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Ablation of Idiopathic Left and Right Ventricular and Fascicular Tachycardias


Key Points

  • The mechanism of idiopathic mitral and tricuspid annular ventricular tachycardias (VTs) is nonreentry (triggered activity or automaticity).

  • Mitral annular VT has a right bundle branch block (RBBB) pattern and monophasic R or Rs in leads V 2 to V 6 . Catheter ablation of mitral annular VT is highly successful.

  • Tricuspid annular VT exhibits a left bundle branch block pattern, R (r) in lead I, and the presence of an R (r) in lead aV L . Catheter ablation eliminates approximately 90% of VTs arising from the free wall portion of the tricuspid annulus, but only 57% of those from the septal portions.

  • Papillary muscle VT appears to be based on a focal (nonreentrant) mechanism.

  • Activation mapping seems to be most useful for ablation of papillary muscle VTs. They typically do not exhibit any recordings of diastolic potentials during sinus rhythm or VT. Catheter ablation is challenging because catheter stability is very difficult because of papillary muscle contractions. Successful catheter ablation usually requires irrigated ablation catheters, and intracardiac echocardiography to visualize the direct contact with the papillary muscle.

  • VTs originating from the crux of the heart are rare and may arise by a focal mechanism from the epicardium; they may be induced with programmed stimulation or burst pacing from the right ventricle, and often require isoproterenol (catecholamine sensitive). Ablation may be performed within the proximal coronary sinus or proximal middle cardiac vein, or by a pericardial approach.

  • The mechanism of verapamil-sensitive idiopathic left fascicular VT is reentry.

  • Diagnosis is based on demonstration of RBBB and superior axis configuration (common type); RBBB and inferior axis configuration (uncommon type); or a relatively narrow QRS and inferior axis configuration (rare type), together with dependence on left ventricular fascicular activation and verapamil sensitivity (termination or slowing of the tachycardia). In some cases, the reentrant circuit of VT can involve the Purkinje network lying around the papillary muscles.

  • Ablation targets are the diastolic potential in the VT circuit or the presystolic fused Purkinje potential at the VT exit. The success rate of ablation is greater than 90% for verapamil-sensitive idiopathic left VT.

  • The mechanism of nonreentrant fascicular VT is abnormal automaticity from the distal Purkinje system. It is difficult to distinguish this VT from verapamil-sensitive idiopathic left fascicular VT by 12-lead electrocardiogram. The ablation target is the earliest Purkinje activation during VT. The recurrence rate after ablation for nonreentrant fascicular VT is much higher than that of verapamil-sensitive idiopathic left fascicular VT.

Sustained monomorphic ventricular tachycardia (VT) is most often related to myocardial structural heart disease, including healed myocardial infarction and cardiomyopathies. However, no apparent structural abnormality is identified in approximately 10% of all sustained monomorphic VTs in the United States and 20% of those in Japan. These VTs are referred to as idiopathic. Idiopathic VTs usually occur in specific locations and have specific QRS morphologies, whereas VTs associated with structural heart disease have a QRS morphology that tends to indicate the location of the scar. Idiopathic VT comprises multiple discrete subtypes that are best differentiated by their mechanism, QRS morphology, and site of origin. The most common idiopathic VT originates from a focus in the outflow tract of the right ventricle (RV) (see Chapter 28 ), and its mechanism is most likely triggered activity. In idiopathic left VT, the following four types exist: left ventricular outflow tract VT, VT from the mitral annulus, papillary muscle VT, VT arising from ventricular crux, verapamil-sensitive left fascicular VT, and nonreentrant fascicular VT ( Box 29.1 ). This chapter focuses on the assessment and nonpharmacologic treatment of idiopathic left and right VTs and left fascicular VTs.

