REVIEW

Focal Atrial Tachycardia II: Management

KURT C. ROBERTS-THOMSON, PETER M. KISTLER, and JONATHAN M. KALMAN
From the Department of Cardiology, Royal Melbourne Hospital, and the Department of Medicine, University of
Melbourne, Melbourne, Australia

Over the last decade there have been significant changes in the treatment of focal atrial tachycardia (AT).
This review concentrates on the different approaches to the treatment of focal AT. Initial therapies included
antiarrhythmic medications and surgery. However, with the advent of radiofrequency ablation, and the
poor efficacy of pharmacological therapy, there has been a shift toward a primary ablative approach.
Several different mapping techniques have been proposed. The different techniques, including P-wave
morphology and advanced three-dimensional mapping, are discussed in this review. (PACE 2006; 29:
769–778)
focal atrial, tachycardia, radio frequency ablation, therapy

Introduction be adenosine-sensitive. AT due to abnormal auto-

The management of focal atrial tachycardia
(AT) has progressed rapidly in recent times. Pre-
viously, the use of antiarrhythmic medication was
the mainstay of therapy. More recently the success
of radiofrequency ablation has seen a shift toward
a primary ablative approach in many patients. Fo-
cal AT is an uncommon arrhythmia and there re-
mains a paucity of trials comparing the efficacy of
different treatment regimes. The efficacy of vari-
ous therapies is also difficult to assess because the
clinical definition of focal AT is often difficult to
rigorously apply and focal AT may spontaneously
regress. No large studies have evaluated the effect
of nonablative therapies on focal AT.
Acute Management
Vagal maneuvers, such as carotid sinus mas-
sage, are normally unsuccessful in terminating fo-
cal AT, but may produce AV block allowing a
clear view of the P-wave and a definitive diag-
nosis. The effectiveness of DC cardioversion is
also limited. It may be successful for those whose
mechanism is microreentry or triggered activity.
However, automatic AT is usually unresponsive
to DC cardioversion.1 Similarly, overdrive pac-
ing suppresses automatic AT but does not result
in termination,2,3 whereas it is often successful
in terminating AT due to microreentry and trig-
gered activity.3 As discussed earlier, focal AT may
Disclosure: Dr. Kurt Roberts-Thomson and Dr. Peter Kistler are
the recipients of a Postgraduate Research Scholarship from the
National Health and Medical Research Council of Australia.
Address for reprints: Jonathan M. Kalman, M.B.B.S., Ph.D.,
F.A.C.C., Department of Cardiology, Royal Melbourne Hospi-
tal, Melbourne 3050, Australia. Fax: 61 3 9347 2808; e-mail:
jon.kalman@mh.org.au
Received June 27, 2005; revised September 21, 2005; accepted
October 12, 2005.
maticity is transiently suppressed and AT due to
microreentry and triggered activity is frequently
terminated.3
AV-nodal blocking agents are useful in con-
trolling the ventricular rate. Nonautomatic AT are
frequently terminated by verapamil.3 Intravenous
β-blockers may also terminate AT due to abnor-
mal automaticity and triggered activity.3,4 Class Ic
drugs have been shown to be efficacious in termi-
nating some focal AT5–7 via suppression of auto-
maticity or action potential prolongation.
Pharmacological Therapy
There are no long-term, randomized, placebo-
controlled studies on the use of antiarrhythmic
therapy in focal AT. The available studies regard-
ing long-term medical therapy of focal AT are ob-
servational, with small numbers. The majority fo-
cus on automatic AT in children and infants, with
only a few studies in adults. There is widespread
agreement that antiarrhythmic agents have low ef-
ficacy in the treatment of focal AT.
Calcium channel blockers and β-blockers are
recommended as first-line agents due to their low
side effect profile.8 However, the evidence for the
use of these medications appears to be limited.
Mehta et al.4 found that in patients on digoxin,
the addition of propranolol suppressed the AT in
5 of 10 children. This is similar to the results of
other pediatric studies.9,10 However, the use of β-
blockers alone in adults appears to have no ef-
fect.11 Prager et al.11 also observed verapamil to be
completely ineffective. These medications, along
with digoxin, have a role in controlling the ven-
tricular rate.
