S52

Ablation of Idiopathic Right Ventricular Outflow TractTachycardia: Current Perspectives

SANDEEP JOSHI, M.D., and DAVID J. WILBER, M.D.

From the Cardiovascular Institute, Loyola University Medical Center, Maywood, Illinois, USA

Ablation of Idiopathic Right Ventricular Outflow Tract Tachycardia. Ventricular tachycardia(VT) arising from the right ventricular outflow tract (RVOT) in the absence of overt structural heartdisease is a common entity. Exclusion of occult structural disease such as arrhythmogenic right ventricularcardiomyopathy is critical as this diagnosis impacts both ablation outcomes and long-term prognosis. VTis most commonly due to triggered activity. Induction of the target arrhythmia in the laboratory is oftenproblematic, and is frequently facilitated by catecholamine infusion. Recent data indicate that high-densitythree-dimensional activation mapping facilitates identification of target sites for ablation, and that thespatial resolution of pacemapping may be more limited than previously recognized. A standard 12-leadelectrocardiogram is useful in providing an initial approximation of the site of origin within the outflowtract, and may contain subtle clues to potentially confounding foci on the left ventricular endocardialor epicardial surface. When sufficient arrhythmia is present to permit mapping, successful ablation canbe expected in 90–95% of patients, with a recurrence risk of approximately 5%. In experienced centers,major complications are ≤1% and outcomes should approach those obtained for the common forms ofsupraventricular tachycardia. (J Cardiovasc Electrophysiol, Vol. 16, pp. S52-S58, Suppl. 1, September 2005)

catheter ablation, ventricular tachycardia, mapping, right ventricle

Introduction

Ventricular tachycardia (VT) arising from the right ven-tricular outflow tract (RVOT) in the absence of overt structuralheart disease is a common entity, representing up to 10% of allVTs evaluated by specialized arrhythmia services.1,2 Clini-cal presentation is variable, with symptom onset typicallybetween the ages of 20 and 40 years. The arrhythmia appearsto be more common in women.2 Nonsustained VT is morefrequent, comprising 60–92% of reported series.3-6 Episodesmost often occur as repetitive salvos (the pattern of repetitivemonomorphic VT)7-8 Occasionally, runs of VT are inces-sant, and premature ventricular beats comprise a substantialproportion of all QRS complexes in a 24-hour-period. Lesscommonly, patients present with paroxysmal sustained tachy-cardia, separated by relatively long intervals of infrequentpremature ventricular beats.9-12 Episodes tend to increase infrequency and duration during exercise and emotional stress.In more than 80% of patients, the QRS configuration is a leftbundle pattern with an inferior axis, reflecting an origin inthe RVOT.

Diagnostic Evaluation and Prognosis

The diagnosis of idiopathic RVOT VT is one of exclusion.Subtle forms of RV disease (arrhythmogenic right ventricu-lar dysplasia or cardiomyopathy [ARVC]) may not alwaysbe detected on the basis of clinical examination and rou-tine echocardiography.13-16 VT associated with ARVC usu-ally manifests multiple QRS configurations during differentepisodes, including tachycardias with a superior QRS axis

Address for correspondence: David Wilber, M.D., Loyola University Med-ical Center, Bldg 110, Room 3262, 2160 South First Ave, Maywood, IL60153. Fax: 708-327-2377; E-mail: dwilber@lumc.edu

doi: 10.1111/j.1540-8167.2005.50163.x

(both uncommon in idiopathic RV tachycardia). However,many patients with ARVC present with a left bundle, infe-rior QRS axis tachycardia alone.17,18 Exclusion of ARVCin patients considered for catheter ablation is more than anacademic exercise, since both long-term prognosis,18-20 andresponse to catheter ablation20-22 may be less favorable.

