825

Clinical Review
Section Editor: Stephen C. Hammill, M.D.
Using the 12-Lead ECG to Localize the Origin of Atrial and
Ventricular Tachycardias: Part 2Ventricular Tachycardia
HARIS M. HAQQANI, M.B.B.S., JOSEPH B. MORTON, M.B.B.S., Ph.D.,
and JONATHAN M. KALMAN, M.B.B.S., Ph.D., F.A.C.C.
From the Department of Cardiology, Royal Melbourne Hospital and Department of Medicine, University of Melbourne, Victoria, Australia
Using the 12-Lead ECG to Localize the Origin of Atrial and VT. Monomorphic ventricular
tachycardia (VT) can arise from multiple different ventricular locations in the context of several different
underlying myocardial substrates. Despite this variability, the surface 12-lead electrocardiograph (ECG)
has proven to be a robust and reproducible initial mapping tool that can provide useful information in
localizing the origin of both focal and reentrant forms of VT. The second part of this review series will look
at the use of the ECG in mapping the various forms of VT encountered in clinical practice. (J Cardiovasc
Electrophysiol, Vol. 20, pp. 825-832, July 2009)
ventricular tachycardia, catheter ablation, electrocardiogram, aortic sinus of Valsalva, epicardial
Introduction
The past decade has seen a tremendous increase in our
understanding of the origins and mechanisms of monomor-
phic ventricular tachycardias (VTs), as well as in our ability
to successfully treat these arrhythmias by catheter mapping
and ablation. Central to this progress has been an improved
understanding of the anatomical basis underlying many of
these arrhythmias and an appreciation of the important role
of the 12-lead electrocardiograph (ECG) as a mapping tool.
In this reviewwe will look at use of the ECGin mapping both
idiopathic VT in structurally normal hearts and scar-related
VT.
General Considerations
The QRS complex during VT is generated from a distinct
site of origin for focal VTs or from the exit site of a con-
strained diastolic isthmus during reentrant VT. Some general
principles related to ventricular geometry and activation gov-
ern the ECG patterns seen in VT. First, left ventricular free
wall VT shows right bundle branch block (RBBB) cong-
uration, while VT exiting from the interventricular septum
or right ventricle displays left bundle branch block (LBBB)
conguration. Second, septal exits are associated with nar-
Dr. Haqqani is the recipient of a Medical Postgraduate Scholarship from
the National Health and Medical Research Council of Australia, and a Car-
diovascular Lipid Research Grant. Professor Kalman has received research
funding support from St. Jude Medical and Medtronic.
Address for correspondence: Jonathan M. Kalman, M.B.B.S., Ph.D.,
F.A.C.C., Department of Cardiology, Royal Melbourne Hospital, Grattan
Street, Parkville, Victoria, Australia 3050. Fax: 61-3-9347 2808; E-mail:
jon.kalman@mh.org.au
Manuscript received 11 December 2008; Revised manuscript received 25
January 2009; Accepted for publication 27 January 2009.
doi: 10.1111/j.1540-8167.2009.01462.x
rower QRS complexes consistent with synchronous rather
than sequential ventricular activation. Third, basal sites show
positive precordial concordance, while negative concordance
is seen in apical sites of origin. The QRS axis varies predom-
inantly with shifts in exit along a superoinferior axis but also
may also occur with right-left shifts. These general rules usu-
ally apply even in the presence of signicant structural heart
disease though signicant scarring fromprior infarction, car-
diomyopathy, and congenital heart disease can reduce the
precision of the ECG as a localizing tool. A classical exam-
ple of this is VT seen late after the repair of Tetralogy of
Fallot in which right VT may display a RBBB morphology.
Anatomical variation is the other main factor that can
cause disruption to expected patterns of body surface electri-
cal vectors for a given arrhythmia origin. This can arise from
translational, rotational, or attitudinal shifts in the normal re-
lationship of the heart to the chest wall, or from variations
within the cardiomediastinal anatomy itself. Antiarrhythmic
drugs, by affecting myocardial conduction characteristics,
may be expected to affect the surface ECG appearance of
VT.
