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A Case of Narrow Ventricular Tachycardia
Fascicular ventricular tachycardia is often confused with supraventricular tachycardia because of its relatively narrow QRS and termination with verapamil. Prompt recognition of this arrhythmia is necessary because it is curable with catheter ablation. In this case report, the author revises the key features to successfully diagnose and treat this arrhythmia.
lightheadedness. A 12-lead ECG showed a tachycardia with right bundle morphology, QRS width of 120 ms, and left superior axis with a cycle length of 280 ms (Figure 1). Adenosine 6 mg and amiodarone 150 mg failed to terminate this rhythm, but a 200 J cardioversion restored sinus rhythm.
A heart catheterization revealed normal coronary arteries. Transthoracic echocardiogram was also unrevealing.
Induction of the arrhythmia during atrial pacing is shown in Figures 2 and 3. Atrial and ventricular pacing during tachycardia is shown in Figures 4 and 5, respectively. What is the mechanism of this tachycardia?
width less than 140 ms, double peak R wave in V1 with a taller left peak) and also VT (R
fusion, dissociating the His bundle and atrial electrogram from the ventricular activation (Figure 4), which is diagnostic of VT. Electrocardiographic recognition of RBB and left superior axis morphology is characteristic of fascicular VT, but it is not sufficient to make the diagnosis. Electrophysiology pacing maneuvers are necessary to correctly make the diagnosis (Figure 5). Pacing from left ventricular mid apical septum produced entrainment with concealed fusion, and post-pacing interval minus VT cycle length difference was within 30 ms, indicating the ventricular septum was within the arrhythmia circuit (not shown). Induction of tachycardia occurred with atrial 
pacing (Figure 3). The constellation of all these features makes fascicular VT the most likely diagnosis.
Arrhythmia Mechanism. The mechanism of fascicular VT is presumably reentry. Zipes et al1 postulated that such a narrow ventricular rhythm would originate near the posterior fascicle of the left bundle. The reentrant circuit is composed of a verapamil-sensitive zone, activated anterogradely, and the fast conduction purkinje fibers activated retrogradely recorded as the pre-purkinje and the purkinje potentials, respectively, with the turnaround site in the lower third of the septum. QRS axis depends of the fascicle involved. More often a left axis deviation is observed (i.e., the posterior fascicle is involved). A third form, normal axis fascicular VT, has been described.2 Catheter mapping reveals earliest activation site at the mid and apical ventricular septum and the tachycardia may be induced, entrained and terminated with atrial pacing due to proximity of the circuit to the conduction system (Figure 5). This tachycardia is usually paroxysmal and affects young males (15 to 40 years old).3 It has been characterized by its termination with verapamil (i.e., “verapamil sensitive”).4Differential Diagnosis. Fascicular VT is frequently misdiagnosed as supraventricular tachycardia with aberrancy because of the narrow QRS duration during tachycardia (120 ms), responsiveness to intravenous verapamil, and the occurrence in young patients with structurally normal hearts. Other ventricular arrhythmias in the differential are interfascicular VT, LVOT and LV aortic cusp VT.
Interfascicular VT has a typical RBBB morphology and left or right axis deviation during VT, mimicking fascicular VT. However, interfascicular VT is most commonly seen in patients with an anterior infarction and either left anterior or posterior fascicular block.5 During EP study, the ventricular depolarization is preceded by His bundle depolarization, i.e., positive HV interval, which is not seen in fascicular VT (negative HV interval). The circuit goes down the LBBB and one of the fascicles and up the blocked fascicle. Spontaneous oscillations in the ventricular tachycardia cycle length are preceded by changes in the LB-LB (left bundle) interval. Interfascicular VT terminates with ventricular extrastimuli or RF ablation that produces block in LAF or LPF.
Idiopathic LVOT and aortic cusp VTs are triggered arrhythmias with inferior axis, early R wave transition in the precordial leads. Idiopathic mitral annulus VTs tend to have a wider RBBB morphology with R waves until V6, allowing a confident diagnosis using only the surface ECG.
Catheter Ablation. Catheter ablation in this young group of patients is a very attractive therapy. Success is over 80%, with infrequent complications plus the benefit of avoiding long-term adverse drug reactions.6
Ablation can be performed during tachycardia by targeting the rapid purkinje potentials or the slow pre-purkinje potentials. Because the proximity of the pre-purkinje potentials to the LBB and His bundle, targeting the rapid purkinje potentials is usually desirable.6,7
In this case a purkinje potential was targeted and ablated (Figure 6). Application of RF energy at this site terminated the tachycardia in 5.2 seconds.
Fascicular VT is easily catheter bump terminated and it might not be induced again during the case. Thus, ablation may need to be done during sinus rhythm. A perpendicular ablation line around the inferoposterior septum or ablation targeting the purkinje potentials in the 2/3 inferior septum is usually successful.
Introduction
A 50-year-old man presented to the emergency department with palpitations and
lightheadedness. A 12-lead ECG showed a tachycardia with right bundle morphology, QRS width of 120 ms, and left superior axis with a cycle length of 280 ms (Figure 1). Adenosine 6 mg and amiodarone 150 mg failed to terminate this rhythm, but a 200 J cardioversion restored sinus rhythm.
A heart catheterization revealed normal coronary arteries. Transthoracic echocardiogram was also unrevealing.
Induction of the arrhythmia during atrial pacing is shown in Figures 2 and 3. Atrial and ventricular pacing during tachycardia is shown in Figures 4 and 5, respectively. What is the mechanism of this tachycardia?