The ACC/AHA/ESC Guidelines for the Man-
agement of Supraventricular Arrhythmias8 regard
class Ia, class Ic, and class III agents as second-
line agents. However, the efficacy of these med-
ications is variable. Studies have demonstrated


C 2006, The Authors. Journal compilation 
C 2006, Blackwell Publishing, Inc.

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 ROBERTS-THOMSON, ET AL.
success rates of only 10–20% with quinidine and
procainamide, with acceleration of the tachycar-
dia sometimes observed.4,11 Class Ic medications
appear relatively efficacious. In 13 patients, Kuck
et al.6 showed that flecainide completely sup-
pressed the AT in seven patients, with partial sup-
pression in another five patients. Its effectiveness
has been confirmed by some studies5,12 but not
others.11,13 Other class Ic agents, encainide and
propafenone, have shown some success.1,5,7,13,14
The class III antiarrhythmic drugs, sotalol and
amiodarone, appear to provide the best results. In
five patients, who had failed a mean of three antiar-
rhythmic drugs, the addition of sotalol to digoxin
suppressed the AT in all patients.15 Although po-
tentially limited by its side effects, several investi-
gators have reported a good response of automatic
AT to amiodarone.4,16,17
In view of the limited long-term efficacy
of pharmacologic therapy, radiofrequency abla-
tion may be considered as a first-line therapeutic
modality for patients with significant symptoms.
Radiofrequency Ablation
Mapping Techniques
P-wave morphology can provide a noninva-
sive guide to the site of origin prior to electrophys-
iological study. In the electrophysiological labora-
tory, a range of different techniques have been used
for mapping and ablation of focal AT.
Stable AT or frequent atrial ectopics are re-
quired to commence mapping. If there is no
spontaneous ectopic atrial activity, atrial pacing
maneuvers should be performed in an attempt to
induce the AT. If this is unsuccessful, the use of iso-
proterenol may stimulate atrial ectopy. Once there
is sufficient atrial activity, mapping may proceed
in patients with structurally normal hearts and a
P-wave morphology and behavior consistent with
focal AT. Further atrial pacing maneuvers should
be performed if there is doubt about the diagnosis.
P-Wave Morphology
The morphology of the P-wave can provide
useful clues to the likely site of tachycardia origin.
The P-wave morphology is determined by the site
of origin of atrial activity and the pattern of atrial
activation. Studies looking at P-wave morphology
have mainly involved patients with structurally
normal atria and these P-wave configurations
cannot be extrapolated to patients with abnor-
mal atrial anatomy. Analysis of P-wave morphol-
ogy is frequently compromised by being totally
or partially obscured by the preceding T-wave.
When evaluating the P-wave morphology it is very
important to analyze the initial P-wave vector and
ensure that this is not partially obscured by the
770 July 2006
Figure 1. Continuous 12-lead ECG of a patient with
atrial tachycardia from the CS ostium. Note the diffi-
culty in assessing P-wave morphology when the P-wave
is buried within the T-wave. In this case a burst of ven-
tricular pacing separated the T-wave from the P-wave al-
lowing clear assessment of the P-wave morphology. This
may also be achieved with vagal maneuvers or adeno-
sine.
T-wave. To this end, we analyze only those P-
waves clearly preceded by an isoelectric base-
line. When necessary, the P-wave may be sepa-
rated from the T-wave by vagal maneuvere, adeno-
sine or following termination of ventricular pacing
(Fig. 1). Analysis of the P-wave morphology is also
limited by its spatial resolution. Man et al.18 as-
sessed the spatial resolution of P-wave morphol-
ogy using unipolar atrial pace mapping at different
sites. Pacing at sites as far apart as 32 mm in the
coronary sinus (CS) and 17 mm in the right atrium
(RA) resulted in P-waves identical in appearance.
Despite these limitations, P-wave morphology re-
mains a useful guide to the location of the AT focus.