1
Idiopathic RVOT VT
Outow tract ventricular tachycardia (OTVT) is the com-
monest form of idiopathic VT and accounts for around 10%
of all VT seen in referral centers.
2
The outow tract re-
gion consists of a number of essentially contiguous struc-
tures within a small 3-dimensional space (Fig. 1). These
include the right ventricular outow tract (RVOT), the pul-
monary artery, the parahisian region, the left ventricular out-
ow tract (LVOT), the mitral annulus (MA) (particularly
the region of the aortomitral continuity), aortic sinuses of
Valsalva (ASOV), and the left ventricular (LV) epicardium
(particularly in the region of the conuence between the an-
terior interventricular vein and the great cardiac vein). OTVT
has been described to arise from all the outow tract region
structures, but the endocardium of the RVOT is by far the
826 Journal of Cardiovascular Electrophysiology Vol. 20, No. 7, July 2009
Figure 1. Basal view of the annular and outow tract region after removal of both atrial chambers. The close 3-dimensional anatomical relations of the
various outow tract and annular structures around the central brous cardiac skeleton can be appreciated. (A) Shows the typical surface ECG appearance
of VT arising from the posterior aspect of the free wall of the right ventricular outow tract. An LBBB conguration with inferior axis is seen with late
precordial transition after V
3
and notching in the inferior leads. The positive forces in lead I imply a posterior (or rightward) focus. In (B) is a typical example
of the surface ECG appearance of VT with an anteroseptal RVOT origin. An early precordial transition before V
3
is seen with a negative lead I morphology.
(C) Shows the multiphasic notched conguration in lead V
1
that can be seen in outow tract VT arising from the left coronary cusp of the aortic sinus of
Valsalva. (D) Displays an example of VT arising from the epicardium of the left ventricular outow tract that was mapped to the anterior interventricular
vein region (where activation occurred 45 ms prior to the onset of the QRS). The ECG shows a left bundle branch block (LBBB), inferior axis conguration
with broad QRS complexes of 149 ms and slurred intrinsicoid deections. The earliest time to maximal deection in any precordial lead occurs in lead V3
at 101 ms. Thus, the maximum deection index (MDI) for this tachycardia morphology is 0.68. PA = pulmonary artery; RVOT = right ventricular outow
tract; LCC = left coronary cusp; RCC = right coronary cusp; LCA = left coronary artery; RCA = right coronary artery.
most common site of origin and accounts for up to 75% of
OTVT cases. Despite the close anatomical proximity of the
distinct origins of OTVT, the 12-lead ECG is still able to
serve as a useful initial mapping tool. The classical ECG pat-
tern of OTVT is an LBBB conguration monomorphic VT
with an inferiorly directed frontal plane QRS axis and deeply
negative QS complexes in leads aVL and aVR. Stereotypical
variations to this basic pattern have been described for the
different sites of origin of OTVT.
In axial cross-section the RVOT is generally a crescent-
shaped structure that wraps anteriorly around the aortic root
and LVOT, leftward of the interventricular septum. It extends
from the top of the tricuspid valve below to the pulmonary
valve above. The so-called septal aspect of the RVOT ac-
tually abuts the supravalvular aorta, not the interventricular
septum, with the pulmonary valve located superior to the
aortic valve leaets (Fig. 1). The anteroseptal tip of this cres-
cent is actually directed leftward and is closely related to the
bifurcation of the left main coronary artery and the anterior
interventricular vein on the epicardial aspect of the LV, as
well as to the left ASOV. The posteroseptal tip points right-
ward and is closely apposed to the right ASOV. These basic
anatomic relations are important in understanding the ECG
patterns of OTVT, which are summarized in Table 1.
