Ventricular tachycardia (VT) arising from the region of the right ventricular outflow tract (RVOT) is readily recognized, both in its electrocardiographic (ECG) expression and clinical behavior. The distinctive QRS pattern has a left bundle branch block (LBBB)-like complex with tall, smoothly contoured R-waves in the inferior ECG leads. Arrhythmia episodes may occur as rare or frequent isolated premature ventricular complexes (PVCs), bursts of nonsustained VT, or as discrete episodes of sustained tachycardia, often facilitated by catecholamines. Most often, there is no evidence of underlying structural heart disease. The syndrome of idiopathic RVOT ectopic activity or VT is generally benign, with an excellent long-term survival even if untreated. It must be distinguished from other disorders associated with RV VT, such as RV dysplasia and sarcoidosis. RVOT VT is usually amenable to catheter ablation in patients who require treatment. In this review, we will discuss the approach to catheter mapping and radiofrequency (RF) ablation to treat this disorder; a discussion of its pathophysiology and details of clinical presentation can be found elsewhere.

Patient Selection

Patients with RVOT PVCs or VT have a wide spectrum of symptoms, ranging from none, to palpitations, lightheadedness, dyspnea, presyncope, or syncope. Patients with bothersome symptoms not readily treated with well-tolerated medications are candidates for ablation. An ECG showing PVCs or VT can suggest the likely region of origin of the arrhythmia. A number of ECG algorithms have been developed that correlate QRS morphology with region of origin, to assist in mapping.^[1] Successful elimination of PVCs/VT hinges on having adequate amounts of the arrhythmia during the procedure; enough should be present to provide both ample opportunity to map the origin of the arrhythmia carefully, as well as a reliable means of assessing the success of ablation.

Preparation

Patients are prepared for the procedure in a standard fashion, ideally having discontinued beta-blockers or antiarrhythmic agents for a minimum of five half-lives prior to the procedure. At the beginning of the procedure, if spontaneous PVCs or VT are absent, isoproterenol or epinephrine may be infused intravenously to provoke ectopic complexes or VT; venous access may be obtained by passing a single catheter to the right atrium or ventricle where stimulation may be performed with or without catecholamine infusion. If these methods do not provoke enough arrhythmia to adequately map, there is little point in placing additional catheters in the heart and the procedure should be terminated. Sedation administered during the procedure can decrease the amount of spontaneous or inducible arrhythmia. When VT or PVCs occur, one should record simultaneous 12-lead ECG leads of the target QRS morphology for later reference. This is useful for comparing pacemapping results to the spontaneous VT as well as ensuring that catheter-induced PVCs that occur during mapping are not mistaken for the target arrhythmia. We position catheters at the right ventricular apex (to serve as a stable timing reference), the His bundle location for a fluoroscopic reference, and right atrium. The latter can help in discerning whether a P-wave distorts the onset of the ECG during isolated PVCs. A mapping/ablation catheter (4-mm tip usually suffices) is advanced into the right atrium, across the tricuspid valve, and into the RVOT with a clockwise motion as though one were performing right-heart catheterization. It is important to monitor multiplane fluoroscopy during this process in order to avoid inadvertent perforation of the thin RVOT. One should not attempt to advance the catheter when the tip is perpendicular to the RVOT wall. The catheter tip can usually be passed easily into the pulmonary artery. This serves as a good starting point for mapping, since many VT foci are just below the pulmonic annulus. Catheter mapping and ablation can be undertaken successfully without advanced mapping systems; these may be useful in specific instances in which some, but relatively infrequent, ventricular ectopy is encountered or when the target for ablation is near an important structure that one wishes to avoid injuring, such as the His bundle.