BOX 29.1
Classification of Left and Right Ventricular and Fascicular Tachycardias

Outflow Tract VTs ( triggered activity, reentry, or automaticity )

  • Left ventricular outflow tract, aortic sinus of Valsalva, or epicardial VT

  • Right ventricular outflow tract or pulmonary artery VT

Mitral Annular VT ( triggered activity, reentry, or automaticity )

  • Anterolateral, anteromedial (aorto-mitral continuity), lateral, posterior, or posteroseptal mitral annular origin

Tricuspid Annular VT ( triggered activity, reentry, or automaticity )

  • Posterior–posterolateral, anterior–anterolateral, posteroseptum, anteroseptal (parahissian), or midseptal mitral annular origin

Papillary Muscle VT ( triggered activity, reentry, or automaticity)

  • Left posterior papillary muscle, left anterior papillary muscle, or right papillary muscle origin

VT Arising From Ventricular Crux ( triggered activity, reentry, or automaticity )

  • Middle cardiac vein approach or epicardial approach

Left Ventricular Reentrant Fascicular VTs (reentry)

  • Left posterior septal fascicular VT

  • Left posterior papillary muscle fascicular VT

  • Left anterior septal fascicular VT

  • Left anterior papillary muscle fascicular VT

  • Left upper septal fascicular VT

Nonreentrant Fascicular VT (triggered activity or automaticity)

  • Left Purkinje origin

  • Right Purkinje origin

VT, Ventricular tachycardia.

Mitral Annular Ventricular Tachycardia

Mitral annular VTs are found in 5% of symptomatic, idiopathic VTs/premature ventricular complexes (PVCs) and occur with equal frequency in both sexes or with a male predominance (male, 53%–69%). Mitral annular VTs were noted in 5% of all cases of idiopathic VT ; however, a previous study showed that mitral annular VT accounts for 49% of idiopathic repetitive monomorphic VTs arising from the left ventricle (LV; other sites included the coronary cusps and inferoseptal region).

Pathophysiology

Classification

Mitral annular VT can be classified by the anatomic location. The majority originate from the anterolateral portion of the mitral annulus (in close proximity to the aorto-mitral continuity), and less commonly the lateral, posterior, or posteroseptal annulus ( Fig. 29.1 ). The anterior and anteromedial portion of the mitral annulus, that is the aorto-mitral continuity, may also be the origin of the VT.

Fig. 29.1, Representative 12-lead electrocardiograms of premature ventricular complexes originating from the anterolateral (A), posterior (B), and posteroseptal (C) portions of the mitral annulus. The arrows indicate notching of the late phase of the QRS complex in the inferior leads.

Mechanism

The mechanism of this arrhythmia appears to be nonreentry, and it may be a triggered activity based on the response to adenosine, verapamil, and pacing maneuvers. It has been proposed that a remnant of the atrioventricular conduction system close to the aorto-mitral continuity, such as a dead-end tract, might be important in the genesis of the nonreentrant mechanism for the tachycardia. The close proximity of the anterolateral mitral valve to the right ventricular outflow tract, left ventricular outflow tract, and left ventricular epicardial myocardium near the left coronary cusp suggests that idiopathic VT from these sites could likely originate from a single focus, with different exit points or activation of alternate pathways between the VT focus and an exit point.

