Twelve-lead ECG features to identify ventricular tachycardia
arising from the epicardial right ventricle
Victor Bazan, MD, Rupa Bala, MD, Fermin C. Garcia, MD, Jonathan S. Sussman, MD,
Edward P. Gerstenfeld, MD, Sanjay Dixit, MD, David J. Callans, MD, Erica Zado, PA,
Francis E. Marchlinski, MD
From the Cardiovascular Division, Department of Medicine, Hospital of the University of Pennsylvania,
Philadelphia, Pennsylvania.
BACKGROUND Usefulness of 12-lead ECG for predicting an epi-
cardial origin for ventricular tachycardia (VT) arising from the
right ventricle (RV) has not been assessed. An epicardial approach
is sometimes warranted to eliminate RV VT.
OBJECTIVES The purpose of this study was investigate the hy-
pothesis that specific ECG features identify an epicardial origin for
RV VT.
METHODS To mimic an endocardial or epicardial origin, we paced
representative sites in 13 patients undergoing RV endocardial/
epicardial mapping (134/180 pace map sites).
RESULTS QRS duration from epicardial vs endocardial sites was
not different (183 27 ms vs 185 28 ms, P .3). Reported
cut-off values for identifying epicardial left ventricular origin,
pseudo-delta wave (34 ms), intrinsicoid deflection time (85
ms), and RS complex (121 ms) did not apply to the RV. A Q wave
in lead II, III, or aVF was more likely noted from inferior epicardial
Introduction
Successful catheter ablation for both left ventricular (LV)
and right ventricular (RV) tachycardia (VT) sometimes re-
quires an epicardial approach.1 6 Specific 12-lead ECG pat-
terns have been described as helpful for identifying an
epicardial VT origin in the LV, including pseudo-delta
wave 34 ms, intrinsicoid deflection time 85 ms, RS
complex duration 121 ms, and delayed precordial maxi-
mum deflection index 0.55.7,8 The 12-lead ECG is useful
for identifying ventricular arrhythmias from specific regions
of the RV endocardium, especially from the RV outflow
tract (RVOT).9 11 However, its usefulness in predicting an
epicardial site of origin in the RV has not been established.
Thus, characterizing ECG patterns to predict an epicardial
origin in the RV is of interest. We sought to describe ECG
features that predict an epicardial site of origin for RV
arrhythmias by mimicking the origin of VT with RV endo-
cardial and epicardial pace mapping.
Address reprint requests and correspondence: Dr. Francis E. March-
linski, Hospital of the University of Pennsylvania, 9 Founders Pavilion,
3400 Spruce Street, Philadelphia, Pennsylvania 19104. E-mail address:
francis.marchlinski@uphs.upenn.edu. (Received April 27, 2006; accepted
June 23, 2006.)
1547-5271/$ -see front matter 2006 Heart Rhythm Society. All rights reserved.
vs endocardial sites (53/73 vs 16/43, P .01). A Q wave in lead I
was more frequently present from epicardial vs endocardial ante-
rior RV sites (30/82 vs 5/52, P .001). QS in lead V2 was noted
from anatomically matched epicardial anterior RV sites (22/33 vs
13/33, P .05). In the RV outflow tract, no ECG feature distin-
guishing epicardial/endocardial origin reached statistical signifi-
cance.
CONCLUSION A Q wave or QS in leads that best reflect local
activation suggest an epicardial origin for RV depolarization and
may help in identifying a probable epicardial site of origin for RV
VT. QRS duration and reported criteria for epicardial origin of VT
in the left ventricle do not identify a probable epicardial origin
in the RV.
KEYWORDS Epicardium; Ventricular tachycardia; Pace mapping;
Right ventricle
(Heart Rhythm 2006;3:11321139) 2006 Heart Rhythm Society.
All rights reserved.
Methods
Patient population
Twenty-five patients underwent endocardial and epicardial
catheter mapping and ablation for drug-refractory ventricu-
lar arrhythmias. In each patient, the risks of mapping/abla-
tion were discussed in detail, and all patients gave written
informed consent in accordance with institutional guidelines
of the University of Pennsylvania Health System. Each
patient underwent detailed voltage mapping, pace mapping,
and activation mapping in an attempt to characterize the VT
substrate and target/ablate their arrhythmia.
Study protocol
To be included in this study analysis, each patient was
required to undergo detailed pace mapping from both en-
docardial and epicardial free-wall surfaces of the RV. Each
pace mapping site was tagged on an electroanatomic map
(CARTO, Biosense Webster, Diamond Bar, CA, USA) of
the RV chamber of interest for detailed offline analysis. A
detailed electroanatomic map in sinus rhythm was per-
formed using a 4-mm-tip catheter maintaining a fill thresh-
old of 20 mm, with the entire surface of the RV endocar-
dium and epicardium documented to be sampled. Pace
mapping was performed using bipolar pacing (distance be-
tween poles 1 and 2 1 mm) at threshold from both
doi:10.1016/j.hrthm.2006.06.024
Bazan et al ECG Features for Epicardial Right Ventricle VT 1133