Pace mapping and activation mapping studies have
demonstrated several important generalizations in ECG lo-
calization of RVOT VT. First, septal sites on the RVOT tend
to have narrower LBBB QRS complexes with earlier pre-
cordial transition (positive QRS by V
3
or earlier) and larger
amplitudes in the inferior leads (Fig. 1B).
3
In contrast, free
wall sites in the RVOT, which account for up to 34%of RVOT
VT foci,
2
have later precordial transitions, with broader QRS
complexes and notching in the inferior leads (Fig. 1A).
3
It
should be remembered, however, that even from the free
wall, conduction velocity in idiopathic OTVT is rapid, and
signicantly wide QRS complexes should prompt a thor-
ough evaluation for the presence of structural heart disease
and myocardial brosis. Second, posterior sites in the RVOT
are distinguished by their leftward initial vector that tends to
produce a positive QRS complex in limb lead I (Fig. 1A).
4
Anterior sites have either isoelectric or negative, often multi-
phasic, forces in lead I (Fig. 1B).
3
It is important that the limb
lead electrodes are placed correctly as the lead I vector will be
reversed with posteroseptal sites with electrode placement on
the chest rather than the shoulders.
5
As a majority of RVOT
VT foci lie at the top of the RVOT within a 12 cm cranio-
caudal band subjacent to the pulmonary valve, they produce
a negative QS pattern in lead aVL.
6
Isoelectric or positive
forces in aVL strongly imply a more caudal site of origin at
the base of the RVOT, potentially adjacent to the His bun-
dle.
2,7
Compared to the RVOT, these parahisian foci also tend
to display lower R-wave amplitude and shorter QRS duration
in the inferior leads, larger R-wave amplitude in lead I, V
5
and V
6
, and a QS pattern in V
1
.
7
Given the close anatomical
proximity of the aortic root, parahisian VT may overlap with
OTVT arising from the noncoronary cusp (NCC) or right
coronary cusp (RCC) of the aortic valve, and no specic
ECG criteria reliably differentiate these sites.
8
Haqqani et al. Using the 12-Lead ECG to Localize the Origin of Atrial and VT 827
TABLE 1
Typical ECG Patterns of Idiopathic VTs
Location of VT Exit/Focus BBB Axis V
1
V
6
Other Features
RVOT
Anteroseptal LBBB Inferior rS R Early transition with lead I negative, isoelectric or multiphasic
Posterior free wall LBBB Inferior rS R Late transition; broad late notched inferior leads and lead I positive
Parahisian LBBB Inferior QS R Isoelectric or positive AVL, large R amplitude in I, V
5
and V
6
PA LBBB Inferior rS R Earlier transition with taller inferior R waves; QS in AVL > qs in AVR
TA
Anteroseptal LBBB Inferior QS R Positive, isoelectric, or multiphasic in AVL
Posterolateral LBBB Variable QS R Notching in limb leads; discordant forces in inferior leads if inferior
ASOV
LCC LBBB Inferior rS, RS R Atypical LBBB; notched M or W pattern in V
1
; QS or RS in lead I
RCC LBBB Inferior rS, RS R Atypical LBBB; early transition; broad R in V
2
, positive in lead I
LCC/RCC junction LBBB Inferior qrS R Atypical LBBB with multiphasic QRS in V
1+
LVOT
Anterolateral MA RBBB Inferior R R Late inferior lead notching; wider QRS with lead I negative
Septal sites LBBB Left inferior rS R Positive forces in lead I
AMC RBBB Inferior qR R May also have R in V
1
with positive precordial concordance and no S V
6
Epicardial
AIV/GCV junction LBBB Inferior rS R Precordial pattern break with abrupt loss of R waves in V
2
; MDI > 0.55
Crux LBBB Left superior rS R Early transition; MDI > 0.55; slurred intrinsicoid deection
Papillary m.