Determining the Atrium of Origin
Leads V 1 and aVL have been described as the
best leads to distinguish between left and right
atrial foci.19,20 Tang et al.19 assessed P-wave mor-
phology in 31 patients, 14 with left atrial foci. All
but one of the left atrial AT had a positive P-wave
in V 1 . This is due to the posterior midline loca-
tion of the left atrium and subsequent anterior ac-
tivation. The criterion that a positive P-wave in
V 1 indicated a left atrial focus had a sensitivity
of 93%, specificity of 88%, positive predictive ac-
curacy of 87%, and negative predictive accuracy
of 94%.19 A negative P-wave in V 1 predicted a
right atrial focus. Care must be taken to observe
the initial P-wave vector as P-waves in V 1 with
an initial isoelectric segment followed by an up-
right component frequently indicate an origin near
the CS ostium or from the right septum. If the iso-
electric segment is overlooked and the P-wave is
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 FOCAL ATRIAL TACHYCARDIA II
Figure 2. P-waves from atrial tachycardia from the low
and high CT. Note the positive-negative morphology in
lead V 1 . These sites may be differentiated by the P-wave
morphology in the inferior leads. The P-wave from infe-
rior sites is negative in the inferior leads and the superior
sites are positive.
simply described as upright, this will lead to in-
correct localization to the left atrium. A positive
or biphasic P-wave in lead aVL indicates a right
atrial focus with a sensitivity of 88%, specificity
of 79%, positive predictive accuracy of 83%, and
a negative predictive accuracy of 85%.19
While these criteria are useful to predict the
atrium of origin of AT foci, certain anatomic loca-
tions tend to be associated with specific P-wave
morphologies.
Crista Terminalis
The crista terminalis (CT) extends the length
of the RA and so there are a variety of P-wave mor-
phologies from AT foci located on this structure
(Fig. 2). The majority of AT from the mid and su-
perior CT has biphasic P-waves in lead V 1 , sim-
ilar to the sinus P-wave, with an initial positive
component followed by a negative component.21
AT from the low CT often have negative P-wave in
V 1 .21 The P-wave in lead I is positive from most CT
sites. Lead aVR is negative.22 Tada et al.22 used this
to differentiate posteriorly located crista sites from
more anteriorly located sites in the RA, which had
upright P-waves in aVR. The P-wave vector in the
inferior leads is useful to determine where on the
CT the AT focus arises.21 Foci located in the supe-
PACE, Vol. 29 July 2006
Figure 3. P-waves from the CS ostium and the supe-
rior mitral annulus at the aortic-mitral continuity. Note
the similar P-wave morphologies in the precordial leads.
Atrial tachycardia arising from the CS ostium has neg-
ative P-waves in the inferior leads and positive P-waves
in lead aVL. The P-wave is negative in lead aVL in atrial
tachycardia from the superior mitral annulus and the in-
ferior leads are positive. The P-waves in the limb leads
are of low amplitude.
rior CT have positive P-waves in the inferior leads,
whereas the P-waves are isoelectric or biphasic in
these leads for mid cristal locations and negative
for inferior foci.
CS Ostium
The precordial leads display characteristic P-
wave morphology in AT arising from the CS ostium
(Fig. 3). Lead V 1 has an initial component that is
either isoelectric or mildly inverted followed by an
upright component.23 Across the precordial leads
the initial component becomes more negative and
the second component becomes isoelectric. Lead
aVL is positive and the P-waves are deeply nega-
tive in the inferior leads. The P-wave morphology
is similar to that of typical atrial flutter that has an
exit zone at the CS ostium.24 Foci located within
the body of the CS will have a P-wave in V 1 , which
is upright from the onset without an isoelectric seg-
ment and P-waves are frequently upright across the
precordial leads.
Atrial Septum
P-waves originating from an AT focus on
the anterior and midseptum are narrower than
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 ROBERTS-THOMSON, ET AL.
Figure 4. P-waves from the right perinodal region and
the left side of the septum. P-wave morphology from both
these regions may be variable. Note, in this case, the P-
wave from the right perinodal region is isoelectric in V 1 .