epicardial and endocardial free-wall surfaces at cycle

lengths of 400 to 600 ms. This allowed for analysis of the
QRS obtained as a consequence of local and not distant
capture. Data acquisition created an anatomic shell of the
RV that allowed for identification of pace mapping sites in
specific regions of the RV endocardium and epicardium.
The 12-lead ECG QRS complex acquired from each pace
mapping site was recorded and subsequently analyzed using
the Prucka CardioLab recording system (Houston, TX,
USA). The following ECG features were assessed: (1) QRS
duration; (2) initial Q wave or QS complex in leads V2, I, II,
III, and aVF; (3) QRS polarity amplitude ratio between II/III
and between aVL/aVR (if the QRS vector was more posi-
tive or less negative in lead II or aVL, respectively, the ratio
was considered 1); and (4) pseudo-delta wave, intrinsi-
coid deflection time, and shortest RS complex values, as
described in reported data that successfully identified an LV
Figure 1 Schematic right anterior oblique view of the right ventricle
epicardial origin.7 (RV) divided into regions to identify the site-specific influences on ECG
We hypothesized that, comparing epicardial to endocar- criteria for distinguishing endocardial vs epicardial site of origin (see text
dial pace mapping sites, (1) QRS duration would be in- for details).
creased from the epicardium; (2) initial Q waves would
more likely be present from the epicardium with an initial
negative QRS vector in leads I and V2 for anterior (left- for each patient (Figure 1). Of note, the anterior margin
ward) sites and in lead II, III, or aVF for inferior RV sites; of the RV was always established from the endocardium
(3) epicardial sites in the RVOT region would be more to avoid epicardial pace mapping sites obtained from the
leftward and thus would produce polarity ratio 1 for leads interventricular septum. This segmentation allowed us to
II/III and aVL/aVR; and (4) reported criteria for predicting group regions to assess the impact of an outflow tract
epicardial origin in the LV do not apply to the RV. location (RVOT), anterior location (apical superior and
Each pace mapping site had to be separated by at least apical inferior), basal location (basal superior and basal
5 mm as confirmed by electroanatomic mapping in order to inferior), and inferior location (basal inferior and apical
be included as a distinct pace mapping site. QRS duration inferior) on ECG characteristics.
was assessed from the pacing stimulus to the latest QRS in We also measured the QRS duration from RV septal sites
any of the 12 recorded leads. The reviewer was blinded to with the goal of comparing these values to the QRS duration
the location of the pacing site at the time of all measure- of free-wall endocardial and epicardial pace mapping sites.
ments.
Anatomically matched RV epicardial/endocardial
Epicardial access site analysis
Epicardial access for activation and pace mapping was ob- In order to avoid unequal weighting of certain ECG patterns
tained using the techniques described by Sosa et al.12 After
related to the heterogeneous sampling of pace mapping for
pericardial puncture, which was guided by use of contrast, a
the RV free wall among patients and between endocardium
wire was deployed into the pericardial space and the needle
and epicardium, a more restrictive analysis was performed
withdrawn. A standard 8Fr sheath was introduced. A 4-mm-
comparing individually epicardial pace mapping sites with
tip CARTO was advanced through the sheath for mapping
and ablation on the epicardial surface. the corresponding (just opposite) endocardial pace mapping
sites. The average anatomic distance between endocardial
RV free-wall sites and epicardial matched sites was 17 6 mm, and no site
To facilitate the identification of region-specific ECG fea- was more than 25 mm apart.
tures that might suggest an epicardial origin, pace mapping
sites in the RV were grouped into distinct anatomic seg- Statistical analysis
ments: from the pulmonic valve to the top of the tricuspid Continuous variables are expressed as mean SD and were
valve (outflow tract region), top of the tricuspid valve to mid compared using a paired or unpaired Student t-test as ap-
tricuspid valve (mid RV region), and mid tricuspid valve to propriate. Categorical variables were compared using Chi-
bottom of the RV (inferior RV region). The mid and infe- square or Fisher exact test as appropriate. P .05 was
rior RV regions were further divided into two equal considered significant. Sensitivity and specificity values
portions basal and apicalin the vertical direction. were determined for each ECG feature that reached statis-
Thus, a total of five distinct anatomic segments were tical significance in anatomically matched pace mapping
defined from either the endocardium or the epicardium analysis.
1134 Heart Rhythm, Vol 3, No 10, October 2006