Diagnostic Criteria

Surface Electrocardiogram

The electrocardiogram (ECG) in mitral annular VT has a right bundle branch block (RBBB) pattern and a monophasic R or Rs in leads V 2 to V 6 (see Fig. 29.1 ). Further, an ECG analysis can precisely distinguish among the different subtypes by the polarity of the QRS complex in the inferior and lateral leads. In anterolateral VTs, the polarity of the QRS complex in leads I and aV L is negative and positive in the inferior leads. Posterior VTs and posteroseptal VTs have a negative polarity in the inferior leads and positive polarity in leads I and aV L . VT arising from the free wall portion of the annulus, such as an anterolateral VT or posterior VT, has a longer QRS duration (sometimes also described as a δ-wave–like morphology ) and notching in the late phase of the R wave/Q wave in the inferior leads. This feature is not observed in posteroseptal, anterior, or anteromedial VTs. Notching of the late phase of the QRS complex in the inferior leads and widening of the QRS complex observed in these VTs may result from phased excitation from the LV free wall to the RV. Posterior VTs have a dominant R in V 1 , whereas posteroseptal VTs have a negative QRS component in V 1 (qR, qr, rs, rS, or QS). The Q wave amplitude ratio of lead III to lead II is greater in posteroseptal VTs than in posterior VTs. Anterior and anteromedial VTs arising from the aorto-mitral continuity exhibit an absence of S waves in lead V 6 and RBBB or left bundle branch block (LBBB) with an early transition as noted in aortic cusp VTs ( Fig. 29.2 ). A proposed algorithm to predict the precise focus of a VT/premature ventricular contractions originating from the mitral annulus is shown in Fig. 29.3 .

Fig. 29.2, A representative case of a successful ablation of a ventricular tachycardia originating from the aortomitral continuity. A, A 12-lead electrocardiogram. No notching of the QRS complex was found. B, Intracardiac recordings. During the premature ventricular complex, a distinct local activation recorded by the ablation catheter (ABL) preceded the onset of the QRS complex by 24 ms. C, Radiographs obtained in the right anterior oblique (RAO) 35 degrees and left anterior oblique (LAO) 45 degrees projections showing the ablation sites. The distal electrode of the ablation catheter was positioned at the aorto-mitral continuity just beneath the aortic valve. AIV, Anterior interventricular vein; CS, coronary sinus; d, distal; GCV, great cardiac vein; HRA, high right atrium; p, proximal; Uni, unipolar electrogram.

Fig. 29.3, Proposed algorithm to predict the precise focus of a ventricular tachycardia/premature ventricular contractions originating from the mitral annulus based on the QRS wave configuration in 12-lead electrocardiogram recordings. VT, Ventricular tachycardia.

Mapping and Ablation

Catheter ablation using radiofrequency (RF) energy to cure patients with mitral annular VT is associated with a high success rate because of the focal origin of this form of VT ( Figs. 29.4 and 29.5 ). The 12-lead ECG is a useful initial guide to localize the site of the origin of the tachycardia. Intracardiac mapping to select the optimal site for ablation (see Figs. 29.4 and 29.5 ) includes activation mapping (earliest local intracardiac electrogram that precedes the onset of surface QRS during VT) and pace mapping (pacing the ventricle from a selected site during sinus rhythm to match the 12-lead morphology of the spontaneous or induced VT). All successful ablation sites have atrial and ventricular electrogram amplitudes satisfying the criteria for a mitral annular origin, with a ratio of the atrial to ventricular electrograms of less than 1 and an amplitude of the atrial and ventricular electrograms of more than 0.08 and 0.5 mV, respectively, at the successful ablation site. Some patients have a potential noted before the local ventricular electrogram. The use of 3-dimensional electroanatomic mapping systems may reduce the fluoroscopic exposure and improve the efficacy of the catheter ablation by providing activation maps during VT that identify the site of origin and also provide the ability to maneuver the ablation catheter easily to recorded sites of interest.

Fig. 29.4, A representative case of successful ablation of a ventricular tachycardia originating from the anterolateral portion of the mitral annulus (Patient 1). A, Intracardiac recordings. During the premature ventricular complex, a low-amplitude presystolic potential recorded by the ablation catheter (ABL) preceded the onset of the QRS complex by 34 ms (arrow). The timing of the second peak of the notched R wave corresponded precisely with that of the activation of the right ventricle free wall (dotted line), which was recorded with the catheter in the high right atrium (HRA). B, Radiographs obtained in the right anterior oblique (RAO 35 degrees) and left anterior oblique (LAO 45 degrees) projections showing the ablation sites. The distal electrode of the ablation catheter was positioned at the anterolateral mitral annulus. A, Atrial activation; Bi, bipolar electrogram; Uni, unipolar electrogram; V, ventricular activation.

