S52

Ablation of Idiopathic Right Ventricular Outflow Tract

Tachycardia: 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 heart
disease is a common entity. Exclusion of occult structural disease such as arrhythmogenic right ventricular
cardiomyopathy is critical as this diagnosis impacts both ablation outcomes and long-term prognosis. VT
is most commonly due to triggered activity. Induction of the target arrhythmia in the laboratory is often
problematic, and is frequently facilitated by catecholamine infusion. Recent data indicate that high-density
three-dimensional activation mapping facilitates identification of target sites for ablation, and that the
spatial resolution of pacemapping may be more limited than previously recognized. A standard 12-lead
electrocardiogram is useful in providing an initial approximation of the site of origin within the outflow
tract, and may contain subtle clues to potentially confounding foci on the left ventricular endocardial
or epicardial surface. When sufficient arrhythmia is present to permit mapping, successful ablation can
be 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 of
supraventricular tachycardia. (J Cardiovasc Electrophysiol, Vol. 16, pp. S52-S58, Suppl. 1, September 2005)

catheter ablation, ventricular tachycardia, mapping, right ventricle

Introduction (both uncommon in idiopathic RV tachycardia). However,

Ventricular tachycardia (VT) arising from the right ven-
tricular outflow tract (RVOT) in the absence of overt structural
heart disease is a common entity, representing up to 10% of all
VTs evaluated by specialized arrhythmia services.1,2 Clini-
cal presentation is variable, with symptom onset typically
between the ages of 20 and 40 years. The arrhythmia appears
to be more common in women.2 Nonsustained VT is more
frequent, comprising 60–92% of reported series.3-6 Episodes
most often occur as repetitive salvos (the pattern of repetitive
monomorphic VT)7-8 Occasionally, runs of VT are inces-
sant, and premature ventricular beats comprise a substantial
proportion of all QRS complexes in a 24-hour-period. Less
commonly, patients present with paroxysmal sustained tachy-
cardia, separated by relatively long intervals of infrequent
premature ventricular beats.9-12 Episodes tend to increase in
frequency and duration during exercise and emotional stress.
In more than 80% of patients, the QRS configuration is a left
bundle pattern with an inferior axis, reflecting an origin in
the 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 always
be detected on the basis of clinical examination and rou-
tine echocardiography.13-16 VT associated with ARVC usu-
ally manifests multiple QRS configurations during different
episodes, 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, IL
60153. Fax: 708-327-2377; E-mail: dwilber@lumc.edu
doi: 10.1111/j.1540-8167.2005.50163.x
many patients with ARVC present with a left bundle, infe-
rior QRS axis tachycardia alone.17,18 Exclusion of ARVC
in patients considered for catheter ablation is more than an
academic exercise, since both long-term prognosis,18-20 and
response to catheter ablation20-22 may be less favorable.
The diagnosis of ARVC remains problematic. The 1994
European Society of Cardiology Task Force criteria provide
widely accepted guidelines.23 An abnormal signal-averaged
electrocardiogram (SAECG) is uncommon in patients with
idiopathic RVOT VT, while an abnormal time or frequency
domain SAECG is present in 50–80% of patients with
ARVC.24,25 The 12-lead electrocardiogram is usually nor-
mal. Widespread T-wave inversion in the anterior precordial
leads, and incomplete or complete right bundle branch block
suggests ARVC.20
Cine magnetic resonance imaging (MRI) and radionuclide
right ventriculography provide useful information regarding
right ventricular size and function. However, several groups
have reported a substantial incidence of MRI abnormalities
(65–76%) in patients with idiopathic RVOT VT without other
evidence of ARVC.26-28 These abnormalities included focal
thinning and segmental contraction abnormalities, and were
equally distributed between the outflow tract and the anterior
free wall. In addition, focal fatty infiltration was observed
in approximately 25% of patients. The clinical significance
of 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 with
caution.28
Long-term prognosis in patients with truly idiopathic
RVOT VT is excellent, despite frequent recurrences of tachy-
cardia.3-12,29 Sudden death is rare in patients with initially
normal left and right ventricular function; in such patients,
occult cardiomyopathy is usually identified on postmortem
examination. Similarly, progression to diffuse cardiomyopa-
thy is rare.
 Joshi and Wilber Ablation of Idiopathic Right Ventricular Outflow Tract Tachycardia S53

