No apparent structural abnormality is identified in approximately 10% of all sustained monomorphic ventricular tachycardias (VTs) in the US1 and in 20% of those in Japan.2 These VTs are referred to as 'idiopathic'. Idiopathic VTs usually occur in specific locations and have specific QRS morphologies, whereas VTs associated with structural heart disease have a QRS morphology that tends to indicate the location of the scar. The most common idiopathic VT originates from a focus in the outflow tract of the right ventricle, and its mechanism is most likely triggered activity. In idiopathic left VT, four types of VT exist: verapamil-sensitive left fascicular VT (re-entry), VT with a focal origin in the distal Purkinje system (abnormal automaticity), left ventricular outflow tract VT (triggered activity, re-entry or automaticity) and VT from the mitral annulus (triggered activity, re-entry or automaticity). This article focuses on the diagnosis and ablation of verapamil-sensitive left fascicular VT.
Verapamil-sensitive fascicular VT is the most common form of idiopathic left VT. It was first recognised as an electrocardiographic entity in 1979 by Zipes et al.,3 who identified the characteristic diagnostic triad: induction with atrial pacing, right bundle branch block (RBBB) and leftaxis configuration and manifestation in patients without structural heart disease. In 1981, Belhassen et al.4 were the first to demonstrate the sensitivity of the tachycardia to verapamil, a fourth identifying feature. In 1988, Ohe et al.5 reported another type of this tachycardia, with RBBB and a right-axis deviation. More recently, Shimoike et al.6 described the upper septal form of this tachycardia. According to the QRS morphology, verapamil-sensitive left fascicular VT can be classified into three subgroups: left posterior fascicular VT, whose QRS morphology exhibits an RBBB configuration and a superior axis (see Figure 1A); left anterior fascicular VT, whose QRS morphology exhibits an RBBB configuration and right-axis deviation (see Figure 1B); and upper septal fascicular VT, whose QRS morphology exhibits a narrow QRS configuration and normal or right-axis deviation (see Figure 1C). Left posterior fascicular VT is the most common type of verapamil-sensitive fascicular VT and may account for up to 90% of cases, left anterior fascicular VT is uncommon and left upper septal fascicular VT is rare.
Substrate and Anatomy
Some data suggest that the tachycardia may originate from a false tendon or fibromuscular band in the left ventricle.7-9 Suwa et al.8 described a false tendon in the left ventricle of a patient with idiopathic VT in whom the VT was eliminated by surgical resection of the tendon. Using transoesophageal transthoracic and echocardiography, Thakur et al.9 found false tendons extending from the posteroinferior left ventricle to the basal septum in 15 of 15 patients with idiopathic left VT, but in only 5% of control patients. Maruyama et al.10 reported a case with the recording of sequential diastolic potentials (DPs) bridging the entire diastolic period and a false tendon extending from the midseptum to the inferoapical septum. However, Lin et al.11 found that 17 of 18 patients with idiopathic VT had this fibromuscular band, but also found it in 35 of 40 control patients. They concluded that the fibromuscular band was a common echocardiographic finding and was not a specific arrhythmogenic substrate for this tachycardia, although they could not exclude the possibility that the fibromuscular band was a potential substrate of the VT. Small fibromuscular bands, trabeculae carneae and small papillary muscles cannot be detected by echocardiography. The Purkinje networks in these small anatomical structures are important when considering the re-entry circuit of verapamil-sensitive left posterior fascicular VT. This circuit is not completely defined but may comprise fascicular tissue and ventricular myocardium.
The mechanism of verapamil-sensitive left VT is re-entry, because it can be induced, entrained and terminated by programmed ventricle or atrial stimulation. To confirm its re-entry circuit and the mechanism, my colleagues and I performed left ventricular septal mapping using an octapolar electrode catheter in 20 patients with left posterior fascicular VT.12 In 15 of 20 patients, two distinct potentials, P1 and P2, were recorded during the VT at the midseptum (see Figure 2). Although the middiastolic potential (P1) was recorded earlier from the proximal rather than the distal electrodes, the fused pre-systolic Purkinje potential (P2) was recorded earlier from the distal electrodes. During sinus rhythm, recording at the same site demonstrated P2, which was recorded after the His-bundle potential and before the onset of the QRS complex; however, the sequence of the P2 was the reverse of that seen during the VT.