Fig. 29.5, A representative case of a successful ablation of a ventricular tachycardia originating from the posteroseptal portion of the mitral annulus. A, Intracardiac recordings. During the premature ventricular complex, the local ventricular activation recorded by the ablation catheter (ABL) preceded the onset of the QRS complex by 20 ms. No notched QRS complex was found in the surface electrocardiogram. B, Radiographs obtained in the right anterior oblique (RAO) 35 degrees and left anterior oblique (LAO) 45 degrees projections showing the ablation sites. The distal electrode of the ablation catheter was positioned at the posteroseptal mitral annulus. A, Atrial activation; Bi, bipolar electrogram; HRA, high right atrium; Uni, unipolar electrogram; V, ventricular activation.

Success and Recurrence Rates

Catheter ablation is highly successful with ablation delivered at the site of the earliest ventricular activation or sites with a 12/12 pace-map match. However, there was a recurrence rate of 8% in one series. Most cases may be successfully ablated by an endocardial approach, but ablation in the coronary venous system, specifically the great cardiac vein, has been described. Comparing the morphology of the coronary sinus ECG with that at the site of ablation on the mitral annulus may be helpful for determining the optimal ablation site.

Tricuspid Annular Ventricular Tachycardia

Tricuspid annular VTs are found in 8% of all the cases of idiopathic VTs/PVCs (including right- and left-sided VT/PVC) and approximately 5% of all patients with a right-sided VT origin. A recent study reported that tricuspid annular VT arising from the free wall portion is more common in males than in females (male/female ratio, 1.83), whereas the incidence of that arising from the septum is distributed almost equally between males and females.

Pathophysiology

Classification

Tricuspid annular VT can be classified by the anatomic location. Septal sites were more common than free wall sites in a previous study (74%) and less common in the series presented by another study (43%). Of the septal locations, the majority were anteroseptal or parahissian (72%).

Mechanism

The mechanism of this arrhythmia appears to be nonreentrant based on the findings that it typically occurs spontaneously and cannot easily be induced by pacing maneuvers.

Diagnostic Criteria

Surface Electrocardiogram

All VT/PVCs arising from the tricuspid annulus demonstrate an LBBB QRS morphology and positive QRS polarity in leads I, V 5 , and V 6 ( Figs. 29.6 and 29.7 ). No negative component of the QRS complex is found in lead I. The R wave in lead I is usually greater because the tricuspid annulus is more rightward and inferior to the right ventricular outflow tract. A positive component (any r or R) is recorded in lead aV L in 95% of patients, and the overall polarity in aV L is positive in 89%.

Fig. 29.6, Representative 12-lead electrocardiograms of premature ventricular contractions originating from the (A) posterolateral, (B) anterior, and (C) anteroseptal portions of the tricuspid annulus. The arrows indicate the second peak of the notched QRS complex in the limb leads.

Fig. 29.7, A representative case of a successful ablation of a premature ventricular complex (PVC) originating from the anteroseptal (parahissian) portion of the tricuspid annulus. A, A 12-lead electrocardiogram. No notching of the QRS complex in the inferior lead was found. B, Intracardiac recordings. During the PVC, a distinct local activation recorded by the ablation catheter (ABL) preceded the onset of the QRS complex by 30 ms (arrow). C, An activation map during a PVC that was created by a 3-dimensional mapping system (CARTO, Biosense Webster, Diamond Bar, CA; upper) and a radiograph obtained in the right anterior oblique (RAO) 35 degrees projection (lower) show the ablation site. The distal electrode of the ablation catheter was positioned at the anteroseptal (parahissian) portion of the tricuspid annulus. To avoid a potential complication of impairment of atrioventricular conduction, the power delivery was increased gradually from 10 W. The radiofrequency (RF) energy was delivered using a maximum power of 35 W and maximum electrode–tissue interface temperature of 55°C. During the RF energy application, the location of the ablation catheter was verified by multiplane fluoroscopic views and a 3-dimensional mapping system. A, Atrial activation; Dist, distal; HBE, His-bundle electrogram; HRA, high right atrium; Prox, proximal; Uni, unipolar electrogram.