Electrophysiologic Evaluation Endocardial Mapping

The large majority of idiopathic outflow tract tachycardias
are due to cyclic AMP mediated triggered activity.10,12,30 In
contrast, tachycardias associated with ARVC are commonly
due to reentry.20,28 Adenosine rarely influences tachycardias
due to reentry,31 and in particular has no effect on VT associ-
ated with ARVC. In patients who present with sustained VT
due 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 critical
range 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 required
to 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, and
coupling intervals during ventricular pacing. Aminophylline
and atropine, though theoretically useful in facilitating trig-
gered activity, are rarely effective. Sedation may suppress this
VT, particularly the use of benzodiazepines and propafol.
The QRS morphology during RVOT VT typically has a left
bundle configuration with QS or rS patterns in leads V1 and
V2, and a right or left inferior axis (Figs. 1A and 2A). Minor
variations in QRS morphology between complexes during
tachycardia may occur, associated with minor variations in
local electrograms recorded near the site of tachycardia ori-
gin.32 However, multiple morphologically distinct VTs due
to triggered activity are rare, and should raise suspicion of
alternate mechanisms and occult underlying heart disease.
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 successful
ablation sites tends to be only modestly early, ranging from
10–60 msec prior to onset of the surface QRS.32-39 Bipo-
lar endocardial electrograms have high amplitudes and rapid
slew rates. Fractionated complex electrograms and diastolic
potentials are rarely if ever seen, and should raise suspicion
of 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 10
msec 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 the
manual assignment of activation time, it is not surprising that
electrogram timing alone has been reported to have relatively
limited utility as a predictor of successful ablation sites. How-
ever, high-density simultaneous display of activation time and
anatomic location with three-dimensional electroanatomical
mapping systems facilitates discrimination between minor
differences 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 with
noncontact arrays41-43 and multielectrode basket catheters44
have been similarly effective in identifying target sites for
ablation.
Pacemapping was initially thought to be more useful as
a means of localizing target sites; most investigators report