Posteromedial RBBB Superior rsR RS Late R to S transition
Anterolateral RBBB Inferior rsR RS Later R to S precordial transition
Fascicular
Left posterior fascicular RBBB Left superior rsR RS Loss of late precordial R waves with more apical exits
Left anterior fascicular RBBB Right rsR RS Similar to posterior fascicular apart from axis
Upper septal Narrow Normal or right rS Rs Narrow QRS complex with VA dissociation
AIV = anterior interventricular vein; AMC = aortomitral continuity; ASOV = aortic sinus of valsalva; GCV = great cardiac vein; LBBB = left bundle
branch block; LCC = left coronary cusp; LVOT = left ventricular outow tract; MDI = maximum deection index; PA = pulmonary artery; RBBB = right
bundle branch block; RCC = right coronary cusp; RVOT = right ventricular outow tract; TA = tricuspid annulus.
Another right-sided structure that may give rise to idio-
pathic VT is the tricuspid valve annulus.
9
While this does
not strictly reside in the RVOT, the majority of VTs arising
from the tricuspid annulus (TA) do so from the anteroseptal
aspect in proximity to the His bundle. Thus, there is further
overlap between these and parahisian VTs arising from the
base of the RVOT or the NCC. Lead aVL is either monopha-
sic positive or multiphasic and low amplitude, in addition to
the usual left bundle branch conguration with inferior axis.
For TA VT arising from the free wall of the valve ring off
the septum, a similar conguration is seen but with notch-
ing in the limb leads. This situation is analogous to RVOT
free wall VT. TA VT arising from the posterolateral portion
has discordant forces in the inferior leads depending on how
inferiorly the focus is located.
9
Analogous to the arrhythmogenic structure of pulmonary
veins with regard to initiation of atrial brillation, the great
arteries are invested with variable sleeves of myocardium ex-
tending above the semilunar valves.
10
In certain cases these
may harbor arrhythmogenic foci and give rise to OTVT. Pul-
monary artery VT arises 0.52.1 cmcranial to the pulmonary
valve and consequently has an ECG appearance similar to
typical RVOT VT, sometimes with taller R waves in the in-
ferior leads.
11
However, given that the pulmonary trunk is a
more leftward structure than the infundibulum, the ECGmay
exhibit earlier precordial transition and a deeper QS in aVL
than in aVR.
12
Idiopathic VT Arising from Aortic Sinus of Valsalva
VT arising from the aortic sinuses of Valsalva (ASOV)
accounts for up to 21% of idiopathic VT.
13
This arrhythmia
more commonly arises from the left coronary cusp (LCC)
than the right and rarely arises from the NCC,
14,15
and is
once again thought to be related to myocardial extensions
projecting above the aortic valve, into the sinuses of Val-
salva.
10
Characteristically, the surface ECG exhibits earlier
precordial transition with broader and taller R waves in V
1
or V
2
, taller inferior R waves, an S wave in lead I with a
characteristic absence of S waves in V
5
and V
6
.
16
Ouyang
et al.
14
found that in these leads an R-wave duration of >50%
of the total QRS duration or an R/S ratio of more than 30%,
were strongly predictive of an aortic cusp (particularly a
LCC) origin. Pace mapping from the LCC by Lin et al.
17
showed a characteristic multiphasic notched pattern in V
1
with an M or W pattern, presumably due to transseptal
activation after initial LV activation from the LCC (Fig. 1C).
In comparison, RCC pace mapping again produced an early
precordial transition, but this time with a broad R in V
2
and a
longer mean QRS duration. Lead I may also be distinguish-
ing with LCC foci tending to have either QS or rS complexes
here and RCC foci generating more positive forces in this
lead, but this is variable and depends critically on annular
location and orientation.
5
NCC VT has no pathognomonic
ECG pattern and pace mapping here results in atrial cap-
ture due to its proximity to the interatrial septum.
17
Yamada
et al.
