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Fascicular ventricular tachycardia (VT) represents a subset of the idiopathic left ventricular tachycardias (ILVT). Fascicular VT is an uncommon but well-studied ventricular arrhythmia that has several characteristic features: (1) a verapamil-sensitive mechanism, (2) induction with atrial pacing, (3) occurrence in patients without structural heart disease.1 These tachycardias also have an excellent prognosis and thus do not require an implantable cardioverter-defibrillator after a successful ablation.² Given its origin in the fascicles of the left ventricle, each subtype of ventricular tachycardia has a characteristic electrocardiogram (ECG) morphology¹ and can be classified as:

1. Left posterior fascicular VT (LPF VT)—right bundle branch block (RBBB) with left-axis deviation (common form)

2. Left anterior fascicular VT (LAF VT)—RBBB with right-axis deviation (uncommon form)

3. Left upper septal fascicular VT (Septal VT) – narrow QRS and normal frontal-plane axis (rare form)

Although a number of studies have demonstrated the presence of mid and late diastolic potentials during VT, the presence of a slow conduction zone during entrainment, and the presence of constant and progressive fusion,^3–8 not all fascicular tachycardias demonstrate features of a reentrant mechanism.^9,10 As a result, one should not assume that a fascicular tachycardia is purely dependent upon a microreentrant and/or macroreentrant circuit involving the Purkinje network. Focal fascicular ventricular tachycardias produce a centrifugal pattern of activation from a focal fascicular source. These focal tachycardias fail to satisfy criteria of a reentrant arrhythmia with entrainment.

Recently, multiform fascicular tachycardias with an interfascicular reentrant mechanism have also been described.^11–14 Fortunately, the electrocardiogram (ECG) morphology of these multiform VTs is based on the fascicular circuit(s) involved and can be elucidated with a combination of fascicular potential mapping and entrainment pacing. Defining the mechanisms and circuits of fascicular tachycardias has led to an improved understanding of the ideal ablation targets and a long-term success rate of > 95% with a single ablation.¹⁵

Preprocedural Planning

Since by definition fascicular VTs occur in patients without structural heart disease, standard preprocedural planning involves screening with a history and physical, imaging, and work-up to exclude structural or ischemic heart disease. Since a retrograde aortic approach is commonly taken to access the left ventricle for mapping and ablation, the presence of significant peripheral vascular or aortic disease should be identified as well. If anatomic considerations or coexistent medical conditions preclude retrograde aortic access, an antegrade transseptal approach can be pursued. If possible, all antiarrhythmic medications are stopped at least 5 half-lives prior to the procedure.

Reviewing the electrocardiogram (ECG) morphology of the VT serves to confirm the diagnosis as well as to plan on the approaches of endocardial mapping and ablation. Both LPF and LAF VTs have proximal and distal subtypes corresponding to the exit site of the VT along the proximal or distal aspect of the respective fascicle. Nogami and colleagues have shown that the LAF proximal subtype (midseptal exit site) is characterized by a “RS” or “Rs” morphology in leads I, V₅, and V₆, whereas the LAF distal subtype (anterolateral wall exit site) manifests a “QS” or “rS” morphology in those leads6 (Figure 38.1). Unfortunately, the proximal and distal subtypes of LPF VT cannot be distinguished by QRS morphology variations, so they are distinguished by the location of the late diastolic potentials during LV endocardial mapping. The LPF proximal subtype is characterized by late diastolic potentials in the basal-mid inferior septum, whereas the LPF distal subtype has late diastolic potentials found in the apical inferior septum.

Procedure

Patient Preparation

Most patients presenting for electrophysiology study and ablation of fascicular VTs are generally healthy without significant comorbid illnesses, and unless otherwise indicated, conscious sedation or monitored anesthesia care are preferred methods of analgesia. In addition, some fascicular VTs occur in the setting of exercise or heightened sympathetic tone, which may be inhibited with the use of general anesthesia.

