right axis deviation (uncommon form, left anterior fascicular [LAF] VT, 10%), and (3) narrow QRS morphology with normal axis (rare form, upper septal [US] VT, <1%) (Fig. 82.1). 

Mechanism and Ventricular Tachycardia Circuit The mechanism of verapamil-sensitive fascicular VT is reentry as ventricular or atrial programmed stimulation can induce, entrain, and terminate VT. A multitude of studies investigating the role

of the Purkinje system in the VT circuit has been conducted. Several groups demonstrated that the Purkinje network at the LPF region is a critical component of the most common VT circuit on the basis of the high success rate of ablation at this site. Nakagawa and coworkers first reported the importance of Purkinje potentials at the successful ablation site.7 Ablation sites were at the apical inferior septum of the LV. Tsuchiya and associates reported the significance of a late diastolic potential (DP) and emphasized the role of late DPs and presystolic potentials (PPs) in the VT circuit.8 Their successful ablation sites were located at the basal septal region close to the main trunk of the left bundle (LB) branch. In 2000, Nogami and colleagues first demonstrated the macroreentrant circuit of this verapamil-sensitive fascicular VT using a multielectrode catheter placed at the LV midseptal area.9 During sinus rhythm, Purkinje potentials preceding the QRS complex were recorded along the septal wall from proximal to distal electrodes (basal to apical direction) (Fig. 82.2A). During VT, two distinct types of potentials were recorded: DPs and PPs. DP indicated the propagation of excitation in the basal to apical direction, but PP showed propagation from apical to basal direction, which is the reverse of the activation sequence during sinus rhythm (Fig. 82.2B). Entrainment mapping at the exit site where PP and the earliest ventricular activation were fused demonstrated orthodromic DP capture with a postpacing interval identical to the VT cycle length. When entrainment pacing was performed with a shorter cycle length, DP was antidromically captured and VT was terminated. Furthermore, the administration of verapamil during VT significantly prolonged both the DP-PP and PP-DP intervals but not the PP-QRS interval, suggesting that the location of slow conduction was from DP to PP. From the abovementioned findings, it was concluded that DP arose from abnormal Purkinje fibers with verapamil sensitivity and were a critical component of the VT circuit. In contrast, PP, representing the activation of LPF or Purkinje fibers adjacent to LPF, might not be involved in the VT circuit. Recent reports electrophysiologically demonstrated that LPF was more likely to be a bystander as PP could be captured by a sinus beat without affecting the VT cycle length.10,11 These authors advocated the hypothesized VT circuit shown in Fig. 82.3A. Endocardial mapping during the uncommon type of verapamil-sensitive fascicular VT, namely LAF VT, exhibits DP in the LV midseptum and PP near the LAF region. The VT activation is considered to antegradely propagate over the midseptal area similar to the common type of LPF VT and then retrogradely propagate over the area near the LAF. Kottkamp and associates reported a patient who had two VTs with left and right axis QRS configurations.12 Radiofrequency (RF) energy delivered to the area between the LPF and the LAF successfully eliminated both VTs, suggesting that both LPF and LAF VT shared the midseptal area as an antegrade limb of the circuit. Fig. 82.3B depicts a schema of the hypothesized LAF VT circuit. Details of the reentrant circuit of the rare form of verapamilsensitive fascicular VT, USVT, were unclear until recently. Ahmed and coworkers reported that the VT activation propagated antegradely in the LAF or the LPF and then retrogradely in abnormal Purkinje tissue in the LV septum, which is the reverse direction of propagation as observed for LPF and LAF VT13 (Fig. 82.3C). USVT is known to develop following ablation of other types of verapamil-sensitive fascicular VTs. Ahmed and 793

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FIGURE 82.1  Twelve-lead electrocardiograms of verapamil-sensitive fascicular ventricular tachycardia (VT).  (A) Common form (left posterior fascicular VT) shows right bundle branch block (RBBB) with left axis configuration. (B) Uncommon form (left anterior fascicular VT) shows RBBB with right axis configuration. (C) Rare form (upper septal VT) shows narrow QRS with normal axis.

colleagues reported that half of their USVT cohort previously underwent LPF region ablation. Conduction delay in the fascicular region created by ablation seems to provide a new substrate of USVT. However, the remaining half of their cohort had no previous ablation but presented with minor electrocardiogram (ECG) abnormalities, such as small Q waves in the inferior leads and/or S waves in leads I and/or aVF. Regardless of iatrogenic or idiopathic causes, the presence of conduction abnormalities in the midseptum could be a substrate for USVT. 