18
have recently described a group of OTVTs arising
from the junction of the LCC and RCC. These have a char-
acteristic multiphasic QRS conguration in V
1
and require
ablation from the LVOT aspect of the aortic valve cusps.
However, it is likely that there is signicant overlap between
this group and the multiphasic notched V
1
pattern seen in
standard LCC foci.
828 Journal of Cardiovascular Electrophysiology Vol. 20, No. 7, July 2009
Figure 2. Fascicular VT due to reentry involving the left posterior fascicle in a 22-year-old male. The ECG is remarkable for the relatively narrow QRS
complex and AV dissociation seen in lead V
3
. There is a right bundle branch block (RBBB) and left axis deviation, while the early precordial S-wave transition
is consistent with the relatively apical exit where this VT was ablated.
Idiopathic LVOT VT
Precordial R-wave transitions earlier than V
2
are sug-
gestive of a left ventricular origin of OTVT.
19
A major-
ity of these tachycardias arise from the anterolateral MA,
13
and in this location they exhibit positive precordial concor-
dance with an RBBB conguration in V
1
usually with late
notching in the inferior leads. This has been conrmed with
pace mapping studies
20
that demonstrate that, compared to
septal sites, anterolateral and lateral sites of origin exhibit
a longer QRS duration along with predominantly negative
forces in lead I. Septal sites in the parahisian region display
an LBBB conguration more akin to RV foci and have a
dominant R in lead I, usually with left inferior axis. The
most distinctive ECG pattern of basal LVOT VT belongs
to VT arising from the aortomitral continuity (AMC) that
characteristically displays a qR pattern in V
1
as a result of
the left brous trigone deecting initial electrical activation
leftward.
20
Depending on anatomical factors, however, par-
ticularly the position and extent of the trigone, AMC VT
may not display this ECG signature and may instead have
an RBBB pattern with positive concordance and no late pre-
cordial S waves as described by Kumagai et al.
21
This group
also showed that both AMCVT and MA VT had earlier tran-
sitions than a group of ASOV VTs and that they had longer
intrinsicoid deection times. However, there was no differ-
ence in inferior lead R-wave amplitude between the groups.
Idiopathic Epicardial Outow Tract VT
Tachycardias in this region may arise from perivascular
myocardial tissue associated with the coronary venous sys-
tem, particularly at the junction of the great cardiac vein and
anterior interventricular vein but also from other epicardial
sites.
22
The surface ECG generally displays an LBBB con-
guration with inferior axis and transition around V
3
. While
there is no specic ECG signature that is pathognomonic
for these epicardial outow tract VTs, their remote origin
from the rapidly conducting His-Purkinje system would be
expected to delay the intrinsicoid deection of the QRS.
Daniels et al.
22
quantied this by developing a dimension-
less metric called the precordial maximum deection index
(MDI), which is dened by the shortest time to maximal pos-
itive or negative deection in any precordial lead divided by
the QRS duration. A cut-off value of 0.55 had high sensitiv-
ity and specicity in discriminating between epicardial foci
and other outow tract sites of origin. (Fig. 1D). Another
clue to an epicardial LVOT tachycardia is the presence of
precordial pattern break (Dr. Marchlinski, 2nd Annual VT
Symposium, Philadelphia, PA, 2007), also known as R-wave
regression/progression, in which there is an abrupt loss of R
wave in V
2
followed by a resumption in R waves from V
3
to
V
6
. The positive and negative predictive value of this marker
for predicting an epicardial VT location are unclear.
Some of these epicardial foci may be ablated transve-
nously, while others may require a percutaneous epicardial
or even left atrial appendage approach. Recently, Doppala-
pudi et al.