Table 1 Clinical characteristics of the patient population A total of 180 epicardial and 134 endocardial free-wall
Age (yr) 50 18
pace mapping sites were analyzed. The proportion of epi-
Male/female 10/3 cardial/endocardial pace mapping sites was as follows: an-
Structural heart disease CAD: 2 terior RV 84/52; inferior RV 76/43; basal RV 59/62; and
DCM: 4 RVOT 37/20.
RV CM: 2 Anatomically matched epicardial and endocardial sites
No SHD: 5
Clinical arrhythmia:
were identified for 94 of the 134 endocardial sites, or an
Premature ventricular complex/ 4 average of 7.3 4 sites per patient. In addition, the QRS
nonsustained VT duration was assessed for 51 RV septal sites.
Sustained VT 9
Pace mapping sites performed QRS duration
(epicardium/endocardium) The QRS duration for endocardial septal sites was signifi-
Right ventricular outflow tract 37/20 cantly shorter than both epicardial (154 23 ms vs 183
Basal superior 24/40 27 ms, P .001) and endocardial free-wall (154 23 ms vs
Apical superior 43/31 185 28 ms, P .001) surfaces (Table 2). However, there
Basal inferior 35/22
Apical inferior 41/21 was no difference in QRS duration between epicardial and
Total 180/134 endocardial free-wall sites (P .3). This remained true
Values are presented as number or mean SD.
when only the anatomically matched RV endocardial and
CAD coronary artery disease; DCM dilated cardiomyopathy; RV CM epicardial sites were compared (172 27 ms vs 176 24
right ventricular cardiomyopathy; SHD structural heart disease; VT ms, respectively P .3). No region-specific differences in
ventricular tachycardia. QRS duration were found.
Anterior RV
Results The presence of a Q wave in lead I was noted to be more
Baseline characteristics of the patient population are given frequent when pacing from the epicardial surface (30/84
in Table 1. From a total of 25 patients undergoing epicardial [36%]) than from the endocardial free wall (5/52 [9.6%])
VT procedures, 13 patients (10 men and 3 women; age from RV anterior segments (P .01; Figure 2). In addition,
50 18 years) underwent detailed RV endocardial and the presence of a QS complex in lead V2 was noted from 46
epicardial mapping and were included in the analysis. Eight (55%) of 84 epicardial vs 21 (40%) of 52 endocardial pace
of the 13 patients had structural heart disease, and the mapping sites (P .1). For anatomically matched sites
remaining seven patients presented with idiopathic prema- from the anterior RV region, the presence of Q wave in lead
ture ventricular complexes or sustained VT. I was still significantly more frequent when pacing from the