Anatomical Substrate Verapamil-sensitive fascicular VT is idiopathic and is not usually associated with an abnormal low-voltage area. However, there have been reports of fascicular VT in ischemic cardiomyopathy. Earlier studies using canine infarct models showed that Purkinje fibers over the infarcted region remain almost structurally intact but present abnormal electrophysiological (EP) properties, such as decreased resting potential, lower action potential amplitude, and increased action potential duration. These properties may lead to both triggered and reentrant mechanisms of VT.14,15 Hayashi and associates reported four cases with acute or chronic phase of ischemic cardiomyopathy, who developed VT with similar EP properties.16 The VTs were reproducibly induced by programmed stimulation and entrained by atrial pacing. DP and PP were sequentially recorded along the LV posterior septum during the VT, and ablation at either site successfully terminated the tachycardia in all patients. Verapamil sensitivity was confirmed in only one patient in this study because of unstable hemodynamics. A case of reentrant LAF VT associated with healed myocardial infarction was also reported.17 These VTs present several characteristic differences compared with the usual scar-related VT in patients with ischemic cardiomyopathy: (1) relatively narrow QRS morphology during VT, (2) verapamil sensitivity, (3) PPs or DPs during VT, and (4) VT termination by a few RF energy applications to the site.14

A controversy remains regarding the involvement of false tendons or fibromuscular bands in LV verapamil-sensitive fascicular VT. Several reports have suggested the anatomical or EP involvement of false tendons. Thakur and colleagues reported that false tendons were observed more frequently in patients with fascicular VT (100%) compared with those without VT (5%).18 Maruyama and associates reported that an electrode catheter positioned at the LV mid- to inferoapical septum along a false tendon recorded sequential DPs that encompassed the entire VT cycle length.19 In contrast, Lin and coworkers reported a similar prevalence of a fibromuscular band in patients with or without the fascicular VTs.20 Although small fibromuscular bands or trabeculae not detectable by echocardiography could play roles in reentrant circuits, this has not yet been fully elucidated. 

Differential Diagnosis Other types of idiopathic VTs arising from the posterior papillary muscle (PPM) or cardiac crux can present with a similar QRS morphology. Kawamura and associates described a stepwise ECG algorithm to differentiate these VTs that have an RBBB and a superior axis.21 A lower maximum deflection index (MDI) of <0.55 and a shorter QRS duration of <150 ms diagnosed verap­ amil-sensitive LPF VTs with high sensitivity and specificity. VT originating from the PPM is not typically induced by programmed stimulation and is catecholamine sensitive, suggesting a nonreentrant mechanism.22 Crux VT has also a nonreentrant mechanism and catecholamine sensitivity.23 

Therapy Catheter ablation can be a first-line therapy for verapamilsensitive fascicular VT as both the acute and long-term success rates are high.7–9,24 As the DP is recorded at a critical part of the VT circuit, identification of the potential during the VT is

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FIGURE 82.2  Intracardiac recordings in a patient with left posterior fascicle-ventricular tachycardia.  Ablation catheter is placed at the left ventricular midseptum. The distal electrode (ABL1) is located most apically and the proximal electrode (ABL4) is located more basal.  (A) During sinus rhythm, Purkinje potentials preceding the QRS complex are recorded along the septal wall from proximal to distal electrodes (basal to apical direction). (B) During ventricular tachycardia, two distinct potentials, middiastolic potentials (DP) and Purkinje potentials at the presystolic timing (PP), are recorded. While DP shows propagation in the basal to apical direction, PP shows propagation in the apical to basal direction, which is the reverse of the direction during sinus rhythm. The black triangle indicates DP. The white triangle indicates Purkinje potentials that propagate from proximal to distal during sinus rhythm and from distal to proximal during the ventricular tachycardia. ABL, Ablation; d, distal; DP, diastolic potential; HBE, His bundle electrogram; HRA, high right atrium; PP, presystolic potential; RVA, right ventricular apex.