23
have described epicardial idiopathic VT arising
from the crux of the heart in the pyramidal space adjacent
to the posterior descending artery. The QRS morphology of
this VT showed early precordial transition at or before V
2
in addition to a left superior axis and an MDI >0.55. The
inferior leads exhibited deeply negative QS complexes with
slurred intrinsicoid deections, and as the authors point out,
this is very similar to the pattern of maximal preexcitation
seen with manifest posteroseptal pathways that share a sim-
ilar ventricular insertion into the pyramidal space.
Fascicular VT
This idiopathic arrhythmia, also known as left septal VT
or verapamil-sensitive VT, is due to reentry involving altered
Purkinje-bers on the left ventricular aspect of the septum.
There are 3 main variants of this arrhythmia, each with char-
acteristic ECGmanifestations. By far the most common form
is due to reentry involving the left posterior fascicle with an
exit at the inferoapical LV septum.
24
This displays an RBBB
conguration QRS complex with left superior axis and RS
complexes in V
5
and V
6
. There is a loss of these late pre-
cordial R waves in cases with more apical exits (Fig. 2). A
minority of cases are due to the second type, which is due
to reentry involving the left anterior fascicle. These exhibit
an RBBB conguration with right axis deviation.
25
The third
type, upper septal fascicular VT, is very rare and involves the
proximal left bundle branch. It is remarkable for its narrow
QRS complex with normal or rightward axis.
Postinfarction VT
The general principles described earlier can give a rst
approximation to VT exit in the setting of scarring due to
previous myocardial infarction. It should be noted, however,
that in the presence of stable myocardial scar-related reentry,
Haqqani et al. Using the 12-Lead ECG to Localize the Origin of Atrial and VT 829
Figure 3. An electroanatomical bipolar
voltage map of a 55-year-old male pa-
tient with a ventricular tachycardia (VT)
storm is shown in a caudal right poste-
rior oblique projection. Bipolar voltage
of <0.5 mV (suggestive of dense scar) is
depicted in red and normal myocardium
(with bipolar voltage >1.5 mV) is repre-
sented in purple, with other colors corre-
sponding to the intermediate signal am-
plitude seen in the scar border zone. The
patient had a basal inferior aneurysm fol-
lowing remote inferior myocardial infarc-
tion and had 4 readily inducible mor-
phologies of unmappable VT. In (A and B)
are 2 LBBB conguration VTs with sep-
tal exits, (A) being basal and (B) apical.
(C and D) Display 2 RBBB morphology
tachycardias with lateral exits. (D) Has
positive precordial concordance consis-
tent with its basal exit. The basal circuits
in (Aand D), are examples of mitral isth-
mus VTs that exit from the periannular
region on either side of the dense inferior
scar.
subtle changes in the exit from these circuits can lead to
profound changes in the surface ECG morphology.
26
In the postinfarct context, VT usually arises from the left
ventricle with RBBB congurations suggesting a free wall
exit and LBBB conguration seen with septal exits. Neg-
ative forces in lead aVL further point to a free wall site.
Knowledge of scar location is helpful in further regional-
izing the exit.
27
With inferior infarction, most VT has a
basal exit and thus has relatively preserved precordial R
waves (Fig. 3A,D), although apical exits sites also occur
(Fig. 3B, C). Lateral basal exits will show RBBB congura-
tion with positive precordial concordance and right superior
axis (Fig. 3D). The axis in this VT tends to become increas-
ingly more inferior as the exit site shifts progressively higher
up the lateral wall. Septal basal exits show an LBBB con-
guration with left axis deviation (Fig. 3A). Some inferior
infarction-related VTs displaying these ECG patterns have
been shown to have a slow zone of constrained diastolic ac-
tivation abutting the MA.
28
These so called mitral isthmus
tachycardias may exit the inferior slow zone on the septal
side when they have an LBBB left superior axis congu-
ration (Fig. 3A), or they may exit on the parietal free wall
side, where the morphology is RBBBwith right superior axis
(Fig. 3D).