VT could be entrained from the atrium and from the ventricle. Entrainment pacing from the atrium or ventricle captured P1 orthodromically and reset the VT. The interval from the stimulus to P1 was prolonged as the pacing rate increased. The intravenous administration of a low dose of verapamil (0.02-0.04mg/kg) prolonged the cycle length of the VT. Both the P1-P2 and P2-P1 intervals were proportionally prolonged after verapamil administration; however, the interval from P2 to the onset of the QRS complex remained unchanged. These findings demonstrated that P1 is a critical potential in the circuit of the verapamil-sensitive left posterior fascicular VT and suggested the presence of a macro-re-entry circuit involving the normal Purkinje system and abnormal Purkinje tissue with decremental properties and verapamil sensitivity. Although P1 has proved to be a critical potential in the VT circuit, whether the left posterior fascicle or Purkinje fibre (P2) is involved in the retrograde limb of the re-entrant circuit remains unclear.10,13 Morishima et al.14 reported a case with negative participation of the left posterior fascicle to the VT circuit. While selective capture of the left posterior fascicle by sinus beat did not affect the cycle length of VT, the post-pacing interval after the entrainment from left ventricular septal myocardium was equal to the cycle length of VT. Ouyang et al.15 suggested that idiopathic left VT re-entry might be a small macro-re- entry circuit consisting of one anterograde Purkinje fibre with a Purkinje potential, one retrograde Purkinje fibre with retrograde Purkinje potential and the ventricular myocardium as the bridge.
With left posterior fascicular VT, the earliest ventricular activation is recorded from the apical septum, and DPs are recorded from the midseptum (see Figure 2). His activation follows QRS onset by 5-30msec.12 During sinus rhythm, recording from the same site demonstrates the Purkinje potentials after the His-bundle potential and before the onset of the QRS complex. Another type of Purkinje-related VT is the focal tachycardia from the Purkinje system. This VT is classified as propranolol-sensitive automatic VT.1 While this VT is usually observed in patients with ischaemic heart disease,16 it is also observed in patients with a structurally normal heart.17,18 Focal Purkinje VT from the left ventricle can present with an RBBB configuration and either a left- or right-axis deviation on the 12-lead electrocardiogram (ECG), depending on the origin.
It is difficult to distinguish this VT from re-entrant fascicular VT by 12-lead ECG. This VT can be induced by exercise and catecholamines (e.g. isoproterenol and phenyrlephline); however, it cannot be induced or terminated by programmed ventricular stimulation. While this VT is responsive to lidocaine and beta-blockers, it is usually not responsive to verapamil. This can be used as a differentiation from verapamil-sensitive fascicular VT. This VT is transiently suppressed by adenosine and with overdrive pacing.