The P-wave from the left septum is negative-positive in
V 1 , similar to P-waves from the superior mitral annulus
and CS ostium. P-waves arising from the septum tend to
be narrower than the sinus P-wave.
the sinus P-wave.25,26 Lead V 1 is isoelectric or
biphasic, with an initial negative or isoelectric
component, followed by a positive component
(Fig. 4). Anteroseptal foci have positive P-waves
in the inferior leads, whereas midseptal foci tend
to be negative.27 Foci from the left side of the sep-
tum tend to have a completely positive P-wave
in V 1 , although the morphology may be variable
(Fig. 4).25,26
Tricuspid Annulus
The tricuspid annulus (TA) is an anterior atrial
structure and AT arising from this site result in
atrial activation in the posterior direction. Hence,
focal AT from this site have negative P-waves in
V 1 , which may also be notched (Fig. 5).22,28 Lead
aVL is invariably positive. The morphology of the
P-wave in the other leads depends on the site of the
focus on the TA. Inferior foci tend to have negative
P-waves in leads II, III, and aVF, whereas superior
foci are usually isoelectric or positive.28 The su-
perior TA and right atrial appendage are in close
proximity and AT from these sites may have simi-
lar P-wave morphologies.
772 July 2006
Figure 5. P-waves from atrial tachycardia located on
the inferior and superior TA. Note the negative P-waves
in the precordial leads, which are commonly notched.
Inferior locations have negative P-waves in the inferior
leads. Superior locations have low amplitude P-waves
in the inferior leads. The P-wave morphology of atrial
tachycardia from the right atrial appendage is similar
to the superior TA.
Pulmonary Veins
Focal AT from the pulmonary veins (PV) have
characteristic P-wave configurations (Fig. 6). The
P-wave is positive across the precordium, from V 1
to V 6 .19,29 The P-wave morphology also assists in
the localization of the focus to a particular PV. P-
waves from the left-sided PVs are generally broad
in V 1 , and are notched, particularly in the infe-
rior leads, but also in V 1 .29 A positive P-wave in
lead I is highly suggestive of a focus in the right-
sided PV and an inverted P-wave suggestive of a
left-sided PV. An upright P-wave in aVL is consis-
tent with a right-sided PV focus.20,29–31 However,
right-sided PV may also have negative P-waves in
aVL.19,29 Left pulmonary vein sites generally have
broader P-waves than right-sided pulmonary vein
sites.29 An algorithm by Ellenbogen and Wood32
used a P-wave duration of ≥80 ms to differentiate
left pulmonary veins from right. The inferior leads
may be used to differentiate superior from inferior
PV sites as the P-waves from the superior PV are
upright with high amplitude and lower amplitude
P-waves from the inferior PV. The left atrial ap-
pendage is adjacent to the left superior pulmonary
vein (LSPV) and AT from these structures has
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 FOCAL ATRIAL TACHYCARDIA II
Figure 6. P-waves originating from the LSPV, left inferior
pulmonary vein (LIPV), right superior pulmonary vein
(RSPV), and the right inferior pulmonary vein (RIPV).
Left-sided pulmonary veins are characterized by notch-
ing of the P-waves in the inferior leads and V 1 , signif-
icantly broader V 1 , and isoelectric or negative lead I.
Large amplitude P-waves in the inferior leads suggest a
superior vein, low amplitude or isoelectric P-waves sug-
gest inferior veins. (From Kistler et al. Circulation 2003;
108:1968–1975. Reproduced with permission.)
similar P-wave configurations. However, in con-
trast to foci from the LSPV, the P-waves from foci
in the left atrial appendage tend to be deeply neg-
ative in lead I.
Mitral Annulus
Focal AT arising from the superior mitral an-
nulus at the aortomitral continuity had biphasic
P-waves in V 1 , with an initial sharp negative de-
flection followed by positive deflection (Fig. 3).33
P-waves in the limb leads for AT at this site are of
low amplitude, with negative P-waves in aVL and
positive P-waves in the inferior leads.30,33,34
Endocardial Activation Mapping
The most commonly used technique to lo-
cate the AT focus is endocardial activation map-
ping (Fig. 7). In our center, endocardial activation
mapping begins with catheters placed in the bun-
dle of His area and the CS. Other specially de-
signed catheters that accommodate specific struc-
tures, the 20-pole Cristal (CT) catheter and Halo
(TA) catheter, may help to locate the focus. How-
PACE, Vol. 29 July 2006
Figure 7. Activation mapping from a patient with atrial
tachycardia arising from the high CT. Shown are surface
leads I, II, V 1 , and V 6 together with intracardiac record-
ings from the His bundle (HBE), CS, 20-pole catheter
placed on the septal side of the CT and an ablation
catheter (Abl d = distal; Abl p = proximal). In this case
the mapping reference point was CT 5, 6. The high CT
(lateral aspect) was mapped with an ablation catheter
and the site of earliest activation was 38 ms ahead of
CT 5, 6. Note the fractionated signal on the distal abla-
tion catheter, which is commonly seen at the successful
ablation site for CT tachycardias.