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 of
R-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 are
shown in red. The brown dots represent ablation sites. Orange dots represent the His bundle. PV = pulmonary valve.
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 duration
of 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 identical Initial reports suggested that VT invariably arose from a
matches in all 12 surface leads.12,33,34,37,39 The use of body relatively well-circumscribed area on the superior mid and
surface mapping and computerized algorithms for compari- anterior septal surface, just under the pulmonary valve.38
son of paced and tachycardia QRS configurations may im- However, an early report of surgical cryoablation of adeno-
prove the precision of pacemapping.45,46 However, recent sine sensitive RVOT tachycardia identified a free wall fo-
data suggest that the spatial resolution of pacemapping in the cus.47 Subsequently, a free wall site of origin has been re-
RVOT is modest at best. While the probability of obtaining ported in 20–30% of patients undergoing radiofrequency
an exact pacemap match increases with decreasing distance (RF) ablation of RVOT VT.32,35-37,39,48,49 The vast major-
of the pacing site from the site of VT origin, exact matches ity of RVOT VT, both septal and free wall, originates from
could be obtained from multiple sites in all patients, some at myocardium within the first 1–2 cm beneath the pulmonary
pacing sites more than 2 cm away from the site of origin.40 valve. VT may also originate from the muscular sleeve in-
Moreover, pacemapping and activation mapping were highly vesting the proximal pulmonary artery above the valve.50 In
correlated, such that pacemapping added little additional pre- our laboratory, 72 patients have undergone high-density elec-
cision to sites selected on the basis of three-dimensional ac- troanatomical mapping of the RVOT during tachycardia, per-
tivation mapping alone. mitting more precise localization of site of origin (Fig. 4). A
free wall focus was identified in 34%.
Location of Tachycardia Focus and Role of the 12-Lead
Electrocardiogram
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 His
bundle. 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 posterior
to the outflow tract. It is this interface, which is designated,
if imprecisely, as the septal surface. Confusion also arises
with respect to the terminology anterior and posterior, which
typically refer to the location of a site in the right anterior
oblique (RAO) radiographic projection. These directions are
more accurately referred to as leftward (toward the left arm)
for “anterior” locations, and rightward (toward the right arm)
for “posterior” locations. These relationships are summarized Figure 3. Schematic demonstrating the orientation of the right ventricular
in Figure 3. outflow tract (RVOT) in the chest cavity. AO = aorta.
 Joshi and Wilber Ablation of Idiopathic Right Ventricular Outflow Tract Tachycardia
Figure 4. Schematic of the RVOT endocardium opened along the anterior
junction between the free wall and the septum. The schematic is divided into
16 segments to characterize the location of successful ablation sites (and
site of VT origin) in 72 patients undergoing electroanatomical mapping of
idiopathic RVOT VT. The number inside each segment indicates the number
of tachycardias localized to that segment.
Several investigators have used pacemapping as a tool to
evaluate the potential utility of surface ECG characteristics
in localizing the site of VT origin within the outflow tract. A
QS complex in lead I suggests an anterior (leftward) while an
R or qR indicates a more posterior (rightward) focus.49,51,52
Precordial lead transition (R ≥ S) moves leftward as the origin
moves caudally from the pulmonary valve, or away from
the septum.51,52 Wider QRS duration, and notching of the
R-wave in the inferior leads was associated with free wall
VT. Finally, VT arising within 2 cm of the pulmonary valve
virtually always has a negative QRS in lead avL.49
In a series of 46 patients with RVOT VT presenting for
catheter ablation, we prospectively examined the potential
role 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 site
of 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 predictors
of location (P < 0.001), and the sensitivity, specificity, and
positive predictive value of each are presented in Table 1.
A QRS duration ≥140 msec and R-wave notching in ≥2 of
leads II, III, and avF, were highly specific, but somewhat less
TABLE 1
Evaluation of Electrocardiographic Criteria for Localization of the Origin
of RVOT Tachycardia
Sensitivity Specificity
Free wall versus
septal sites
QRS duration ≥140 msec 0.74 0.93
R-wave notching in inferior leads 0.79 0.99
Lead V3 R/S ratio ≤1 1.00 0.74
Anterior (leftward) versus
Posterior (rightward) sites
Negative or isoelectric QRS in lead I 0.96 0.67
Caudal (>2 cm from PV)
versus Cranial Sites
Isoelectric or positive QRS in lead avL 0.86 1.00
PPV = positive predictive value; PV = pulmonary valve; RVOT = right
ventricular outflow tract.
S55
sensitive in predicting a free wall origin. An R/S ratio ≤1 in
lead V3 (reflecting more leftward precordial transition) was
highly sensitive, but less specific for a free wall origin. QRS
polarity in lead I (negative or isoelectric) was a sensitive, but
less specific predictor of an anterior (leftward) site of origin.
Finally, an isoelectric or negative QRS in lead avL strongly
predicted a site caudally in the outflow tract adjacent to the
His bundle. Localization algorithms based on similar criteria
have been reported by others.54,55
Tachycardias with an inferior QRS axis and a very early
precordial transition zone (RS ratios ≥1 in leads V1 or V2)
usually arise from the left ventricular outflow tract (basal
septum 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 target
sites for ablation. Once the center of the early activation area
is identified, pacemapping at this site invariably produces
an excellent or exact pacemap match. Temperature-guided
RF application is important in this region, as cooling of the
catheter tip by circulating blood flow is relatively poor in
some regions of the RV; electrode tip temperature may in-
crease rapidly with relatively low power applications. In our
experience, and that of Wen and colleagues,48 termination
of tachycardia at ultimately successful sites generally occurs
within 10 seconds. Acceleration of the tachycardia during
RF application, followed by gradual slowing or abrupt ter-
mination may also be observed.12 Application of RF energy
in sinus rhythm at sites near the tachycardia origin also may
result in induction of repetitive responses or tachycardia with
QRS characteristics similar to that seen during spontaneous
VT.58 These observations may be due to thermal facilitation
of triggered activity,59 but may also simply reflect thermally
induced abnormal automaticity. 60 Neither phenomenon is a
specific marker for a successful ablation site.
Persistent difficulty in identifying optimal target sites, or
eliminating VT during ablation is uncommon, but may arise
for several reasons. The induced VT may not be of RVOT ori-
gin.61 Occasionally, preexcited tachycardia with antegrade
conduction through a right sided accessory AV connection
(either passively or as the antegrade limb of AV reciprocat-
ing tachycardia) may cause diagnostic confusion, particularly
when preexcitation is intermittent or latent.62 Finally, a small
number of RVOT VTs with typical left bundle (QS or mini-
mal R-wave in leads V1 and V2) inferior QRS patterns, and
a QS complex in lead aVL, mimicking a typical anteroseptal
location, may originate in the epicardium near the AIV.63
PPV Outcome of Ablation
Table 2 summarizes available data with respect to the out-
0.88 come of RF catheter ablation of RVOT VT. Series of greater
0.94 than 10 patients were included if adequate outcome data were
0.73 provided. Acute procedural success was reported in 93% of
patients. In patients with successful ablation, 5% had recur-
0.77
rent VT during a variable period of follow-up. The majority
of recurrences were within the first year, and patients under-
went repeat ablation with long-term freedom from additional
1.00 recurrences. Recurrence more than 1 year postablation was
rare despite follow-up of several years in substantial number
of patients. Procedural variables influencing the probability
S56 Journal of Cardiovascular Electrophysiology Vol. 16, No. 9, Supplement, September 2005