Table 2 Results of region-specific ECG features distinguishing RV epicardial vs endocardial pace mapping sites

Anterior RV Inferior RV Basal RV RVOT RV all sites

No. of pace mapping sites
Epi 84 76 59 37 180
Endo 52 43 62 20 134
QRSd (ms)
Epi 178 24 190 30 197 28 173 18 183 26
Endo 176 25 192 31 197 27 169 18 185 28
Q lead II, III, or aVF
Epi (%) 42 78* 61* 0 38*
Endo (%) 29 40 32 5 27
Q lead I
Epi (%) 36* 18 5 24 23*
Endo (%) 10 9 3 10 12
QS lead V2
Epi (%) 55 28 36 59 46*
Endo (%) 40 33 27 20 31
aVL/aVR 1
Epi (%) 25 8 2 59 24
Endo (%) 23 9 10 40 19
II/III 1
Epi (%) 18 3 2 51 19
Endo (%) 21 7 5 30 15
QRS duration is presented as mean SD. Values are presented as percentage of pace map sites from the corresponding specific RV region and surface
that meet a particular criteria.
*P .05 comparing epicardial to corresponding free-wall endocardial pace mapping sites.
Endo endocardium; Epi epicardium; QRSd QRS complex duration; RV right ventricle; RVOT right ventricular outflow tract.
Bazan et al ECG Features for Epicardial Right Ventricle VT
Figure 2 Site-specific ECG features for identifying an epicardial site of origin. Distance distance between epicardial and just opposite matched
endocardial pace mapping site for each anatomically matched pace mapping; RV right ventricle; RVOT right ventricular outflow tract.
epicardium (P .001), as was a QS complex in lead V2
(P .05; Figure 3). Sensitivity and specificity values for Q
wave in lead I in this region were 52% and 94%, respec-
tively, whereas those of a QS complex in lead V2 were 67%
and 61%, respectively. Both a Q wave in lead I and a QS
complex in lead V2 were present in 24 (29%) of 84 epicar-
dial pace mapping sites but in only 5 (9.6%) of 52 endo-
cardial pace mapping sites (P .01) and did not enhance the
predictive value of the observed with the individual leads.
Inferior RV
The presence of a Q wave in inferior leads was noted to be
more frequent when pacing from the epicardial surface than
from the endocardium from the RV inferior segments. For
lead II, initial Q wave was present when pacing from the
epicardial surface in 53 (70%) of 76 pace mapping sites vs
16 (37%) of 43 sites from the endocardium (P .001). For
lead III, the proportion was 59 (78%) of 76 vs 16 (37%) of
43, respectively (P .001). For lead aVF, an initial Q wave
was present for 53 (70%) of 76 epicardial pace mapping vs
17 (40%) of 43 endocardial pace mapping sites (P .01).
This remained significant for anatomically matched sites
obtained from the inferior region in the RV (Figure 3). A Q
wave in lead II, III, or aVF was present for 71% of epicar-
dial inferior pace mapping sites vs 26% of pace mapping
sites from the endocardium (P .001). The sensitivity and
specificity values for Q wave in lead II, III, or aVF when
pacing from the epicardium were 71% and 74%, respec-
tively, from this inferior RV region.
Basal RV
The presence of Q wave in lead II, III, or aVF was also more
frequently observed with epicardial pace mapping in this
1135
region of the RV (P .01). However, excluding inferior
sites in the basal RV (basal inferior), a Q wave in inferior
leads no longer distinguished an epicardial from an endo-
cardial origin. For basal superior RV sites, the presence of
a Q wave in lead V2 was significantly more frequent when
pacing from the epicardial surface: 17 (71%) of 24 from the
epicardium vs 10 (25%) of 40 endocardial pace mapping
sites (P .01). However, these results did not remain sta-
tistically significant after anatomically matched site analysis
was performed in this RV segment (P .25).
RV outflow tract
None of the described criteria were noted to be significantly
more prevalent in the RVOT region when pacing from the
epicardial surface. However, leads III and aVR tended to be
more positive and less negative, respectively, when pacing
from the epicardium compared with endocardial pace map-
ping sites in this region. As a result, there was a trend for
lead II/III and aVL/aVR polarity amplitude ratios to be 1
from the epicardium. For aVL/aVR, 22 (59%) of 37 epicar-
dial pace mapping sites had a ratio 1 vs 8 (40%) of 20 in
the free-wall endocardium (P .1). Likewise, II/III ratio
was 1 if pacing was performed from the epicardium in this
area: 19 (51%) of 37 from epicardium vs 6 (30%) of 20
from the endocardial surface (P .1). When anatomically
matched pace mapping sites analysis was performed in the
RVOT region, these differences did not reach statistical
significance.
Previously reported criteria for assessing
epicardial origin
Region-specific differences between epicardial and endo-
cardial surfaces with respect to the presence of a pseudo-
1136 Heart Rhythm, Vol 3, No 10, October 2006