For vascular access, we place a decapolar coronary sinus catheter from the right internal jugular vein, a quadripolar catheter to the high right atrium (HRA), a quadripolar catheter to the His bundle, and a quadripolar catheter to the right ventricular apex (RVA) through the femoral vein. The high right atrial catheter can be moved to the right ventricular outflow tract (RVOT) after an atrial burst pacing and extrastimulus protocol are completed. The right femoral artery is used for placement of an 8-Fr sheath through which a bidirectional 7-Fr, 4-mm quadripolar ablation catheter with 2-mm distal electrode spacing is navigated to the left ventricle (LV) via retrograde aortic access. Given that patients with fascicular VTs lack significant pathologic LV dilatation, an ablation catheter that has a medium-size curve is usually sufficient for LV mapping/ablation. Once arterial access is obtained, an intravenous bolus of unfractionated heparin at a dose of 70 U/kg is given and an infusion at 1000 U/hr is started. Additional heparin boluses and adjustment of the heparin infusion are titrated for a goal ACT of 250–350 seconds measured every 15 minutes.

Diagnosis

Baseline electrophysiology measurements are obtained. Then, burst pacing and programmed electrical stimulation with up to 3 extrastimuli at twice diastolic threshold and a 2 millisecond (ms) pulse width are initiated from the HRA, RVA, and the LV. Burst pacing is usually pursued up to a minimum cycle length of 200 ms. The HRA catheter can be moved to the RVOT if VT cannot be initiated from the RVA and LV. If VT is still not induced, an isoproterenol infusion is started and the same protocol is repeated. The isoproterenol infusion is titrated up to (10 mcg/min) in order to achieve a goal 20% increase in heart rate.

The reentrant circuit of fascicular VT was elegantly described by Nogami and colleagues4 (Figure 38.2). The orthodromic limb is hypothesized to be an accessory Purkinje fiber or a branch of the Purkinje network demonstrating decremental conduction and verapamil-sensitivity. This limb of the VT circuit is oriented parallel to the fascicle with/without an intervening myocardial bridge to the antidromic limb of the circuit, with the antidromic limb being the fascicle itself. Thus, during sinus rhythm, Purkinje potentials (PP) are noted to proceed in a basal to apical activation pattern with the distal PP demonstrating fusion with the earliest ventricular activation (VT exit site). Conversely, during VT, late diastolic potentials (DP) can be visualized to proceed in a basal to apical activation pattern with Purkinje potentials demonstrating a distal to proximal activation pattern (Figure 38.3).

Once ventricular tachycardia is induced, several diagnostic maneuvers are employed to confirm the diagnosis of fascicular VT and to define the location of the circuit. First, Purkinje potentials and diastolic potentials preceding ventricular activation (V) are mapped. Second, changes in the PP-PP and DP-DP intervals should precede changes in the V-V intervals. Third, in the case of LPF and LAF tachycardias, His activation should follow the QRS onset. In left upper septal fascicular VT, a short HV interval is present. This short HV interval during VT will be shorter than the HV interval during sinus rhythm. Careful mapping can also reveal the presence of a left bundle branch potential prior to the His potential during VT (Figure 38.4). Finally, the tachycardia should demonstrate entrainment with ventricular and/or atrial pacing.

Entrainment from the RVA or the RVOT is favored for the demonstration of constant and progressive fusion (Figure 38.5). In addition, as the pacing rate is increased, a prolongation of the stimulus-DP interval should be identified. During entrainment, we seek to identify constant and progressive fusion as well as changes in the stimulus-DP interval or DP-PP interval in order to prove that the diastolic potential is in a zone of slow conduction critical to maintenance of the tachycardia.

If a suitable diastolic potential cannot be mapped, pacing from the VT exit site can be used to demonstrate concealed entrainment. In addition, a postpacing interval (PPI) – tachycardia cycle length (TCL) of < 20 ms confirms that the VT exit site is within the circuit of the tachycardia. As pacing rates are progressively increased, there is an increase in the stimulus to DP interval, thus demonstrating decremental conduction of the VT slow conduction zone (Figure 38.6). With continued decremental pacing, eventually the tachycardia should terminate upon cessation of pacing, thus, providing evidence for the upper limit of the excitable gap.

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