The diagnosis of ARVC remains problematic. The 1994European Society of Cardiology Task Force criteria providewidely accepted guidelines.23 An abnormal signal-averagedelectrocardiogram (SAECG) is uncommon in patients withidiopathic RVOT VT, while an abnormal time or frequencydomain SAECG is present in 50–80% of patients withARVC.24,25 The 12-lead electrocardiogram is usually nor-mal. Widespread T-wave inversion in the anterior precordialleads, and incomplete or complete right bundle branch blocksuggests ARVC.20

Cine magnetic resonance imaging (MRI) and radionuclideright ventriculography provide useful information regardingright ventricular size and function. However, several groupshave reported a substantial incidence of MRI abnormalities(65–76%) in patients with idiopathic RVOT VT without otherevidence of ARVC.26-28 These abnormalities included focalthinning and segmental contraction abnormalities, and wereequally distributed between the outflow tract and the anteriorfree wall. In addition, focal fatty infiltration was observedin approximately 25% of patients. The clinical significanceof these abnormalities, both in the pathogenesis of tachy-cardia and as prognostic markers, is uncertain. The diag-nosis of ARVC based on MRI alone should be made withcaution.28

Long-term prognosis in patients with truly idiopathicRVOT VT is excellent, despite frequent recurrences of tachy-cardia.3-12,29 Sudden death is rare in patients with initiallynormal left and right ventricular function; in such patients,occult cardiomyopathy is usually identified on postmortemexamination. Similarly, progression to diffuse cardiomyopa-thy is rare.

Joshi and Wilber Ablation of Idiopathic Right Ventricular Outflow Tract Tachycardia S53

Electrophysiologic Evaluation

The large majority of idiopathic outflow tract tachycardiasare due to cyclic AMP mediated triggered activity.10,12,30 Incontrast, tachycardias associated with ARVC are commonlydue to reentry.20,28 Adenosine rarely influences tachycardiasdue to reentry,31 and in particular has no effect on VT associ-ated with ARVC. In patients who present with sustained VTdue to triggered activity, the tachycardia usually can be repro-duced by programmed stimulation. 12,31 Burst pacing is usu-ally more effective than ventricular extrastimuli, and a criticalrange of paced cycle lengths for induction is often observed,which may shift with changing levels of adrenergic activa-tion. The tachycardia may be induced in the baseline state,but more often catecholamine infusion is generally requiredto facilitate induction. Occasionally, epinephrine or phenyle-phrine is more effective than isoproterenol. Tachycardia in-duction may be inconsistent,12 reflecting the complex inter-play between heart rate, degree of adrenergic activation, andcoupling intervals during ventricular pacing. Aminophyllineand atropine, though theoretically useful in facilitating trig-gered activity, are rarely effective. Sedation may suppress thisVT, particularly the use of benzodiazepines and propafol.

The QRS morphology during RVOT VT typically has a leftbundle configuration with QS or rS patterns in leads V1 andV2, and a right or left inferior axis (Figs. 1A and 2A). Minorvariations in QRS morphology between complexes duringtachycardia may occur, associated with minor variations inlocal electrograms recorded near the site of tachycardia ori-gin.32 However, multiple morphologically distinct VTs dueto triggered activity are rare, and should raise suspicion ofalternate mechanisms and occult underlying heart disease.

Figure 1. (A) Electrocardiogram of a tachycardia arising from the anterior (leftward) septum. Note the QS complex in lead I, QRS duration of 130, absence ofR-wave notching in the inferior leads, and R > S in lead V3. (B,C) Electroanatomical maps in the LAO and cranial projections acquired during tachycardia.The color-coded isochrones represent activation times during tachycardia with peak QRS voltage in lead II as the fiducial point. Earliest activation times areshown in red. The brown dots represent ablation sites. Orange dots represent the His bundle. PV = pulmonary valve.

Endocardial Mapping

Optimal techniques for localizing the site of origin of idio-pathic RVOT VT have received considerable attention. As ex-pected for focal rhythms, endocardial activation at successfulablation sites tends to be only modestly early, ranging from10–60 msec prior to onset of the surface QRS.32-39 Bipo-lar endocardial electrograms have high amplitudes and rapidslew rates. Fractionated complex electrograms and diastolicpotentials are rarely if ever seen, and should raise suspicionof underlying structural disease.