In the context of anterior infarction, ECG localization is
more difcult due to the presence of a larger scar mass,
particularly if there is anteroapical aneurysm formation. An
LBBB conguration with left axis deviation is typical for
inferoapicoseptal exits, and negative precordial concordance
with QS complexes from V
4
to V
6
suggests an apical exit.
It is difcult to distinguish septal apical and lateral apical
sites, although the former are more likely to have LBBB left
superior axis morphology, while the latter tend to have right
superior axis. At more basal locations, the R-wave ratio in
aVR to aVL increases for lateral sites. The most difcult
VTs to localize following anterior infarction are the RBBB
right or left superior axis morphologies that can arise from
multiple segments,
27
including septal sites. It is likely that the
ECG loses further localizing power for VT in the situation
of multiple infarctions across territories as seen in ischemic
cardiomyopathy patients.
Segal et al.
29
developed an algorithmto predict postinfarc-
tion VT exit sites in the absence of prior knowledge of infarct
location and in patients with multiple infarctions. They used
noncontact mapping of VT exits as the gold standard in 121
VTs in 51 patients. Their algorithm considers in turn the po-
larity in the inferior leads, in lead I, aVL, as well as aVR, and
is applied to both LBBB and RBBB tachycardias. It results
in a comparative accuracy but can be applied in more general
circumstances. Interestingly, this group found that precordial
R-wave concordance and transition was not helpful in exit
site localization.
Recently, the characteristics of VT arising from the pap-
illary muscles in the postinfarction context have been de-
scribed by Bogun et al.
30
Generally, these have an RBBB
conguration and late R- to S-wave transition. They have a
superior axis with posteromedial papillary muscle origin, and
inferior axis when they arise from the anterolateral papillary
muscle. The same group has also described an idiopathic fo-
cal VT originating from noninfarcted papillary muscles with
similar morphology.
31
VT in Nonischemic Cardiomyopathy
The majority of VT in this setting is due to myocardial
reentry, and similar considerations apply to the surface ECG
morphology as in other scar-related conditions. A signicant
proportion of exit sites in nonischemic cardiomyopathy will
be found in the epicardium and these are considered below.
Bundle Branch Reentry
An important cause of VT in this substrate is bundle
branch reentry (BBR) and related arrhythmias due to His-
Purkinje conduction delay.
32
These are important to recog-
nize, as they readily lend themselves to curative catheter
830 Journal of Cardiovascular Electrophysiology Vol. 20, No. 7, July 2009
Figure 4. Atypical bundle branch reen-
try (BBR) VT in a 30-year-old male pa-
tient with severe aortic valve calcication
is shown. The clinical tachycardia was of
right bundle branch block (RBBB) cong-
uration, similar to the sinus rhythm (A)
morphology, and is seen in (B). This oc-
curred due to antegrade activation over
the left bundle branch with the retrograde
limb being the right bundle branch. In this
patient, typical left bundle branch block
(LBBB) conguration BBR VT could also
be induced with programmed stimulation
(C). Catheter ablation of the right bundle
branch to abolish retrograde conduction
was performed, and no arrhythmias could
be induced following this.
ablation. In sinus rhythm, the diseased His-Purkinje sub-
strate produces LBBB or RBBB in practically all patients.
A majority of cases of BBR are characterized by antegrade
activation over the right bundle branch and retrograde ac-
tivation of the left bundle branch. This produces a typi-
cal LBBB morphology VT with normal or leftward axis
(Fig. 4C), usually very similar to the baseline QRS appear-
ance and usually with very short cycle lengths. In a minority
of patients, the reverse circuit can be seen clinically or in-
duced in the electrophysiology lab with retrograde conduc-
tion over the right bundle branch, and this produces a typical
RBBB morphology VT (Fig. 4B). Some patients develop LV
VT related to the distal His-Purkinje system arborization and
this may be due to interfascicular reentry or fascicular au-
tomaticity. The VT morphology in these cases is usually an
RBBB conguration tachycardia of variable axis depending
on which fascicle conducts in the antegrade direction, and
these again have similar morphology to the sinus rhythm
QRS complex.
