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The ventricular outflow tracts and ASCs are major sites of origin of ventricular arrhythmias with or without structural heart diseases.1–11 The ventricular arrhythmias arising from these regions are being increasingly recognized as targets for catheter ablation.^2–12 Although the ECG and EP characteristics of these ventricular arrhythmias may be helpful for identifying the site of origin, it is well known that the complex anatomy of this region may limit the reliability of algorithms based on those characteristics.^9–14 In these ventricular arrhythmias, endocardial catheter ablation is usually successful, but an epicardial catheter approach to ablation via the cardiac vein and subxiphoidal pericardial approach may sometimes be required.^2–18 In this chapter, we discuss our approach to catheter ablation of outflow tract and ASC ventricular arrhythmias.

Preprocedural Planning

Although the RVOT, LVOT, and ASCs are located anatomically close to each other,^19,20 the techniques and equipment used for mapping and catheter ablation may differ among these regions. Therefore, a preprocedural planning of the mapping and catheter ablation approach is important to save procedural time and to reduce costs and complications. The preprocedural planning is usually based on the ECG characteristics and several other considerations.

ECG Diagnosis

ECG characteristics are helpful for predicting the site of origin of ventricular arrhythmias originating from these regions.^5,8–11,21 The most important diagnosis to make by an ECG may be whether the ventricular arrhythmias originate from the right or left side. It is often challenging because anatomically the RVOT and LVOT are located next to each other. The bundle branch block pattern, the precordial transition zone, and some ECG algorithms may be helpful for localizing the site of origin. An RBBB QRS morphology clearly suggests the ventricular arrhythmia originates on the left side. When a left bundle branch block (LBBB) QRS morphology is observed, it is often difficult to predict whether the ventricular arrhythmia (VA) originates from the right or left side. Because the LVOT is anatomically located posterior to the RVOT, LVOT VAs exhibit a taller and wider R wave in the right precordial leads than RVOT VAs. Therefore, the precordial transition zone is helpful for predicting whether a VA originates from the RVOT or LVOT. The precordial transition of > lead V₄ most likely predicts a RVOT VA origin while a precordial transition of < lead V₂ predicts an LVOT VA origin. When there is a precordial transition in lead V₃, it is most difficult to predict RVOT or LVOT VA origins. Several ECG algorithm to predict RVOT or LVOT VA origins have been proposed, and the authors would like to recommend two ECG algorithms: R/S amplitude index and R wave duration index (Figure 33.1) and the V2S/V3R ratio (Figure 33.2) because they are simple and accurate and also can make a diagnosis by looking at the ECG of the VA alone. The R/S wave amplitude ratio in leads V₁ and V₂ is calculated using the amplitude of the QRS complex peak or nadir to the isoelectric line. The R/S wave amplitude index, which is a greater value of the R/S wave amplitude ratio in lead V₁ or V₂, is considered more useful than the R/S wave amplitude ratio alone in lead V₁ or V₂. The R-wave duration index is calculated by dividing the longer R-wave duration in lead V₁ or V₂ by the QRS-complex duration. A precordial transition later than lead V₄ or R/S amplitude index of < 0.3 and R-wave duration index of < 0.5 may strongly suggest a ventricular arrhythmia origin on the right side (Figure 33.1).⁸ Otherwise, a ventricular arrhythmia origin on the left side may be suggested (Figure 33.1). A V2S/V3R ratio is calculated by dividing an S wave amplitude in lead V₂ by an R wave amplitude in lead V₃ (Figure 33.2). Ratios of the V2S/V3R of > 1.5 and < 1.5 predict RVOT and LVOT VA origins, respectively. This ECG algorithm has proven to be useful in VAs with a precordial transition in lead V₃, and may be the most accurate among the previously proposed ECG algorithms. The presence of S waves in lead I may also be helpful for differentiating ventricular arrhythmia origins in the ASCs or RVOT.5,8 The presence of “notching” in the middle of the QRS complex strongly suggests a ventricular arrhythmia origin in the free wall of the RVOT.²² The presence of S waves in lead V₆ may suggest a ventricular arrhythmia origin in the endocardial LV, which indicates the area below the aortic valve.⁵ A qrS pattern in the right precordial leads may be highly specific for a ventricular arrhythmia origin at the junction between the left and right ASCs.⁹

The ECG features as to whether ventricular arrhythmias can be successfully ablated from the endocardial or epicardial side are also important to recognize. The maximum deflection index (MDI), which is calculated by dividing the shortest time to the maximum deflection in any precordial lead by the QRS duration and the ratio of the Q-wave amplitude in leads aVL to aVR (aVL/aVR ratio), may be helpful for making such a diagnosis.^21,23 An MDI of > 0.55 and aVL/aVR ratio of > 1.4 suggest that ventricular arrhythmias may be ablated epicardially, although these algorithms are reliable for ventricular arrhythmias arising from the endocardial LVOT and less reliable for those arising from the ASCs and epicardial LVOT.