With left anterior fascicular VT, the earliest ventricular activation is recorded from the anterolateral left ventricle, and DPs are recorded from the anterior midseptum (see Figure 3). There have been several reports that describe a left VT with an RBBB configuration, right-axis deviation and a different mechanism. Yeh et al.19 reported four cases with an RBBB configuration and right-axis deviation. This VT was adenosine-sensitive and was successfully ablated from the anterobasal left ventricle. The chest leads exhibited an atypical RBBB configuration with wide 'R' morphology. This VT may be the focal tachycardia from the Purkinje system at the distal anterior fascicle. Crijns et al.20 reported a rare case of interfascicular re-entrant VT with an RBBB configuration and right-axis deviation. In their patient, the VT circuit used the anterior fascicle as the anterograde limb and the posterior fascicle as the retrograde limb. Interfascicular VT usually has a His-bundle potential recorded in the diastolic phase during the VT as well as posterior fascicular potentials. During left anterior fascicular VT, left posterior fascicle activates from proximal to distal as a bystander. However, it may be difficult to distinguish between interfascicular VT and fascicular VT.21 The differential diagnosis of upper septal VT includes supraventricular tachycardias (SVTs) with bifascicular block aberrancy. With left upper septal fascicular VT, the retrograde activation of the His bundle is recorded before the onset of the QRS complex (see Figure 4A). If there is 1 to 1 retrograde ventriculoatrial conduction during the tachycardia, it mimics atrioventricular nodal re-entry tachycardia or atrioventricular reciprocating tachycardia. The response of these tachycardias to verapamil and the ability to initiate and entrain them by atrial pacing may also lead to diagnostic confusion. To avoid a misdiagnosis, recognition of the retrograde sequence of the His-bundle activation and measurement of a shorter His-to-ventricular (HV) interval during the tachycardia than in sinus rhythm is important.
An earlier potential than the His-bundle potential is recorded from the left ventricular upper septum, where the left bundle potential is recorded during sinus rhythm. VT can be slowed or terminated by the intravenous administration of verapamil; however, it is unresponsive to adenosine or the Valsalva manoeuvre. Class IA and IC drugs are also effective. Rare cases of adenosine responsiveness occur, but only if the tachycardia shows catecholamine dependency.
In bundle branch re-entry the His activation precedes activation of the left bundle to produce a RBBB QRS morphology. In idiopathic left fascicular VT, the HV interval is shorter and negative and follows left fascicular activation.
Mapping and Ablation
Radiofrequency (RF) catheter ablation may be considered a potential first-line therapy for patients with fascicular VT because this VT can be eliminated by ablation in a high percentage of patients.
Conventional left ventricular septal mapping using a multipolar electrode catheter is useful in patients with left posterior fascicular VT.12 Two distinct potentials, P1 and P2, can be recorded during the VT from the midseptum (see Figure 2B). Because the DP (P1) has been proved to be a critical potential in the VT circuit, this potential can be targeted to cure the tachycardia. Nakagawa et al.22 first reported the importance of Purkinje potentials in the ablation of this VT, and Tsuchiya et al.23 reported the significance of a late DP and emphasised the role of late diastolic and pre-systolic potentials in the VT circuit. However, the successful ablation sites identified by these two research groups were different. Whereas Nakagawa's ablation sites were at the apical-inferior septum of the left ventricle, Tsuchiya's ablation sites were at the basal septal regions close to the main trunk of the left bundle branch. These findings suggest that any P1 during VT can be targeted for catheter ablation. We usually target the apical third of the septum to avoid the creation of left bundle branch block (LBBB) or atrioventricular block.
In our study, P1 was recorded during the VT in 15 of 20 patients. RF ablation was successfully performed at this site in all 15 patients. During energy application, the P1-P2 interval was gradually prolonged, and the VT was terminated by block between P1 and P2. After termination of the tachycardia, the P1 was noted to occur after the QRS complex during sinus rhythm, whereas the P2 was still observed before the QRS complex. The P1 occurred after the QRS complex during sinus rhythm, with an identical activation sequence to that observed during the VT. When the distal segment of P1 is ablated, the P1 activation proceeds orthodromically around the circuit and subsequently blocks from a proximal to distal direction during sinus rhythm. This explains why P1 appears after ablation in the mid-diastolic period and with the same activation sequence as during the VT. The P1 that appears after ablation exhibits decremental properties during atrial pacing and/or ventricular pacing, and the intravenous administration of verapamil significantly prolongs the His-to-P1 interval during sinus rhythm. Pace mapping at the successful ablation site is usually not good, because the selective pacing of P1 is difficult and there is an antidromic activation of the proximal P1 potential. Pace mapping after successful ablation is sometimes better than before ablation because the antidromic activation of P1 is blocked.21 In the remaining five of our 20 patients, the DP (P1) could not be detected, and a single fused P2 was recorded only at the VT exit site. Successful ablation was performed at this site in all five patients. We can speculate that the circuit in these patients may have involved less of the Purkinje system or that the area of slow conduction may not have been close to the endocardial surface.