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FIGURE 82.3  Schematic representation of macroreentrant circuits of three types of verapamilsensitive fascicular ventricular tachycardia (VT).  (A) In left posterior fascicle (LPF)-VT, activation propagates antegradely in the midseptum where abnormal Purkinje tissue distributes and conducts retrogradely near the LPF. In the past, LPF was considered as part of the circuit, but recent reports suggest the LPF is a bystander. (B) In left anterior fascicle (LAF)-VT, activation propagates antegradely in the midseptum and conducts retrogradely near the LAF. (C) In USVT, activation propagates antegradely in the LPF or LAF and then conducts retrogradely in the midseptum. RB, Right bundle.

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ABL1-2 RVA FIGURE 82.4  Intracardiac recordings in left posterior fascicular ventricular tachycardia (VT).  Radio­frequency energy was applied at the site where a diastolic potential (DP) was identified. The DP-presystolic potential (PP) interval gradually prolonged, and then the VT was terminated at the timing of the DP-PP block. After VT termination, a delayed potential is seen after the QRS complex. ABL, Ablation; HBE, His bundle electrogram; HRA, high right atrium; RVA, right ventricular apex.

important. Although the DP can be widely recorded from the basal to apical LV septum, targeting the earliest DP is not necessary; rather, targeting potentials in the apical third of the septum is advisable, as the RF application to the proximal portion of the LV septum could result in LBBB or atrioventricular (AV) block. When RF is applied during the VT, the DP-PP interval gradually prolongs, and DP to PP block terminates the VT. Following successful ablation, the DP is recorded after the QRS complex during sinus rhythm (Fig. 82.4). If no DP is identified, the earliest PP at the VT exit is an alternative target. Verapamil-sensitive fascicular VT can sometimes be noninducible or self-terminating during the EP study. Catheter contact during mapping can mechanically suppress the conduction over the VT circuit (so-called “bump” phenomenon).25 On such occasions, activation mapping can still be performed if a ventricular echo beat with the same QRS morphology as the VT is observed. If no echo beat is inducible, anatomical linear ablation through the inferior mid-LV septum perpendicular to its long axis can be successful. Following the ablation, DPs could be observed after the QRS complex if the ablation line crosses the antegrade limb of the VT circuit. The ablation target for LAF VT is also the region of DPs recorded in the midseptum or PPs in the LV anterolateral region.26 USVT can be eliminated by RF delivery to the upper midseptum where DPs appear during the VT.13 

Focal Ventricular Tachycardia and Ventricular Premature Contraction Originating From the Purkinje System Mechanism

Focal Purkinje VT arising from the LV demonstrates RBBB morphology with either left or right axis deviation on the 12-lead ECG. Lopera and colleagues reported that 2 (0.8%) of 234 SHD-associated VTs were focal Purkinje VT.27 This type of VT is mainly seen in patients with SHD but can also be seen in patients with structurally normal hearts. Although its surface ECG configuration is very

similar to verapamil-sensitive VT, the mechanism is considered nonreentrant. Focal Purkinje VT can be induced with infusion of catecholaminergic agents, such as isoproterenol, but not usually with programmed ventricular stimulation. In addition, β-blockers, but not verapamil, are effective for terminating the VT. On the basis of these characteristics, the mechanism of focal Purkinje VT is considered to be automaticity or triggered activity.28 As the distal Purkinje network is anatomically linked to PMs, PM has been recognized as a major source of VPCs that can be targeted for ablation.21 

Therapy Catheter ablation for this VT should target the earliest Purkinje activation during the tachycardia. Pace mapping at the successful ablation site shows the identical QRS morphology with the S-QRS interval identical to the Purkinje potential to the QRS onset during the VT.28,29 When the target ablation site is located at a relatively proximal portion, there is a potential risk for LBBB or AV block.27 For VPCs from the PM, real-time imaging with intracardiac echo is very useful.30 The contact and stability of the catheter on the PM can be challenging, and sometimes multiple RF lesions are required to eliminate the VPCs. 

