ReviewNew Insights on Verapamil-Sensitive Idiopathic Left Fascicular Tachycardia
Introduction
Verapamil-sensitive left fascicular monomorphic ventricular tachycardia (LF-VT) is a Purkinje-related arrhythmia mainly occurring in patients with structurally normal heart [1,2]. Underlying mechanism is assumed to be reentry in most cases [1,3] while non-reentrant mechanism is rarely involved [4]. Although the first case was reported in a young white man by Belhassen et al. [5], the arrhythmia largely prevails in South East Asia [2,6]. The most common type called “Belhassen VT” [5,7] exits near the left posterior fascicle (LPF) and exhibits a morphology of right bundle branch block (RBBB) and left axis deviation. Less often LF-VT may exit near the left anterior fascicle [8] or involve the septal fascicle. LF-VT is frequently induced by atrial as well as right ventricular (RV) or left ventricular (LV) stimulation [9]. When indicated, ablation is usually a highly effective treatment [10,11]. In the current mini review our aim is to highlight new aspects of this arrhythmia including its ECG recognition, new understandings about the reentrant circuit, ablation targets in inducible and non-inducible patients and the approach to LF-VT with multiform morphology.
Section snippets
ECG recognition of LPF VT
LPF-VT, the most common type of LF-VT is frequently misdiagnosed as supraventricular tachycardia with RBBB and left anterior hemiblock aberrancy especially when capture, fusion beats or atrioventricular (AV) dissociation are not seen [12,13]. Recently, our group described 4 variables that may help distinguishing the QRS morphology of LPF-VT from aberrancy (Fig. 1). Atypical V1 morphology (no rsR', or R larger than R'), QRS width ≤ 140 ms, R/S ratio ≤ 1 and positive aVR were associated with the
The reentrant circuit
In their seminal work [16], Nogami and colleges showed that in 75% of patients with LPF-VT a diastolic potential “P1”, involving abnormal Purkinje tissue showing decremental properties and Verapamil sensitivity, can be recorded. A second presystolic potential (P2 or LPF potential) with a distal to proximal activation may also be recorded during VT. Thus, initially it was proposed that the abnormal Purkinje tissue (P1) serves as an antegrade limp and the LPF serves as the retrograde limb of the
EP study and ablation (Table 1)
As already mentioned LF-VT can be induced by atrial as well as RV or LV extra-stimulus pacing [9]. The usual targets for ablation include either the diastolic potential (P1) or the earliest presystolic P2 potential [1,16]. Since it is a macro reentrant circuit there is usually >1 target that may lead to successful ablation [1,16]. However, ablation is usually performed at the mid to distal two thirds of the septum to avoid the risk of damaging the left bundle branch system or the AV node when
Multiform morphology
LF-VT usually presents with a single ECG morphology, however 5–30% of cases may manifest changing QRS morphology [[38], [39], [40], [41]]. This change in morphology may occur spontaneously or be related to ablation or catheter induced mechanical injury to one of the fascicles. Mechanisms of multiform morphology include a completely new reentrant circuit [39], ablation of a proximal connection between P1 and P2 with continued reentrant circuit using a more distal connection between P1 and P2
In conclusion
Since the initial description of LPF-VT [5,43] our understanding of this fascinating arrhythmia continues to evolve in terms of its ECG recognition, its mechanism and in treating the common as well as the uncommon and multiform fascicular arrhythmia.
8 major references dealing with the present review
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Belhassen B, Shapira I, Pelleg A, Copperman I, Kauli N, Laniado S. Idiopathic recurrent sustained ventricular tachycardia responsive to verapamil: an ECG-electrophysiologic entity. Am Heart J. 1984;108:1034–7.
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Ohe T, Shimomura K, Aihara N, Kamakura S, Matsuhisa M, Sato I, et al. Idiopathic sustained left ventricular tachycardia: clinical and electrophysiologic characteristics. Circulation. 1988;77:560–8. Erratum in: Circulation 1988;78:A5
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Nakagawa H, Beckman KJ, McClelland JH, Wang X, Arruda M,
Disclosure
None.
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