Figure 3 Anatomically matched pace mapping sites analysis. Site-specific ECG features for predicting an epicardial ventricular tachycardia origin for
anterior right ventricle (RV) (A), inferior RV (B), right ventricular outflow tract (RVOT) (C), and basal RV (D). P .05 is considered statistically significant.
Values are presented as proportion of number of pace mapping (PM) sites that meet particular criteria in that region and as mean SD. Mean distance
between endocardial and epicardial matched pace mapping is shown for every represented RV region.

delta wave, intrinsicoid deflection time, and shortest RS
complex in the precordial leads were assessed. Although
some significant differences between endocardial and epi-
cardial pace map sites were seen (Table 3), none of the
reported cut-off values for predicting an epicardial origin in
the LV (pseudo-delta wave 34 ms, intrinsicoid deflection
time 85 ms, and shortest QRS complex throughout pre-
cordial leads 121 ms) significantly applied to the RV to
differentiate an epicardial origin.
Clinical outcome
All 13 patients had prior unsuccessful endocardial ablation
attempts. After detailed evaluation of both endocardium and
epicardium, a total of six VTs were targeted for ablative
therapy from the epicardial surface in the RV in three
patients. Of these six VTs, 5 (83%) were successfully ab-
lated, with no clinical recurrence over a mean follow-up of
10 2 months. The remaining VT could not be abolished
despite endocardial and epicardial ablation, and indeed epi-
cardial pace mapping did not present a good QRS match of
the VT. Importantly, each of the five VTs that were suc-
cessfully ablated fulfilled the site-specific ECG criteria de-
scribed for identifying an epicardial origin of the arrhythmia.
Two of these patients presented with RV cardiomyopathy.
Figure 4 shows an example of VT QRS match from both the
epicardial and endocardial best pace mapping sites, fulfilling
the described ECG feature for identifying an epicardial RV
VT origin.
Bazan et al ECG Features for Epicardial Right Ventricle VT 1137

Table 3 Reported criteria for predicting epicardial VT origin in the LV applied to the RV

Anterior RV Inferior RV Basal RV RVOT RV all sites

Pseudo-delta wave
Epi 44 16 46 18 54 17 59 13 49 18
Endo 42 14 44 15 53 18 51 13 49 17
P .6 .6 .8 .03 .9
IDT
Epi 16 20 36 30 36 32 26 22 25 26
Endo 13 14 44 33 20 19 17 14 17 16
P .3 .02 .01 .06 .01
RS complex
Epi 85 17 95 23 106 21 108 21 95 25
Endo 77 13 88 20 99 14 97 16 90 20
P .01 .1 .03 .03 .06
Values are expressed as mean SD (in milliseconds).
P .05 is considered statistically significant.
Endo endocardium; Epi epicardium; IDT intrinsicoid deflection time, distance from stimulation artifact to peak of R wave in lead V2; LV left
ventricle; pseudo-delta wave interval from stimulation artifact to earliest fast deflection in any precordial lead; RS complex shortest distance between
stimulation artifact to nadir of the first S wave in any precordial lead; RV right ventricle; RVOT right ventricular outflow tract. See text for details.

