Chapter 24 Verapamil-Sensitive (Fascicular) Ventricular Tachycardia

Pathophysiology

Verapamil-sensitive left ventricular tachycardia (LV VT) is a reentrant tachycardia. The diagnosis of reentry as the mechanism of fascicular VT is supported by several observations. The VT can reproducibly be initiated and terminated by programmed electrical stimulation, entrainment and resetting with fusion can be demonstrated, and an inverse relationship between the coupling interval of the initiating ventricular extrastimulus (VES) or ventricular pacing cycle length (CL) and the first VT beat can be observed.

The exact nature of the reentry circuit in verapamil-sensitive VT has provoked considerable interest. Some investigators have suggested that it is a microreentry circuit in the territory of the left posterior fascicle (LPF). Others have suggested that the circuit is confined to the Purkinje system, which is insulated from the underlying ventricular myocardium. False tendons or fibromuscular bands that extend from the posteroinferior LV to the basal septum have also been implicated in the anatomical substrate of this tachycardia. Less often, the reentry circuit is located in fibers distal to the left anterior fascicle (LAF) or may arise from fascicular locations high in the septum.¹

Currently, overwhelming evidence suggests that the VT is caused by a reentrant circuit incorporating the posterior Purkinje system with an excitable gap and a slow conduction area.²^–⁴ The VT substrate can be a small macroreentrant circuit consisting of the LPF serving as one limb and abnormal Purkinje tissue with slow, decremental conduction serving as the other limb. The anterograde limb may be associated with longitudinal dissociation of the LPF or contiguous tissue that is directly coupled to the LPF (such as a false tendon) or, alternatively, has ventricular myocardium interposed. The zone of slow conduction appears to depend on the slow inward calcium current, because the degree of slowing of tachycardia CL in response to verapamil is entirely attributed to its negative dromotropic effects on the area of slow conduction.

The entrance site to the slow conduction zone is thought to be located closer to the base of the LV septum. From there, activation propagates anterogradely (from basal to apical along the LV septum) over the abnormal Purkinje tissue with decremental conduction properties and verapamil sensitivity, which serves as the anterograde limb of the circuit and appears to be insulated from the nearby ventricular myocardium. The lower turnaround point of the reentrant circuit is located in the lower third of the septum, where the wavefront captures the fast conduction Purkinje tissue from or contiguous to the LPF, and retrograde activation occurs over the LPF from the apical to basal septum forming the retrograde limb of the reentrant circuit. Also, at the lower turnaround point anterograde activation occurs down the septum to break through (at the exit of the tachycardia circuit) in the posterior septal myocardium below. The upper turnaround point of the reentrant circuit occurs over a zone of slow conduction located close to the main trunk of the left bundle branch (LB) in the basal interventricular septum (Fig. 24-1). The estimated distance between the entrance and exit of the circuit is approximately 2 cm.^3,⁵

FIGURE 24-1 Schematic illustration of the reentrant circuit in verapamil-sensitive left ventricular tachycardia (LV VT). A block of the LV septum is depicted with the left posterior fascicle (LPF) and diastolic pathway (DP) running in parallel until they intersect at the bottom. A 10-pole catheter is shown recording between pathways; electrograms from each pair are shown along with surface ECG leads and His bundle recordings. A, A sinus rhythm complex is shown; the dashed line denotes QRS onset. Note the direction and speed of propagation over the LPF while the DP is activated after the QRS and in both directions (arrows). B, During a VT complex, the DP is activated anterogradely and the LPF retrogradely (arrows). NSR = normal sinus rhythm. See text for discussion.

Clinical Considerations

Epidemiology

Age at presentation is typically 15 to 40 years (unusual after 55 years). Males are more commonly affected (60% to 80%). Verapamil-sensitive VT is the most common form of idiopathic LV VT, and it accounts for 10% to 15% of all idiopathic VTs.^2,⁶

Clinical Presentation

Most patients present with mild to moderate symptoms of palpitations and lightheadedness. Occasionally, symptoms are debilitating, and include fatigue, dyspnea, and presyncope. Syncope and sudden cardiac death are very rare. The VT is typically paroxysmal and can last for minutes to hours. Although idiopathic LV VT can occur at rest, it is sensitive to catecholamines and often occurs during exercise, after exercise, or emotional distress. Occasionally, the VT can be incessant, may be sustained for a long period (days), and does not revert spontaneously to normal sinus rhythm (NSR). Patients with incessant tachycardia can develop cardiomyopathy.⁷ The clinical course is benign and the prognosis is excellent. Spontaneous remission of the VT may occur with time.

Initial Evaluation

Diagnostic features of fascicular VT include induction with atrial pacing, right bundle branch block (RBBB) with left (or, less commonly, right) axis deviation, structurally normal heart, and verapamil sensitivity. Evaluation to exclude structural heart disease is necessary and typically includes echocardiographic examination, stress testing, and/or cardiac catheterization, depending on patient age and risk factors.

Electrocardiographic Features

ECG during Normal Sinus Rhythm

The resting ECG is usually normal. Symmetrical, inferolateral T wave inversion can be present after termination of the VT.

ECG during Ventricular Tachycardia

The QRS during VT typically has RBBB with LAF block configuration. The R/S ratio is less than 1 in leads V₁ and V₂ (Fig. 24-2).³ VTs arising more toward the middle at the region of the posterior papillary muscle have a left superior axis and RS in leads V₅ and V₆, whereas those arising closer to the apex have a right superior axis with a small “r” and deep S (or even QS) in leads V₅ and V₆. In contrast to VT associated with structural heart disease, the QRS duration during fascicular VT is relatively narrow (<140 to 150 milliseconds), and the RS interval (the duration from the beginning of the QRS to the nadir of the S wave) in the precordial leads is relatively short (60 to 80 milliseconds); thus, the VT is frequently called “fascicular” VT. The VT rate is approximately 150 to 200 beats/min (range, 120 to 250 beats/min). Alternans in the CL is frequently noted during the VT; otherwise, the VT rate is stable.