ever, precise localization must be achieved with
detailed mapping in the region of interest. Gener-
ally an activation time of >20–30 ms before the
P-wave is observed at successful sites but this is
highly variable. If the onset of the P-wave is reg-
ularly obscured by the T-wave, mapping can be
performed to a stable intracardiac fiducial point,
such as the CS ostium, with a known relationship
to P-wave onset.
Similar endocardial activation sequences may
be observed in AT arising from the posterior RA
and the right pulmonary veins, due to their close
proximity (Fig. 8). Yamada et al.20 used a multi-
electrode catheter to show double potentials in the
posterior RA in patients with AT from these sites.
During tachycardia, if the amplitude of the first
potential was greater than that of the second po-
tential, this indicated a right posterior atrial focus.
Right PV foci demonstrated a larger second poten-
tial than first potential. The P-wave morphology in
lead V 1 was also found to be helpful to differenti-
ate these two locations.
Paced Endocardial Activation Sequence
Mapping
Paced activation sequence mapping may be
helpful when the tachycardia is nonsustained or
difficult to induce and is often used to complement
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 ROBERTS-THOMSON, ET AL.
Figure 8. Intracardiac recordings during a sinus beat
(SR) and an atrial ectopic beat (AE) arising from the right
upper pulmonary vein (RUPV). Shown are surface ECG
leads I, II, and V 1 , together with intracardiac record-
ings from the His bundle (HBE), CS, a 20-pole catheter
placed along the CT, and an ablation catheter placed
in the RUPV (Abl d = distal; Abl p = proximal). Note
the similar endocardial activation sequences due to the
close proximity of the posterior RA and RUPV. Double
potentials from the posterior RA and RUPV can be seen
on the ablation catheter. During SR the RA potential is
larger than the RUPV potential; however, during the AE,
the RUPV potential is larger than the RA potential. The
reverse may be seen when the ablation catheter is placed
in the posterior RA.
activation mapping. The ablation catheter is ma-
neuvered to a position where the paced activa-
tion sequence reproduces the spontaneous endo-
cardial sequence. Tracy et al.35 matched the paced
endocardial map to the spontaneous map for right
ATs. Using this technique combined with activa-
tion mapping they reported a success rate of 80%.
Using a standardized set of right atrial catheters,
Deen et al.36 demonstrated a characteristic right
atrial activation map created by pacing each pul-
monary vein corresponded closely with the map
from the same pulmonary vein during rapid AT
and initiation of focal AF (Figs. 9 and 10). The
pulmonary vein of origin could be distinguished
on the basis of this characteristic pattern.
Mechanical Interruption
The application of pressure to the focus of
the AT may transiently interrupt the tachycardia
(Fig. 11). Pappone et al.37 evaluated the predictive
value of intentionally applying pressure to identify
successful ablation sites. Mechanical interruption
was observed in 76% of successful ablation sites
but also in 28% of unsuccessful sites, with a sen-
sitivity, specificity, and positive predictive value
774 July 2006
Figure 9. Example of activation sequence maps during
sinus rhythm (SR; left panel), pacing from the RUPV
(middle panel), and right lower pulmonary vein (RLPV;
right panel).When pacing from the RUPV, activation
on the CT catheter occurs before activation on the CS
catheter. When pacing from the RLPV, activation on the
CS and CT catheters occurs simultaneously. Activation
on the CS catheter occurs from proximal (CS 9, 10) to
distal (CS 1, 2) when pacing both the right-sided veins.
Note also the similarity in the activation pattern between
the RUPV and SR originating from the high CT reflecting
the close anatomic proximity of these two sites. (From
Deen et al. J Cardiovasc Electrophysiol 2002; 13:101–
107. Reproduced with permission.)
of 76%, 71%, and 45%, respectively. In this study,
mechanical interruption was nevertheless a bet-
ter predictor of success than pace mapping or an
activation time to P-wave of >30 ms. The speci-
ficity and positive predictive value of the other
techniques were also improved. However, in our
experience this technique may result in an uncer-
tain endpoint and a higher than usual recurrence
rate.