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 0/10

Coggins et al.36 1994 20 17/20 10 1/17
Mandrola et al.35 1995 35 35/35∗ 24 0/35
Movsowitz et al.38 1996 18 16/18 12 5/16
Gumbrielle et al.33 1997 10 10/10 16 0/10
Chinushi et al.32 1997 13 13/13 28 1/13
Rodriguez et al.39 1997 35 29/35 30 4/28
Almendral et al.37 1998 15 13/15∗ 21 1/13
Wen et al.48 1998 44 39/44 41 4/39
Aiba et al.44 2001 50 47/50 NA NA
Lee et al.63 2002 35 30/35 NA NA
Freidman et al.41 2002 10 9/10 11 2/9
O’Donnell et al.22 2003 33 32/33 56 1/32
Ribbing et al.43 2003 33 27/33 54 1/27
Ito et al.53 2003 109 106/109 21 0/106
Current article 2005 72 71/72 51 2/71
Total 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 all
other series, success was determined at the end of the initial procedure.
# Following initially successful ablation.

of recurrence following initially successful ablation were
examined by Wen et al. Poor pacemap matches (<12/12),
later activation at the target site, as well as reliance on
pacemapping alone, were each significant predictors of recur-
rence.48 Serious complications occur in approximately 1% of
patients, usually related to cardiac perforation.
Recurrent symptoms or VT occur in 30–40% of patients
during long-term follow-up on pharmacologic therapy.6,64,65
In patients with hemodynamic compromise associated with
tachycardia (syncope and presyncope), ablation should be
considered as primary therapy. When symptoms are less se-
vere, multiple factors, including side effects and inconve-
nience associated with long-term drug therapy, frequency of
symptoms, response to prior drug trials, and patient pref-
erence need to be balanced against the small risk of pro-
cedural complications. Tachycardiomyopathy secondary to
idiopathic RVOT VT is uncommon, but well documented,
and should be considered in the occasional patient with
mild/moderate unexplained left ventricular dysfunction and
frequent tachycardia.66 Successful treatment can lead to nor-
malization of LV function, with current technology, and in
experienced centers, catheter ablation of RVOT VT can be ac-
complished with low morbidity and excellent immediate and
long-term outcome. These results approach those reported
for supraventricular tachycardia.
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