Among all tricuspid annular VTs, the QRS duration and Q wave amplitude in each of leads V 1 to V 3 were greater in VT/PVCs arising from the free wall of the tricuspid annulus compared with the septum. The septal VTs have an early transition in the precordial leads (V 3 ), narrower QRS complexes, and Qs in lead V 1 with the absence of notching in the inferior leads, whereas the free wall VTs are associated with a late precordial transition (>V 3 ), wider QRS complexes, absence of Q waves in lead V 1 , and notching in the inferior leads (the timing of the second peak of the notched QRS complex in the inferior leads corresponds precisely with the left ventricular free wall activation). These ECG characteristics are confirmed by pace mapping. A proposed algorithm to predict the precise focus of a VT/premature ventricular contractions originating from the tricuspid annulus is shown in Fig. 29.8 .

Fig. 29.8, Proposed algorithm to predict the precise focus of ventricular tachycardia/premature ventricular complexes originating from the tricuspid annulus based on the QRS configuration in 12-lead electrocardiogram recordings. LBBB, Left branch bundle block; VT, ventricular tachycardia.

Mapping and Ablation

The 12-lead ECG is a useful initial guide to localize the site of origin of the tachycardia. Intracardiac mapping to select the optimal site for ablation ( Fig. 29.9 ; see Fig. 29.7 ) includes activation mapping (earliest local intracardiac electrogram that precedes the onset of surface QRS during VT) and pace mapping (pacing the ventricle from a selected site during sinus rhythm to match the 12-lead morphology of the spontaneous or induced VT). All successful ablation sites had atrial and ventricular electrogram amplitudes satisfying the criteria for a tricuspid annular origin, with a ratio of the atrial to ventricular electrograms at the ablation site of less than 1, and the amplitudes of the atrial and ventricular electrograms are 0.03 or more and less than 0.35 mV at the ablation site, respectively. VTs originating from near the His bundle have a similar ECG and electrophysiologic characteristics as those from the right coronary cusp or noncoronary cusp adjacent to the membranous septum (see Fig. 29.7 ). Therefore when right ventricular mapping shows the earliest ventricular activation near the His bundle, mapping in the right coronary cusp and noncoronary cusp should be added to identify the origin. The use of 3-dimensional electroanatomic mapping systems may reduce the fluoroscopic exposure and improve the efficacy of catheter ablation by providing activation maps during VT that identify the site of the origin and also provide the ability to maneuver the ablation catheter easily to recorded sites of interest. The use of these systems is especially useful for ablating VTs arising from the anteroseptal or parahissian portion (see Fig. 29.7 ). Confirmation of the distance between the ablation site and His-bundle recording site is important to avoid impairing atrioventricular conduction during RF energy applications.

Fig. 29.9, Site of the successful ablation of a premature ventricular complex (PVC) originating from the inferolateral portion of the tricuspid annulus. A, Intracardiac recordings. During the PVC, a ventricular potential recorded by the ablation catheter (ABL) preceded the onset of the QRS complex by 25 ms (arrow). The timing of the second peak of the notched QRS complex corresponded precisely with that of the activation of the left ventricular free wall (dotted line), which was recorded with the catheter within the coronary sinus (CS). B, Radiographs obtained in the right anterior oblique (RAO 35 degrees) and left anterior oblique (LAO 45 degrees) projections showing the ablation sites. The distal electrode of the ablation catheter was positioned at the inferolateral portion of the tricuspid annulus. A, Atrial activation; Bi, bipolar electrogram; Dist, distal; HRA, high right atrium; Prox, proximal; Uni, unipolar electrogram.

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