Ventricular Premature Contractions and Ventricular Fibrillation Triggered From the Purkinje System Although the majority of VPCs are considered to be benign and with little clinical impact, recent reports demonstrated that the VPCs originating from RV or LV fascicles can trigger VF (see Chapter 129).31,32 VF triggered by the fascicular-origin VPC has been reported in ischemic cardiomyopathy, long QT syndrome,33 early repolarization,34 and catecholaminergic polymorphic VT.35 Elimination of the VPC by ablation successfully prevents recurrent VF. Mapping and ablation strategies are similar to those of the focal Purkinje VT. 

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B FIGURE 82.5  Schematic representation of the bundle branches and interfascicular ventricular tachycardia (VT).  (A) Bundle branch reentrant VT includes the right and left bundle (RB and LB) in the circuit. In this schema, activation propagates the RB from distal to proximal and the LB from proximal to distal, but the VT propagating the opposite direction is also possible. (B) Interfascicular VT (IFVT) involves the left anterior and posterior fascicles (LAF and LPF) in the circuit. Both fascicles can be antegrade and retrograde limbs of the circuit. (C) Intracardiac recordings during IFVT. Upper panel shows recording from the catheter placed along LPF. Activation propagates from distal to proximal direction. Lower panel shows a recording from the catheter placed along the LAF. Activation propagates from proximal to distal direction. RB, Right bundle.

Bundle Branch Reentry and Interfascicular Reentry BBRVT (see Chapter 83) is a macroreentrant tachycardia involving RBs and LBs as essential components of the circuit (Fig. 82.5A). Purkinje system conduction disturbances, usually associated with dilated cardiomyopathy,36 valvular diseases,37 ischemic cardiomyopathy, or myotonic dystrophy,38 provide a substrate for BBRVT. However, BBRVT has also been reported in patients with isolated conduction system disease and no apparent structural heart abnormalities.39 The surface ECG during sinus rhythm characteristically shows intraventricular conduction delay: nonspecific or typical bundle branch block patterns with prolonged QRS duration. The surface ECG of BBRVT has an LBBB or RBBB configuration. The HV interval during sinus rhythm is usually prolonged. BBRVT is usually inducible by ventricular programmed stimulation. The diagnosis of BBRVT can be made by demonstrating that the His and RB or LB potentials precede the ventricular activation, and HH and RB-RB or LB-LB interval oscillations precede VV oscillations. An HV interval during the VT is usually longer than that during sinus rhythm but can be equal or shorter depending on the His recording site and upper turnaround point of BBRVT or the balance between antegrade and retrograde conduction times from the upper turnaround point.40 RF ablation is regarded as

the first-line therapy and usually targets the RB. Ablation of LB has been proposed in patients with underlying LBBB pattern to reduce the chance of complete AV block. IFVT is less common compared with BBRVT but is also a macroreentrant tachycardia through the branches of the LV Purkinje system41 (Fig. 82.5B). IFVT has a relatively narrow QRS complex with an RBBB pattern with superior or inferior axis deviation. EP study demonstrates that the LAF or the LPF precedes the ventricular activation, and analysis of oscillations shows that LAF-LAF or LPF-LPF intervals drive the VV intervals. As opposed to BBRVT, the His potential follows the LAF or LPF potential, and the HV interval during the VT is shorter than that during sinus rhythm. Ablation of the IFVT is guided by fascicular potentials and targets either the left anterior or posterior fascicle. 

Conclusions VTs arising from the fascicles or the Purkinje network include a wide spectrum of substrates and mechanisms. The ECG morphologies can mimic each other and sometimes be misleading despite different mechanisms. Careful consideration of the patient’s underlying heart disease and understanding of the ECG and EP characteristics are required for differential diagnosis and appropriate therapy.

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