Initial endocardial activation away from the site of ori-gin is rapid. In a recent series of patients undergoing three-dimensional electroanatomical mapping during RVOT VT,the mean area of myocardium activated within the first 10msec was 3.0 ± 1.6 cm2, ranging from 1.3 to 6.4 cm2.40

Given interobserver variability of up to 5 msec or more in themanual assignment of activation time, it is not surprising thatelectrogram timing alone has been reported to have relativelylimited utility as a predictor of successful ablation sites. How-ever, high-density simultaneous display of activation time andanatomic location with three-dimensional electroanatomicalmapping systems facilitates discrimination between minordifferences in timing and “smooths over” potential measure-ment errors. Ablation directed at the center of the early ac-tivation area is highly effective in eliminating tachycardia40

(Figs. 1 and 2). Three-dimensional activation mapping withnoncontact arrays41-43 and multielectrode basket catheters44

have been similarly effective in identifying target sites forablation.

Pacemapping was initially thought to be more useful asa means of localizing target sites; most investigators report

S54 Journal of Cardiovascular Electrophysiology Vol. 16, No. 9, Supplement, September 2005

Figure 2. (A) Electrocardiogram of a tachycardia arising from the midposterior (rightward) free wall. Note the slightly positive QRS in lead I, a QRS durationof 160 msec, prominent R-wave notching in the inferior leads, and R < S in lead V3. (B,C) Electroanatomical maps in the LAO and cranial projections,respectively, acquired during tachycardia. Format and abbreviations as in Figure 1.

successful ablation at sites with identical or near identicalmatches in all 12 surface leads.12,33,34,37,39 The use of bodysurface mapping and computerized algorithms for compari-son of paced and tachycardia QRS configurations may im-prove the precision of pacemapping.45,46 However, recentdata suggest that the spatial resolution of pacemapping in theRVOT is modest at best. While the probability of obtainingan exact pacemap match increases with decreasing distanceof the pacing site from the site of VT origin, exact matchescould be obtained from multiple sites in all patients, some atpacing sites more than 2 cm away from the site of origin.40

Moreover, pacemapping and activation mapping were highlycorrelated, such that pacemapping added little additional pre-cision to sites selected on the basis of three-dimensional ac-tivation mapping alone.

Location of Tachycardia Focus and Role of the 12-LeadElectrocardiogram

The reported origin of VT within the RVOT varies widely.An important confounding factor is confusion regarding ap-propriate terminology for the complex anatomy of the RVOT.The right coronary cusp is located near the level of the Hisbundle. The bulk of the outflow tract has no true septum,but rather arches anteriorly over the aortic root, which re-places the intraventricular septum as the structure posteriorto the outflow tract. It is this interface, which is designated,if imprecisely, as the septal surface. Confusion also ariseswith respect to the terminology anterior and posterior, whichtypically refer to the location of a site in the right anterioroblique (RAO) radiographic projection. These directions aremore accurately referred to as leftward (toward the left arm)for “anterior” locations, and rightward (toward the right arm)for “posterior” locations. These relationships are summarizedin Figure 3.

Initial reports suggested that VT invariably arose from arelatively well-circumscribed area on the superior mid andanterior septal surface, just under the pulmonary valve.38

However, an early report of surgical cryoablation of adeno-sine sensitive RVOT tachycardia identified a free wall fo-cus.47 Subsequently, a free wall site of origin has been re-ported in 20–30% of patients undergoing radiofrequency(RF) ablation of RVOT VT.32,35-37,39,48,49 The vast major-ity of RVOT VT, both septal and free wall, originates frommyocardium within the first 1–2 cm beneath the pulmonaryvalve. VT may also originate from the muscular sleeve in-vesting the proximal pulmonary artery above the valve.50 Inour laboratory, 72 patients have undergone high-density elec-troanatomical mapping of the RVOT during tachycardia, per-mitting more precise localization of site of origin (Fig. 4). Afree wall focus was identified in 34%.

Figure 3. Schematic demonstrating the orientation of the right ventricularoutflow tract (RVOT) in the chest cavity. AO = aorta.