New Mapping Technology
The mapping and ablation of focal AT has
been augmented by the introduction of three-
dimensional mapping systems. These also allow
a significant reduction in fluoroscopic time and
radiation exposure. The three-dimensional elec-
troanatomic system (CARTO; Biosense Webster,
Diamond Bar, CA, USA) is based on sequential
mapping technology allowing detailed reconstruc-
tion of chamber geometry and activation sequence
(Fig. 12). Natale et al.38 demonstrated that elec-
troanatomic mapping was able to quickly and ac-
curately construct a three-dimensional geometry
of the chamber and map the location of the AT fo-
cus. A number of studies have demonstrated the
ability of electroanatomic mapping to provide a
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 FOCAL ATRIAL TACHYCARDIA II
Figure 10. Example of the activation sequence maps
during sinus rhythm (SR; left panel), pacing from the
left upper pulmonary vein (LUPV; middle panel), and
the left lower pulmonary vein (LLPV; right panel). When
pacing from the LUPV, activation on the CS and CT
catheters occurs simultaneously. When pacing from the
LLPV, activation on the CS catheter occurs before acti-
vation on the CT catheter. Activation on the CS catheter
occurs from distal (CS 1, 2) to proximal (CS 9, 10) when
pacing both the left-sided veins. (From Deen et al. J Car-
diovasc Electrophysiol 2002; 13:101–107. Reproduced
with permission.)
high-resolution map in the region of earliest acti-
vation and precisely locate the focus in relation to
endocardial geometry.38–42 One limitation is the re-
quirement for regular ectopics or sustained tachy-
cardia. Hoffmann et al.39 found that in 12% of
patients, electroanatomic maps were unable to be
constructed due to nonsustained or noninducible
tachycardia.
The noncontact mapping system (EnSite; En-
docardial Solutions, St. Paul, MN, USA) consists
of 64 wires mounted on a 7.6-mL balloon.43 This
allows reconstruction of chamber geometry and si-
multaneous recording of >3,300 virtual unipolar
electrograms enabling entire activation from a sin-
gle beat. One of the difficulties encountered when
mapping AT is its noninducibility in a proportion
of patients. For patients with infrequent AT activ-
ity, the noncontact mapping system allows for a
potential solution, providing detailed maps from
isolated beats and nonsustained AT.44–46 Schmitt
et al.44 used noncontact mapping to identify the
site of earliest activation and found that the tachy-
cardia origin could be localized from the analysis
of only a few tachycardia cycles.
Nonsustained AT may also be mapped using
multielectrode basket catheters. Schmitt et al.47
used a 64-electrode basket catheter to map the RA
in patients with a variety of AT. The basket catheter
PACE, Vol. 29 July 2006
Figure 11. Intracardiac recordings from a patient with
atrial tachycardia. Shown are surface leads II, V 1 , and
V 6 together with intracardiac recordings from the CS,
His bundle (HBE), and ablation catheter. Mechanical
catheter pressure at the site of tachycardia origin (left
superior pulmonary vein) resulted in gradual reduction
in the ablation electrogram amplitude and termination
of the tachycardia. Mechanical mapping or the “bump
technique” has been utilized to identify sites of atrial
tachycardia origin. However, in our experience this may
result in an uncertain endpoint and a higher than usual
recurrence rate.
was able to be deployed in all patients and stable
electrograms were recorded from 88% of the elec-
trodes. Of note, in 60% of cases, no earlier activity
than that reflected with the basket catheter could
be found with a mapping standard catheter. How-
ever, mapping may be limited in the regions of the
isthmus, superior vena cava, and right atrial ap-
pendage as good contact is difficult to achieve in
these areas.
The Ablation Signal
Ablation signal characteristics may also help
identify the AT focus. Fractionated electrograms
are frequently found at the successful ablation site
during AT (Fig. 7)21,46,48–50 ; however, not all stud-
ies have reported this.51–53 In patients with AT lo-
cated mainly on the CT, Kalman et al.21 observed
fractionated signals at the site of successful abla-
tion. In studies by both Lesh et al.48 and Wang
et al.,50 a fractionated ablation signal was seen in
a variety of right and left atrial sites. Fractionated
electrograms may reflect localized abnormalities
in atrial conduction, with poor cell-to-cell cou-
pling causing slowed conduction from a poorly
coupled automatic focus or small reentrant cir-
cuit. Lesh et al.48 suggested that the uncoupling be-
tween the normal surrounding atrial myocardium
and an automatic focus may be a required el-
ement in the arrhythmia mechanism in some
cases.