Figure 5 shows the position of the schematic fascicular VT circuits and the Purkinje potentials during sinus rhythm. The circuit of the left posterior fascicular VT is shown in Figure 5A. P1 and P2 can be recorded during the VT from the midseptum. This type of VT can be named as left posterior slow-fast-type fascicular VT.
Figure 1B shows the 12-lead ECG of verapamil-sensitive left anterior fascicular VT. Some patients with this VT also have a typical left posterior fascicular VT. Left ventricular endocardial mapping during left anterior fascicular VT can identify the earliest ventricular activation in the anterolateral wall of the left ventricle.24 RF current delivered to this exit site suppresses the VT in half of this type.
The fused Purkinje potential was recorded at this site and preceded the QRS complex by 20-35msec, with pace mapping exhibiting an optimal match between the paced rhythm and clinical VT. In the remaining patients, RF catheter ablation at the exit site was unsuccessful. In these patients, a Purkinje potential was recorded in the diastolic phase during the VT at the midanterior left ventricular septum. The Purkinje potential preceded the QRS during VT by 56-66msec, and catheter ablation at these sites was successful (see Figure 3).
Kottkamp et al.25 reported one patient who had two left VT configurations with right- and left-axis deviation. In this patient, RF catheter ablation delivered to the single site between the left anterior and posterior fascicles successfully eliminated both VTs. This suggests that the anterior limb is the common pathway.
The circuit of proximal type of the left anterior fascicular VT was also shown in Figure 5A. In this circuit, DP represents the activation potential in the proximal portion of the specialised Purkinje tissue with a decremental property. The P represents the activation in the left anterior fascicular the Purkinje fibres near the left anterior fascicle.
During VT, the antegrade limb is the DP and the retrograde limb is the P or septal muscle itself. This type of VT can be named as left anterior slow-fast-type fascicular VT.
Figure 4 shows the intracardiac electrograms of the upper septal fascicular VT. A fused Purkinje potential was recorded at the left posterior fascicular (LPF) area during sinus rhythm (see Figure 4A). During VT, recording at the same site also demonstrated a fused pre-systolic Purkinje potential that preceded the onset of QRS by 20msec. The activation sequences of Purkinje potentials at LPF area are similar during sinus rhythm and VT. This site is one of exit during VT, because a fused pre-systolic ventricular potential was recorded. Furthermore, the other exit site during VT may be the left anterior fascicular area because the QRS morphology during VT is quite narrow and exhibited an inferior axis. This VT was successfully ablated at the left ventricular upper septum (see Figure 4B). At this site, a left bundle branch (LF) potential was recorded during sinus rhythm and the Purkinje potential preceded the QRS by 35msec during the VT.
The RF application eliminated the VT without creating an LBBB or atrioventricular block. The 12-lead ECG configuration in a case reported by Shimoike et al.6 was different from that seen in our groups. Their case showed LBBB configurations and a normal axis during the VT. However, the QRS width was narrow, and the successful ablation site was similar to our groups.
The hypothesised circuit of the upper septal fascicular VT is depicted in Figure 5B. In this circuit, DP represents the activation potential of the specialised Purkinje tissue at the left ventricular upper septum. P represents the activation of the left fascicles or Purkinje fibre near the left fascicles. Both left anterior and posterior fascicles are the antegrade limbs of the re-entrant circuit in VT. This explains why this VT exhibits a narrow QRS configuration and inferior axis. DP represents the common retrograde limb of the circuit in VT and can be the ablation target. This type of VT can be named as fast-slow-type fascicular VT.