Joshi and Wilber Ablation of Idiopathic Right Ventricular Outflow Tract Tachycardia S55

Figure 4. Schematic of the RVOT endocardium opened along the anteriorjunction between the free wall and the septum. The schematic is divided into16 segments to characterize the location of successful ablation sites (andsite of VT origin) in 72 patients undergoing electroanatomical mapping ofidiopathic RVOT VT. The number inside each segment indicates the numberof tachycardias localized to that segment.

Several investigators have used pacemapping as a tool toevaluate the potential utility of surface ECG characteristicsin localizing the site of VT origin within the outflow tract. AQS complex in lead I suggests an anterior (leftward) while anR or qR indicates a more posterior (rightward) focus.49,51,52

Precordial lead transition (R≥S) moves leftward as the originmoves caudally from the pulmonary valve, or away fromthe septum.51,52 Wider QRS duration, and notching of theR-wave in the inferior leads was associated with free wallVT. Finally, VT arising within 2 cm of the pulmonary valvevirtually always has a negative QRS in lead avL.49

In a series of 46 patients with RVOT VT presenting forcatheter ablation, we prospectively examined the potentialrole of several ECG criteria in predicting the location of suc-cessful ablation sites. QRS amplitude, notching, duration,and polarity were evaluated for their ability to predict the siteof origin along three perpendicular anatomic axes: septal-free wall, cranial-caudal, and leftward-rightward were evalu-ated.53 Five variables were found to be significant predictorsof location (P < 0.001), and the sensitivity, specificity, andpositive predictive value of each are presented in Table 1.A QRS duration ≥140 msec and R-wave notching in ≥2 ofleads II, III, and avF, were highly specific, but somewhat less

TABLE 1

Evaluation of Electrocardiographic Criteria for Localization of the Originof RVOT Tachycardia

Sensitivity Specificity PPV

Free wall versusseptal sites

QRS duration ≥140 msec 0.74 0.93 0.88R-wave notching in inferior leads 0.79 0.99 0.94Lead V3 R/S ratio ≤1 1.00 0.74 0.73

Anterior (leftward) versusPosterior (rightward) sites

Negative or isoelectric QRS in lead I 0.96 0.67 0.77Caudal (>2 cm from PV)

versus Cranial SitesIsoelectric or positive QRS in lead avL 0.86 1.00 1.00

PPV = positive predictive value; PV = pulmonary valve; RVOT = rightventricular outflow tract.

sensitive in predicting a free wall origin. An R/S ratio ≤1 inlead V3 (reflecting more leftward precordial transition) washighly sensitive, but less specific for a free wall origin. QRSpolarity in lead I (negative or isoelectric) was a sensitive, butless specific predictor of an anterior (leftward) site of origin.Finally, an isoelectric or negative QRS in lead avL stronglypredicted a site caudally in the outflow tract adjacent to theHis bundle. Localization algorithms based on similar criteriahave been reported by others.54,55

Tachycardias with an inferior QRS axis and a very earlyprecordial transition zone (RS ratios ≥1 in leads V1 or V2)usually arise from the left ventricular outflow tract (basalseptum or aortic commissures) or LV epicardium.56,57

Approach to Catheter Ablation

It is our practice to use three-dimensional activation map-ping as the primary localization technique for selecting targetsites for ablation. Once the center of the early activation areais identified, pacemapping at this site invariably producesan excellent or exact pacemap match. Temperature-guidedRF application is important in this region, as cooling of thecatheter tip by circulating blood flow is relatively poor insome regions of the RV; electrode tip temperature may in-crease rapidly with relatively low power applications. In ourexperience, and that of Wen and colleagues,48 terminationof tachycardia at ultimately successful sites generally occurswithin 10 seconds. Acceleration of the tachycardia duringRF application, followed by gradual slowing or abrupt ter-mination may also be observed.12 Application of RF energyin sinus rhythm at sites near the tachycardia origin also mayresult in induction of repetitive responses or tachycardia withQRS characteristics similar to that seen during spontaneousVT.58 These observations may be due to thermal facilitationof triggered activity,59 but may also simply reflect thermallyinduced abnormal automaticity. 60 Neither phenomenon is aspecific marker for a successful ablation site.