The site of tachycardia origin may also
be identified using unipolar recordings.51,54 The
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 ROBERTS-THOMSON, ET AL.
Figure 12. Right atrial three-dimensional electroanat-
omic (CARTO) map in a patient with atrial tachycardia
originating from the right septum (tilted left posterolat-
eral view). The yellow dot marks where the His signal
was recorded. Note the centrifugal activation from the
site of origin (red to blue) and the precise localization
of the focus in relation to endocardial geometry. SVC =
superior vena cava; TA = tricuspid annulus.
presence of a pure negative deflection (QS-pattern)
with a rapid initial slope theoretically localizes the
site of origin of the AT. Tang et al.54 analyzed the
unipolar electrogram at both the successful and
unsuccessful ablation sites of focal AT. All the suc-
cessful sites were characterized by the presence of
the QS-morphology. An RS-pattern was observed
at unsuccessful sites. Poty et al.51 reported an acute
success rate of 86% using unipolar recordings to
identify the target site for ablation.
Radiofrequency Ablation
Direct current shocks were the first form of
catheter ablation therapy for the elimination of
atrial foci.55 With the advent of radiofrequency
ablation this has become the treatment of choice
in patients with significant symptoms. AT abla-
tion series have reported success rates between
69% and 100%,3,21,35,37–39,41,44,46,48,50–53,56–59 with
a low incidence of complications. Reported com-
plications include pericardial effusion and tam-
ponade,56 phrenic nerve paralysis,57 AV block,53,57
776 July 2006
sinus node dysfunction,37,53 and pulmonary vein
stenosis.60 Recurrence rates are generally low,
varying between 0% and 33%. Chen et al.61 an-
alyzed 16 studies and reported a recurrence rate
of 7%. In that study, predictors of success of ra-
diofrequency ablation were analyzed. The only in-
dependent predictor of successful radiofrequency
ablation was a right atrial focus. Lower acute suc-
cess rates have been reported in males, patients
with multiple foci and those with repetitive forms
of AT.57 Older patients, patients with other car-
diac diseases, and those with multiple foci have
a higher risk of recurrence.61
At our institution, radiofrequency ablation
is used for all cases. However, cryoablation has
been reported to be useful in the ablation of
foci near the AV node.62,63 In general, a stan-
dard curve 4-mm ablation electrode is used, with
usual power setting of 50 W, and temperature
of 60◦ C. An asymmetric curve electrode may be
helpful in the ablation of septal foci. In certain
locations, such as the trabeculated RA, irrigated
ablation may be beneficial. Catheter stability is
enhanced by the use of long sheaths and is par-
ticularly valuable with ablation in the perinodal
area.
Surgery
Surgery is efficacious in eliminating AT with
success rates of 66–100%.2,11,64–68 However, anes-
thesia and hypothermia may result in nonin-
ducibility of the AT, preventing intraoperative
mapping.2,11,66 Prior to the advent of radiofre-
quency ablation, surgery was the treatment of
choice for focal AT refractory to medical ther-
apy. However, as ablation techniques have be-
come more advanced surgical treatment for fo-
cal AT is unusual. Surgical techniques performed
include excision, cryoablation, left atrial isola-
tion, and regional isolation. Complications from
surgery include sinus node dysfunction requir-
ing pacemaker implantation11,64 and atrial scar-
ring which may produce the substrate for later
macroreentry.
Conclusion
Assessment of the efficacy of antiarrhythmic
therapy for focal AT is difficult due to the paucity
of randomized controlled trials. However, there is
widespread agreement that antiarrhythmics have
low efficacy in the treatment of focal AT. With the
advent of radiofrequency ablation, there has been
a shift away from pharmacological therapy as long-
term cure may be achieved in a high proportion of
patients.
PACE, Vol. 29
 FOCAL ATRIAL TACHYCARDIA II
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