Because of their anatomical close proximity, ventricular arrhythmias originating from the RVOT, LVOT, and ASCs may exhibit similar ECG features. In addition, the complex anatomy of these regions may limit the reliability of these ECG algorithms. In the preprocedural planning, these limitations should be kept in mind, and all possibilities should be considered.

Other Considerations

RVOT ventricular arrhythmias occur more frequently in women than in men while males consistently predominate with LVOT ventricular arrhythmias.^10,24 The RVOT ventricular arrhythmias are usually caused by abnormal automaticity. They can be induced by exercise or intravenous isoproterenol and may be suppressed by beta-blockers. The LVOT ventricular arrhythmias are likely to occur based on a mechanism of triggered activity and can be induced by ventricular stimulation.

Procedure

Patient Preparation

All patients are brought to the EP laboratory in a fasting state. EP study and catheter ablation are performed under deep sedation with intravenous midazolam, fentanyl, and propofol. In patients with PVCs, the 12-lead surface ECGs of clinical PVCs should be recorded before sedation is initiated, because sedation may sometimes suppress PVCs.

A total of 3 sheaths are inserted in the right femoral vein for catheter placement with an 8-Fr sheath for an ablation catheter. Access in the right femoral artery is obtained with an 8-Fr sheath for LV mapping. A heparin bolus of 100 to 150 units/kg is typically given immediately thereafter, and intravenous heparin is administered to maintain an ACT > 250 seconds during LV mapping and ablation procedure. It is also important to prepare for possible arterial access in the left femoral artery with a 6-Fr sheath for coronary angiography.

EP Study

For mapping and pacing, a quadripolar catheter is positioned at the HB region via the right femoral vein and a 6- or 7-Fr deflectable decapolar catheter in the CS. The CS catheter is advanced into the GCV as far as possible, even into the AIVV, until the proximal electrode pair records an earlier ventricular activation than the most distal electrode pair during the ventricular arrhythmias (Figures 33.3 and 33.4). When this is impossible, a 2.3-Fr micro multi-electrode catheter (Pathfinder™, Cardima, Fremont, CA) is advanced through a 7-Fr Amplatz angiographic guiding catheter via the right femoral vein for mapping within these veins (Figure 33.5). Endocardial mapping and pacing in the ventricular outflow tracts are usually performed using a 7-Fr, 4- or 5-mm-tip ablation catheter via the right femoral vein or artery. When few PVCs are observed at the beginning of the EP study, induction of ventricular tachycardia or PVCs is attempted by burst pacing from the RVOT or right ventricular apex with the addition of an isoproterenol infusion.

Mapping

Because preprocedural ECG diagnosis is imperfect, mapping in the RV should be first performed in all patients with an LBBB QRS morphology. Activation mapping seeking the earliest bipolar activity and/or a local unipolar QS pattern during ventricular arrhythmias is most reliable for identifying a site of origin of the ventricular arrhythmia. In some patients, when the VT or PVCs are frequent, electroanatomic mapping can facilitate the procedure and improve procedural outcomes.²⁴ Pace mapping may be helpful when ventricular arrhythmias are infrequent and can roughly localize a site of origin. Pace mapping is especially helpful for RVOT ventricular arrhythmias^3,12, but may be less helpful for ASC ventricular arrhythmias because pacing in the ASCs may not exactly reproduce the QRS morphology of the ventricular arrhythmias because of preferential conduction (Figure 33.6)¹³ or the inability to obtain myocardial capture despite the use of high pacing current. A comparison of the pace maps from the right and left side may be helpful to predict whether a ventricular arrhythmia can be ablated from the right or left ventricle (Figure 33.7). When an earlier precordial transition during ventricular arrhythmias cannot be reproduced by pace mapping from the right ventricle, a site of origin may be considered to be located in the left ventricle. A comparison of the pace maps from the ASCs, endocardial LVOT, and GCV may be helpful to predict whether a ventricular arrhythmia can be ablated from the endocardial or epicardial side (Figure 33.7). In this comparison, the MDI as well as the pace map score should be evaluated. When the MDI during ventricular arrhythmias is closer to that during pace mapping from the GCV than that during pace mapping from the ASCs and LVOT, the epicardial surface may be considered to be the source of the ventricular arrhythmia. Pace mapping is performed using the distal bipolar electrodes at a pacing cycle length of 500 ms and at a minimum stimulus amplitude required for consistent capture (up to a maximum output of 20 mA and pulse width of 2.0 ms). The score for the pace mapping is determined as the number of leads with an identical height of the R wave/depth of the S wave (R/S) ratio match (12 represents a perfect R/S ratio match in all 12 leads), as well as the number of leads with a fine notching match in the 12-lead ECG as previously reported (perfect pace mapping is equal to 24 points).3 An excellent pace map is defined as a pace map that obtains a score of > 20. The pace map score can also be automatically calculated with computer software by comparing the paced QRS complex with a template of the spontaneous PVC or VT morphology.

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