Persistent difficulty in identifying optimal target sites, oreliminating VT during ablation is uncommon, but may arisefor several reasons. The induced VT may not be of RVOT ori-gin.61 Occasionally, preexcited tachycardia with antegradeconduction through a right sided accessory AV connection(either passively or as the antegrade limb of AV reciprocat-ing tachycardia) may cause diagnostic confusion, particularlywhen preexcitation is intermittent or latent.62 Finally, a smallnumber of RVOT VTs with typical left bundle (QS or mini-mal R-wave in leads V1 and V2) inferior QRS patterns, anda QS complex in lead aVL, mimicking a typical anteroseptallocation, may originate in the epicardium near the AIV.63

Outcome of Ablation

Table 2 summarizes available data with respect to the out-come of RF catheter ablation of RVOT VT. Series of greaterthan 10 patients were included if adequate outcome data wereprovided. Acute procedural success was reported in 93% ofpatients. In patients with successful ablation, 5% had recur-rent VT during a variable period of follow-up. The majorityof recurrences were within the first year, and patients under-went repeat ablation with long-term freedom from additionalrecurrences. Recurrence more than 1 year postablation wasrare despite follow-up of several years in substantial numberof patients. Procedural variables influencing the probability

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TABLE 2

Outcome of Radiofrequency Catheter Ablation in Patients with Idiopathic Right Ventricular Outflow Tachycardia

Year N Acute Success Mean Follow-up (mo) Recurrence#

Calkins et al.34 1993 10 10/10 8 0/10Coggins et al.36 1994 20 17/20 10 1/17Mandrola et al.35 1995 35 35/35∗ 24 0/35Movsowitz et al.38 1996 18 16/18 12 5/16Gumbrielle et al.33 1997 10 10/10 16 0/10Chinushi et al.32 1997 13 13/13 28 1/13Rodriguez et al.39 1997 35 29/35 30 4/28Almendral et al.37 1998 15 13/15∗ 21 1/13Wen et al.48 1998 44 39/44 41 4/39Aiba et al.44 2001 50 47/50 NA NALee et al.63 2002 35 30/35 NA NAFreidman et al.41 2002 10 9/10 11 2/9O’Donnell et al.22 2003 33 32/33 56 1/32Ribbing et al.43 2003 33 27/33 54 1/27Ito et al.53 2003 109 106/109 21 0/106Current article 2005 72 71/72 51 2/71Total 542 504/542 (93%) 22/426 (5%)

∗Acute success determined at hospital discharge, with one or more patients undergoing repeat procedures due to early recurrence or initial failure. In allother series, success was determined at the end of the initial procedure.#Following initially successful ablation.

of recurrence following initially successful ablation wereexamined by Wen et al. Poor pacemap matches (<12/12),later activation at the target site, as well as reliance onpacemapping alone, were each significant predictors of recur-rence.48 Serious complications occur in approximately 1% ofpatients, usually related to cardiac perforation.

Recurrent symptoms or VT occur in 30–40% of patientsduring long-term follow-up on pharmacologic therapy.6,64,65

In patients with hemodynamic compromise associated withtachycardia (syncope and presyncope), ablation should beconsidered as primary therapy. When symptoms are less se-vere, multiple factors, including side effects and inconve-nience associated with long-term drug therapy, frequency ofsymptoms, response to prior drug trials, and patient pref-erence need to be balanced against the small risk of pro-cedural complications. Tachycardiomyopathy secondary toidiopathic RVOT VT is uncommon, but well documented,and should be considered in the occasional patient withmild/moderate unexplained left ventricular dysfunction andfrequent tachycardia.66 Successful treatment can lead to nor-malization of LV function, with current technology, and inexperienced centers, catheter ablation of RVOT VT can be ac-complished with low morbidity and excellent immediate andlong-term outcome. These results approach those reportedfor supraventricular tachycardia.

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