The End-point of Ablation
We deliver RF energy during the tachycardia of left posterior and anterior fascicular VTs. If the VT is terminated or slowed within 15 seconds, additional current is applied for another 60-120 seconds. If the test RF current is ineffective, ablation is directed to a more proximal site with the earlier DP. If the mid-DP cannot be detected with upper septal fascicular VT, we deliver RF energy for 30-60 seconds during sinus rhythm to avoid atrioventricular block. We perform catheter ablation in this region using a low power output (i.e. 10W), which can gradually be increased while carefully monitoring for development of a junctional rhythm or atrioventricular block.
After the ablation, programmed stimulation should be repeated. Other than the non-inducibility of VT, there are several electrophysiological findings that can serve as end-points of RF applications for left posterior fascicular VT. After ablation of the distal attachment between P1 and P2, P1 appears after the QRS complex. However, this phenomenon is not sufficient for an end-point because it only indicates conduction block in the direction from P2 to P1.
This unidirectional block can be seen during the baseline state24 or after an insufficient RF application.21 To confirm the creation of bi-directional block between P1 and P2, we perform atrial pacing with various cycle lengths after the ablation. If there is residual conduction from P1 to P2, a premature ventricular complex (i.e. ventricular echo beat) with a similar QRS morphology to that observed during the VT can be repeatedly observed.
Our experience at the time of writing includes 76 patients with left posterior fascicular VT, 12 patients with left anterior fascicular VT and two patients with left upper septal fascicular VT. The success and recurrence rates are, respectively, 97 and 4% for left posterior fascicular VT, 92 and 8% for left anterior fascicular VT and 100 and 0% for left upper septal fascicular VT.
Apart from the complications that may result from any left ventricular electrophysiological procedure (e.g. thrombophlebitis, damage to the femoral artery, ventricular perforation), the only complication that has been associated with catheter ablation of idiopathic left VT has been LBBB and atrioventricular block. Tsuchiya et al.23 reported that two patients (12.5%) had transient LBBB after ablation in their series of 16 patients. They targeted the left basal septum, and the LBBB disappeared within 10 minutes without VT recurrence. In our experience, one of 90 patients (1.1%) had a transient atrioventricular block. This patient had a left posterior fascicular VT, and the DP (P1) at the midseptum was targeted for the ablation. Before the ablation, the patient had catheter-induced RBBB. Approximately 15 seconds into the RF delivery, the VT terminated and second-degree atrioventricular block was observed. The atrioventricular block disappeared immediately after discontinuation of the RF-energy delivery.
The inability to reliably induce VT is a formidable obstacle to successful ablation. Isoproterenol enhances or facilitates induction of sustained VT in 60-70% of those patients without inducible sustained VT at baseline. In some patients, the administration of a low dose of class IA drug enhances the slow conduction at the specialised Purkinje tissue and facilitates induction of stable sustained VT. Catheter mapping sometimes mechanically suppresses the conduction in the VT circuit ('bump' phenomenon).
In such cases, a ventricular echo beat during sinus rhythm or atrial pacing is useful. If premature ventricular complexes with a similar QRS morphology to that observed during the VT are repeatedly seen, activation mapping can be performed. If no ventricular echo beats are inducible, the empirical anatomical approach can be an effective strategy for ablation of left posterior fascicular VT.26 First, the VT exit site is sought by pace mapping during sinus rhythm, and RF energy is delivered to that site. Second, a linear lesion is placed at the midseptum, perpendicular to the long axis of the left ventricle, approximately 10-15mm proximal to the VT exit. During anatomical linear ablation, P1 suddenly appears after the QRS complex if the ablation site is on the descending limb of the VT circuit. This anatomical approach is also useful in patients in whom diastolic Purkinje potential cannot be recorded during VT.
Idiopathic left fascicular tachycardia actually consists of multiple discrete subtypes that are best differentiated by their mechanism, VT morphology and the successful ablation site. In re-entrant fascicular VT, diastolic and pre-systolic Purkinje potentials are recorded; however, the earliest Purkinje potential is not needed for ablation. Recognition of the heterogeneity of this VT and its unique characteristics should facilitate appropriate diagnosis and therapy.