Mapping and Catheter Ablation

If at all possible, mapping should be performed in the absence of catecholamine infusion. More vigorous cardiac motion during catecholamine infusion decreases catheter stability and increases the risk of cardiac perforation. Two main methods of mapping are used to guide ablation: activation mapping and pacemapping. Activation mapping is useful in the presence of frequent PVCs or VT episodes, comparing the timing of activation of the electrogram from the catheter tip electrode with onset of the QRS. The bipolar electrogram is universally used for this purpose, seeking a timing of 10-40 msec prior to the QRS onset. The unipolar recording from the catheter tip is also very helpful; this should have a sharp "QS" deflection that times with the bipolar recording and precedes the QRS onset by a similar amount (Fig. 1).^[2] The operator must be wary of mistaking catheter-induced ectopy for the target arrhythmia. Electrograms from catheter-induced complexes meet all criteria for excellent sites of ablation, since they are derived from endocardial irritation by the catheter tip (Fig. 2). Ablation should not be performed at such sites. Pacemapping (uni- or bipolar) at putative ablation sites at a rate slightly faster than VT can corroborate the activation mapping findings. This should exactly replicate the 12-lead ECG of the previously recorded target QRS complex, including any small notches, indicating that stimulation is being performed from the site of ectopic impulse formation (Fig. 3). Ablation at sites with a so-called "perfect" or "superimposable" pacemap is generally successful. Ablation at sites from which pacing produces a QRS with lesser degrees of resemblance to the target QRS ("10/12 lead match") is less likely to be successful. In patients with too little ectopic activity to perform activation mapping, pacemapping is extremely helpful. One should use as little current as is needed to reliably capture; if capture only occurs at >5 mA, the electrode contact is poor and should be adjusted.^[3] Ablation can be performed with power settings of ≤50 W with a target temperature of 55-70°C and duration of 30-60 seconds. Energy delivery may result in an increased frequency in ectopy or bursts of VT, acceleration of ongoing VT followed by slowing and termination, or sudden cessation of VT or ectopy without prior change in frequency or rate. If there has been no change in the arrhythmia after 15 seconds of power delivery, it should be stopped and catheter contact and stability reassessed. Myocardial damage from power delivery is evidenced by ST elevation on the unipolar recording. About 5% of patients have additional morphologies of PVCs or VT that differ slightly from the originally targeted one. Sites of origin of these secondary forms are usually within 1-2 cm of the site at which the original morphology was ablated. It is unclear whether these additional morphologies represent an altered exit site of the first morphology, or an actual second focus. With an amount of arrhythmia sufficient for thorough mapping, ablation using these methods can eliminate PVCs or VT with the characteristic LBBB/inferior axis morphology in >90% of patients.

(Enlarge Image)

Figure 1. Activation mapping of PVCs in a patient with RVOT ectopy. Five ECG leads and intracardiac recordings from the right ventricular apex (RVA) and ablation (Abl) catheter (U, unipolar tip electrode recording; dist, distal electrode bipolar pair; prox, proximal electrode pair) from five different RVOT sites; dashed line denotes QRS onset. Recordings are all at same amplification. Sites A-D are unsatisfactory; successful ablation occurred at site E. In (A), Abluni-d shows a QS shape but is not pre-QRS; in (B), the electrogram precedes the QRS but has low amplitude and dV/dt due to poor tissue contact; in (C), the distal electrogram recordings are slightly pre-QRS, but proximal electrode recordings are earlier still; in (D), an "rS" complex is present in Abluni-d; in (E), Abluni-d shows a sharp QS that, with Abldist, precedes the QRS by 20 msec.

(Enlarge Image)

Figure 2. Catheter-induced versus target PVC. Recordings as in prior figures; His = His bundle recording. The ablation site electrograms from the two complexes on the left show excellent characteristics for ablation targets (unipolar recording with QS configuration and timing equal to bipolar distal recording, 30 msec pre-QRS onset). However, these complexes are catheter-induced while mapping catheter recordings during actual target PVC (at right) are not acceptable for ablation.

(Enlarge Image)

Figure 3. Pacemapping of RVOT VT. The target QRS during VT is shown at left; recordings similar to Figure 1. A-E show single paced complexes from five different sites attempting to match the VT QRS. In A-D, the QRS appears progressively more similar to the target morphology; successful ablation occurred at site E, where pacing exactly replicates the target QRS.

Although standard mapping and ablation equipment suffices in the majority of cases, specialized mapping systems (CARTO^™ [Biosense-Webster, Diamond Bar, CA, USA], EnSite^™ or Nav-X^™ [St. Jude Medical, St. Paul, MN, USA]) may enable acquisition of activation mapping data during rare ectopic complexes. One must be careful to avoid causing ectopy with the EnSite^™ catheter that could be mistaken for target arrhythmia. When detailed activation mapping reveals no sites with timing >15 msec prior to QRS onset, or pacemapping does not approximate the target QRS morphology, one should consider alternate sites of origin such as epicardial RVOT, supravalvular pulmonary artery, deep septal sites or left ventricular outflow tract or sinus of Valsalva. Mapping in these disorders follows the same principles as noted above.

Success Rates and Complications

As noted above, >90% of patients who have adequate target material for ablation have a successful outcome, defined as lack of spontaneous arrhythmia episodes in the absence of adjunctive medical therapy. Patients with recurrent episodes after an apparently successful outcome may have repeat ablation, which is usually successful. Potential complications of ablation occur in <1% of cases and include myocardial perforation with cardiac tamponade due to catheter manipulation during mapping or rupture during ablation in the RVOT, and very rarely heart block due to inadvertent slippage of the catheter toward the His bundle. Excessive ablation in the septal portion of the RVOT can result in injury to the left anterior descending or left main coronary arteries with resultant myocardial infarction. Death from the procedure is extremely rare.

Summary

The syndrome of focal origin VT or frequent PVCs arising from the RVOT is a common, readily recognized arrhythmia that often causes intolerable symptoms that warrant therapy. Using standard techniques, catheter ablation is an accepted and highly successful and safe treatment that can be applied early in the course of therapy in this patient group.