Discussion present with Q wave or QS complex in lead I and V2, and

The present study shows that when a stimulus rises from the
epicardial surface of the RV, the QRS is more likely to
demonstrate initial negative forces (Q waves) in inferior
leads, lead I, and/or lead V2, depending upon the region of
origin. More specifically, the anterior epicardial sites
inferior RV epicardial sites show an initial Q wave in
inferior leads. These observations were consistently ob-
served overall and when comparative analysis for anatom-
ically matched epicardial and endocardial pace mapping
sites was performed.
ECG characteristics that predict epicardial site of origin
in the LV and aortic cusps have been defined.7,8 These
features result from the slurring initial portion of the QRS
complex from the epicardium.
No ECG features have been described to predict an
epicardial site of origin in the RV.
Pacing from either endocardial and epicardial surfaces
should reproduce the activation pattern present in focal
arrhythmias and from exit sites in reentrant tachycar-
dias.13,14 We previously used this technique to successfully
develop ECG criteria that can accurately localize RVOT
and basal LV VT.10,15
The ECG features described in the present study appear
to be a manifestation of the vector of the initial wavefront of
the RV activation rising from either the epicardium or the
endocardium. Thus, they should apply for defining a site of
origin or exit site near the endocardial or the epicardial
surface for RV tachycardias.

