Idiopathic Ventricular Tachycardias

These tachycardias usually occur in patients who do not have other structural heart disease, and have a focal origin (6-8). The prognosis is good—sudden death is very rare, but symptoms can be severe. Occasionally tachycardia is incessant, and causes

Table 2

Catheter Ablation of VT Definition of Terms

Types of VT

Focal Origin

Tachycardia originates from a small focus, usually not associated with scar. The QRS morphology is a good indicator of the location of the focus and type of tachycardia.

Bundle-branch reentry

Tachycardia caused by circulation of the excitation wavefront down one bundle branch, through the interventricular septum, and up the contralateral bundle branch to complete the circuit.

Scar-Related reentry

Tachycardia caused by circulation of the excitation wavefront through and around regions bordered by scar, often from prior MI.



The process of localizing the source of the tachycardia, usually by moving an electrode catheter around the ventricles.

Activation Sequence Mapping

Recording activation during tachycardia at multiple sites to determine the pattern of ventricular activation. Focal-origin tachycardias can be located by identifying the earliest site of activation.


Pacing from the mapping catheter during sinus rhythm and comparing the resulting QRS morphology to that of the VT. For focal-origin tachycardias pacing at or near the tachycardia focus produces a QRS morphology identical to that of the tachycardia.

Entrainment Mapping

Pacing from the mapping catheter during tachycardia. The effect of pacing can be analyzed to determine the proximity of the pacing site to the tachycardia circuit.

dilated cardiomyopathy. This tachycardia-induced cardiomyopathy may resolve if the tachycardia is suppressed before irreversible left ventricular dilation has occurred (9,10).

Idiopathic RVOT Tachycardia

The most common IVT originates from a focus in the outflow tract of the right ventricle (7,11-13) (Fig. 2). This tachycardia has LBBB configuration in ECG lead V1. The frontal plane axis is directed inferiorly or inferiorly and to the right. Tall monophasic R-waves are present in leads II, III, and AVF. Tachycardia may occur in repetitive bursts (referred to as repetitive monomorphic ventricular tachycardia) (14). Sustained episodes are often precipitated by exercise or emotion. Unifocal premature ventricular contractions (PVCs) with a morphology identical to that of the tachycardia are often present during sinus rhythm. In some patients, the premature beats are severely symptomatic and warrant therapy (15). This tachycardia is most likely caused by a form of automaticity linked to intracellular calcium increases that provoke spontaneous depolarizations known as after-depolarizations (13,14). Initiation often requires bursts of rapid pacing and/or administration of isoproterenol, and usually terminates in response to administration of adenosine (13). Although evidence of heart disease by echocardio-gram, electrocardiogram (ECG), and angiography is generally absent, the possibility of a focal structural abnormality is suggested by one study in which cardiac magnetic resonance imaging (MRI) identified focal areas of thinning, hypokinesis, or fatty infiltration (16). The major differential diagnosis is arrhythmogenic right ventricular dysplasia.

Fig. 2. Two different IVTs. Both have a LBBB configuration and frontal plane axis directed inferiorly, consistent with an origin in the RVOT. The tachycardia in (A) was successfully ablated from the RVOT. Ablation in the RVOT failed to interrupt the tachycardia in (B). This tachycardia has an initial prominent R-wave in V1 (arrow), suggesting a more leftward origin (see text).

Fig. 2. Two different IVTs. Both have a LBBB configuration and frontal plane axis directed inferiorly, consistent with an origin in the RVOT. The tachycardia in (A) was successfully ablated from the RVOT. Ablation in the RVOT failed to interrupt the tachycardia in (B). This tachycardia has an initial prominent R-wave in V1 (arrow), suggesting a more leftward origin (see text).

Right ventricular dysplasia is suggested by multiple morphologies of VT, usually with a LBBB-type configuration, because of reentry (as assessed in the electrophysiology laboratory). Idiopathic tachycardia is often controlled by chronic therapy with verapamil, diltiazem, or beta-blockers. Catheter ablation is a reasonable consideration when phar-macologic therapy is not effective.

Catheter ablation targets the focus. Isoproterenol combined with ventricular pacing is often required for initiation. If VT or frequent premature ventricular contractions (PVCs) are present, activation-sequence mapping can be used to locate the focus. During sinus rhythm, pace-mapping can be used to attempt to locate the arrhythmia focus. Sites which pacing exactly reproduces the tachycardia QRS morphology are at or near the arrhythmia focus. Ablation is successful in approx 85% of patients (7,11,17-20). Failures occur because of two major problems. The first is an inability to reproducibly provoke the tachycardia in the electrophysiology laboratory, preventing adequate localization. The second problem is the occasional location of the focus deep within the septum, or possibly epicardial over the septum, where ablation from the endocardial surface is difficult. Occasionally, ablation from the left side of the interventricular septum is effective (21). Electrocardiographic findings suggestive of an atypical location and lower likelihood of success include a slurred downstroke of the S-wave in lead V1 and a large initial r-wave in lead V1 or V2 (7,11) (Fig. 2, panel B). Complications are rare, but fatal cardiac perforation has been reported (18). Rare cases of coronary-artery occlusion during radiofrequency ablation in the left ventricular outflow tract (LVOT) have also been reported (22).

Idiopathic Left Ventricular, Verapamil-Sensitive Tachycardia

The most common form of idiopathic left ventricular tachycardia has a RBBB configuration with a frontal plane axis that is directed superiorly (8,23) (Fig. 1, middle). This tachycardia can be terminated by administration of intravenous (iv) verapamil, suggesting that slow calcium-channel-dependent tissue is involved. The mechanism is reentry, probably involving the distal fascicles of the posterior division of the LBB. Rarely, tachycardia arises from the anterior division of the LBB and has a RBBB configuration with the frontal plane axis directed to the right (7,24,25). If specifically sought with echocardiography, more than 90% of patients have a left ventricular false tendon identifiable (26). These false tendons can contain Purkinje tissue, raising the possibility that the tendon is involved in causing the tachycardia (27). False tendons are not specific for this arrhythmia; they are also seen in patients without this tachycardia. Similar to idiopathic right ventricular tachycardia, this idiopathic left ventricular tachycardia rarely, if ever, leads to sudden death. Chronic therapy with beta-adrenergic blockers and/or the calcium-channel blockers verapamil or diltiazem often prevents episodes. Catheter ablation is a reasonable therapy for patients who do not respond to or do not wish to take antiarrhythmic medications.

Ablation targets a discrete Purkinje potential that precedes the onset of the QRS complex during tachycardia (23). The target is usually identified along the inferior aspect of the left ventricular septum. When the tachycardia originates from the anterior division of the LBB, the target can be on the anterior wall (24,25,28). Ablation is successful in more than 90% of patients (8,23,24,26,29,30). Occasional failures are usually caused by catheter-induced trauma or "bumping" the arrhythmia focus, preventing its initiation to allow mapping (27). Complications are rare, but damage to the aortic or mitral valve from catheter manipulation can occur (18).

Idiopathic focal tachycardias can occur in other locations, such as along the ventricular aspect of the mitral annulus, and in the epicardial portion of the LVOT (21,31). Successful ablation depends on whether the focus is sufficiently close to the endocardium to allow damage with present catheter techniques. Success is often unpredictable without performing catheter mapping.

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