Discussion
Diagnosis. Differential diagnosis of a wide QRS tachycardia includes supraventricular tachycardia with aberration, preexcited tachycardia, intraventricular conduction disturbances, paced rhythms, and ventricular tachycardia (VT). Analysis of the electrocardiogram was not conclusive. P waves were visible and there was atrio-ventricular association (Figures 1 and 2). QRS morphological criteria had features of both SVT (QRS
width less than 140 ms, double peak R wave in V1 with a taller left peak) and also VT (Rfusion, dissociating the His bundle and atrial electrogram from the ventricular activation (Figure 4), which is diagnostic of VT. Electrocardiographic recognition of RBB and left superior axis morphology is characteristic of fascicular VT, but it is not sufficient to make the diagnosis. Electrophysiology pacing maneuvers are necessary to correctly make the diagnosis (Figure 5). Pacing from left ventricular mid apical septum produced entrainment with concealed fusion, and post-pacing interval minus VT cycle length difference was within 30 ms, indicating the ventricular septum was within the arrhythmia circuit (not shown). Induction of tachycardia occurred with atrial 
pacing (Figure 3). The constellation of all these features makes fascicular VT the most likely diagnosis.
Arrhythmia Mechanism. The mechanism of fascicular VT is presumably reentry. Zipes et al1 postulated that such a narrow ventricular rhythm would originate near the posterior fascicle of the left bundle. The reentrant circuit is composed of a verapamil-sensitive zone, activated anterogradely, and the fast conduction purkinje fibers activated retrogradely recorded as the pre-purkinje and the purkinje potentials, respectively, with the turnaround site in the lower third of the septum. QRS axis depends of the fascicle involved. More often a left axis deviation is observed (i.e., the posterior fascicle is involved). A third form, normal axis fascicular VT, has been described.2 Catheter mapping reveals earliest activation site at the mid and apical ventricular septum and the tachycardia may be induced, entrained and terminated with atrial pacing due to proximity of the circuit to the conduction system (Figure 5). This tachycardia is usually paroxysmal and affects young males (15 to 40 years old).3 It has been characterized by its termination with verapamil (i.e., “verapamil sensitive”).4Differential Diagnosis. Fascicular VT is frequently misdiagnosed as supraventricular tachycardia with aberrancy because of the narrow QRS duration during tachycardia (120 ms), responsiveness to intravenous verapamil, and the occurrence in young patients with structurally normal hearts. Other ventricular arrhythmias in the differential are interfascicular VT, LVOT and LV aortic cusp VT.
Interfascicular VT has a typical RBBB morphology and left or right axis deviation during VT, mimicking fascicular VT. However, interfascicular VT is most commonly seen in patients with an anterior infarction and either left anterior or posterior fascicular block.5 During EP study, the ventricular depolarization is preceded by His bundle depolarization, i.e., positive HV interval, which is not seen in fascicular VT (negative HV interval). The circuit goes down the LBBB and one of the fascicles and up the blocked fascicle. Spontaneous oscillations in the ventricular tachycardia cycle length are preceded by changes in the LB-LB (left bundle) interval. Interfascicular VT terminates with ventricular extrastimuli or RF ablation that produces block in LAF or LPF.
Idiopathic LVOT and aortic cusp VTs are triggered arrhythmias with inferior axis, early R wave transition in the precordial leads. Idiopathic mitral annulus VTs tend to have a wider RBBB morphology with R waves until V6, allowing a confident diagnosis using only the surface ECG.
Catheter Ablation. Catheter ablation in this young group of patients is a very attractive therapy. Success is over 80%, with infrequent complications plus the benefit of avoiding long-term adverse drug reactions.6
Ablation can be performed during tachycardia by targeting the rapid purkinje potentials or the slow pre-purkinje potentials. Because the proximity of the pre-purkinje potentials to the LBB and His bundle, targeting the rapid purkinje potentials is usually desirable.6,7
In this case a purkinje potential was targeted and ablated (Figure 6). Application of RF energy at this site terminated the tachycardia in 5.2 seconds.
Fascicular VT is easily catheter bump terminated and it might not be induced again during the case. Thus, ablation may need to be done during sinus rhythm. A perpendicular ablation line around the inferoposterior septum or ablation targeting the purkinje potentials in the 2/3 inferior septum is usually successful.
Conclusion
Fascicular ventricular tachycardia is usually misdiagnosed as supraventricular tachycardia. Prompt diagnosis of this arrhythmia is necessary, because if recognized, it is curable with catheter ablation.References
- Zipes DP, Foster PR, Troup PJ, Pedersen DH. Atrial induction of ventricular tachycardia: Reentry versus triggered automaticity. Am J Cardiol 1979;44:1–8.
- Nogami A. Idiopathic left ventricular tachycardia: Assessment and treatment. Card Electrophysiol Rev 2002;6:448–457.
- Ohe T, Aihara N, Kamakura S, et al. Long-term outcome of verapamil-sensitive sustained left ventricular tachycardia in patients without structural heart disease. J Am Coll Cardiol 1995;25:54–58.
- Belhassen B, Rotmensch HH, Laniado S. Response of recurrent sustained ventricular tachycardia to verapamil. Br Heart J 1981;46:679–682.
- Lopera G, Stevenson WG, Soejima K, et al. Identification and ablation of three types of ventricular tachycardia involving the his-purkinje system in patients with heart disease. J Cardiovasc Electrophysiol 2004;15:52–58.
- Klein LS, Shih MH-T, Hackett MFK, et al. Radiofrequency catheter ablation of ventricular tachycardia in patients without structural heart disease. Circulation 1992;85:1666–1674.
- Arya A, Haghjoo M, Emkanjoo Z, et al. Comparison of presystolic purkinje and late diastolic potentials for selection of ablation site in idiopathic verapamil sensitive left ventricular tachycardia. J Interv Card Electrophysiol 2004;11:135–141.
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