33
Epicardial Scar-Related VT
With the more widespread use of percutaneous epicardial
mapping and ablation, it has become apparent that a sig-
nicant proportion of VT circuits have one or more critical
components located in the epicardium. This is particularly
true in nonischemic substrates. Various ECG characteristics
have been used to predict whether an epicardial approach
may be required based on the VT morphology. It should be
remembered, however, that the QRS morphology is related
solely to the VT exit site and this does not imply that some
other component of the circuit (such as a central isthmus or
entrance site) cannot be ablated from the endocardium, even
when an epicardial exit is implied by the ECGcharacteristics.
As a result of this inherent discrepancy, it is unlikely that the
surface ECG by itself will ever be entirely predictive of the
need for epicardial access and mapping for any given VT.
Nevertheless, a number of helpful surface ECG criteria
have been developed to address this issue, all of which gen-
erally rely on the late engagement of rapidly conducting
His-Purkinje bers by exits on the epicardium. Two of these,
the MDI and precordial pattern break, have been discussed
above. There are no data on the performance of these cri-
teria in patients with structural heart disease, but it is likely
that they are still helpful in this context. Berruezo et al.
34
developed 3 ECG criteria in cardiomyopathy patients with
sensitivity and specicity ranging between 76% and 95%
for predicting an epicardial exit in patients with failed endo-
cardial VT ablation. First, they looked at the presence of a
pseudodelta wave in the precordial leads of RBBB VTs.
This was dened as the time from the QRS onset to the ear-
liest rapid deection in any precordial lead and duration of
>34 ms was found to perform best. Second, they found a
delayed intrinsicoid deection to the peak of the R wave in
V
2
of >85 ms was also accurate. And nally, slightly less
predictive was a shortest RS interval of >120 ms in any
precordial lead.
Other criteria have used the presence of regional Q waves
to indicate wavefront propagation away from an epicardial
focus. Bazan et al.
35
developed a regional model of Q-wave
patterns that predicted a left ventricular epicardial exit for
VT in the absence of prior myocardial infarction. These
patients generally had nonischemic cardiomyopathy with a
mean ejection fraction of 40%. Pace mapping and activa-
tion mapping during VT showed that Q waves as part of
the VT morphology better predicted epicardial exits than
the pseuododelta, intrinsicoid deection or shortest RS crite-
ria described in the predominantly ischemic cardiomyopathy
population of the Berruezo et al.
34
study. In particular, an-
terobasal and anteroapical epicardial VT exits showed Q
waves in lead I, and anterobasal sites were especially
more likely if there were no inferior Q waves. Infer-
obasal and inferoapical sites were characterized by inferior
Q waves.
Haqqani et al. Using the 12-Lead ECG to Localize the Origin of Atrial and VT 831
In most cases, RV scar-related tachycardia circuits would
be expected to be ablated from the endocardium regardless
of any epicardial component they may have, due to the rel-
atively thin RV free wall. However, in certain substrates,
notably arrhythmogenic right ventricular dysplasia, the RV
free wall may thicken signicantly due to dense conu-
ent brosis and epicardial ablation may be required. Bazan
et al.
36
also looked at RV epicardial VT and pace maps
and found that Q waves in lead I correlated with anterior
epicardial sites, while QSpatterns in lead V
2
suggested apical
epicardial exits. Inferior epicardial sites were characterized
by the presence of Q waves in the inferior leads. No ECG
features distinguished epicardial outow tract exits. Notably,
none of the QRS characteristics of epicardial LV tachycardia
exits were seen in the RV.
Summary
The surface 12-lead ECG is an important and useful tool
for localization of VT site of origin. While it has inherent
limitations, it remains indispensable in the overall clinical
and procedural strategy for managing patients with these
arrhythmias.
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