Figure 4 Comparison between epicardial ventricular tachycardia (VT)
QRS and epicardial vs endocardial best pace mapping (PM) sites. Site-
specific ECG feature for predicting an epicardial origin for right ventricular
VT is included.
QRS duration
According to our results, differences in QRS width between
RV epicardial and endocardial free-wall sites of origin do
not exist, as has been reported for the LV.7 We hypothesize
that two contributing factors may play a role in this obser-
vation. The first is related to RV wall thickness. Wall
thickness in the RV is less than in the LV; thus, muscle mass
might not play a significant role in delaying stimulus con-
duction from the epicardium. Second, the extent of the
Purkinje network over the RV free wall is less than that
noted from over the LV free wall. Thus, slowing of con-
duction may be more similar from an endocardial and epi-
cardial RV free wall site than noted for the LV. This hy-
1138
pothesis is further supported by the significant difference in
QRS duration that was observed when comparing pace
mapping from the endocardium of RV free wall vs septal
locations. Our study population included a subgroup of
patients with RV cardiomyopathy, and, in this specific sub-
group as well, QRS duration was not noted to be signifi-
cantly longer when pacing from epicardial vs endocardial
locations. Thus, the presence of scar in the RV does not
appear to increase QRS duration from the epicardium.
Site-specific ECG criteria
Ventricular arrhythmias from the basal and inferior free
wall in the RV are common in the setting of RV cardiomy-
opathy, and radiofrequency ablative therapy is frequently
indicated.16,17 Identification of ECG features that predict an
epicardial site of origin is important for defining the opti-
mum ablation strategy in this RV region. The present study
shows that initial Q wave in inferior leads but not a longer
QRS duration may be helpful in determining the need for an
epicardial approach in order to achieve successful ablative
therapy in this region of the RV.
Although the anterior RV is an infrequent site of origin
for ventricular arrhythmias, it also is worthwhile for iden-
tifying criteria that may suggest the need for an epicardial
approach. The presence of a Q wave in lead I and QS
complex in lead V2 for epicardial pace mapping from this
region is more likely than from the endocardium. Epicardial
sites are more anterior (leftward) than are endocardial free-
wall opposite sites in this region. Thus, the initial net vector
is predominantly traveling away from lead I and lead V2
posteriorly or rightward, indicating the initial wavefront
traveling from the epicardium to the endocardium in the
anterior RV.
The superior part of the RV base corresponds to the
His-bundle region and its vicinity. ECG features have been
defined to predict a site of origin for ventricular arrhythmias
in this specific region.18 We believe that the assessment of
an epicardial site of origin based on surface ECG criteria in
basal superior RV requires further investigation.
RVOT region
Ventricular arrhythmias frequently originate from the
RVOT.19,20 A late transition in precordial leads, a broader
QRS, and a less prominent and more notched R wave in lead
II were shown to accurately identify septal vs free-wall sites
of origin of RVOT VT.10 Joshi and Wilber21 reported sim-
ilar criteria that predict a free-wall origin in the RVOT.
Other ECG features predict the site of origin from the LV
outflow tract and from the aortic cusps, as well as from
above the pulmonary valve.2224
No previous studies have described ECG patterns that
might suggest an epicardial origin in the RV outflow tract
and its vicinity, although an epicardial approach is some-
times warranted in this region.25 When pacing from the
epicardium in the RVOT region, we noted a trend toward
aVL/aVR and II/III QRS polarity amplitude ratios 1.
Without overstating the significance of this trend, the anat-
Heart Rhythm, Vol 3, No 10, October 2006
omy of the RVOT would suggest that when a stimulus
arises from the epicardium, it will tend to be more leftward
in origin and support our observations.
Ablation strategy for RV arrhythmias
Epicardial ablation will improve the outcome of ablative
therapy for ventricular arrhythmias when the endocardial
approach fails to suppress the arrhythmia.20,25,26 Of note,
we previously demonstrated the usefulness of irrigated-tip
catheter ablation in the RV when RV cardiomyopathy is
present.17 Thus, this alternative ablation strategy has to be
considered before an epicardial ablation is deemed neces-
sary. Nevertheless, sometimes epicardial ablation may be
warranted, and thus the described ECG criteria are useful
for predicting those cases in which epicardial ablation might
be needed to guarantee a successful outcome.
Study limitations
The number of pace mapping sites obtained for our study
analysis may be limited, and the results may not apply for
ventricular arrhythmias in the setting of RV abnormalities
other than those included in our patient population, such as
congenital heart disease and RV remodeling after pulmo-
nary hypertension.
Data regarding successful VT ablation from the epicar-
dial RV surface reported here, although providing valuable
preliminary confirmation of our results, are limited and
require additional evaluation.
Clinical arrhythmia can occur at faster rates than the
pacing cycle length used in this study. As previously noted,
the QRS occasionally can vary depending on the cycle
length during ventricular tachycardia or ventricular pac-
ing.10 However, differences in QRS morphology related to
the rate are subtle, especially in the absence of structural
heart disease. Thus, in our opinion, the described ECG
features still are applicable.
Inability to capture from the epicardial surface has been
reported.1 However, in our series, ventricular capture was
consistently observed, albeit at a higher output threshold
than from the endocardial surface.
Our results may not apply to patients who have more
extensive LV disease, especially in the setting of coronary
disease with prior infarction, which can manifest on the
ECG with an initial Q wave. Furthermore, the shape of the
RV can vary importantly among individuals.27 This may
affect the initial vector of the wavefront during the ventricu-
lar depolarization on which we based our criteria.
Conclusion
For arrhythmias that arise from the RV, the presence of an
initial Q wave in lead I and QS in lead V2 for anterior sites
in the RV strongly predicts an epicardial origin. Similarly,
an initial Q wave in leads II, III, and aVF is observed with
pace mapping from the inferior epicardial locations in the
RV. Further investigation is required to determine reliable
ECG criteria for suggesting an epicardial origin in the
RVOT. QRS duration does not distinguish an epicardial
Bazan et al ECG Features for Epicardial Right Ventricle VT
from an endocardial origin, nor do reported criteria for
predicting epicardial origin in the LV. These data have
important implications for facilitating the optimum ablation
strategy for managing ventricular arrhythmias from the RV.
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