CLINICAL RESEARCH
Europace (2011) 13, 942–948
doi:10.1093/europace/eur033
Ablation for Atrial Fibrillation
Changes in low right atrial conduction times
during pulmonary vein isolation for atrial
fibrillation: correlation with inducibility
of typical right atrial flutter
José Dizon *, Angelo Biviano, William Whang, Frederick Ehlert, and Hasan Garan
Department of Medicine, Division of Cardiology, Columbia University Medical Center, Columbia University, 630 West. 168th Street, New York, NY 10032, USA
Received 25 September 2010; accepted after revision 19 January 2011; online publish-ahead-of-print 21 March 2011
Aims
Isthmus-dependent right atrial flutter (RAFL) is a common sequela of pulmonary vein isolation (PVI). It is unclear as to
whether RAFL is a result of PVI or a concealed phenomenon unmasked by the elimination of atrial fibrillation (AF).
We measured low right atrial conduction times (LRACTs) before and after PVI and examined their relationship to the
inducibility of RAFL.
.....................................................................................................................................................................................
Methods
Twenty consecutive patients with paroxysmal AF but no history of RAFL were studied during the initial PVI proand results
cedure by radiofrequency ablation. Antiarrhythmic agents were discontinued for at least five half-lives. The clockwise
and counterclockwise LRACTs were measured before and after PVI by pacing the proximal coronary sinus or lowlateral RA. Programmed atrial stimulation was performed post-PVI. Right atrial flutter, if inducible, was confirmed by
entrainment mapping. Right atrial flutter was induced in six patients (Group A). No arrhythmias or only AF was
induced in the remaining 14 patients (Group B). The average change in the clockwise LRACT was 19.8 + 17.5 ms
in Group A vs. 0.3 + 10.7 ms in Group B (P , 0.05). The average change in the counterclockwise LRACT was
25.7 + 30.4 ms in Group A vs. 0.0 + 6.7 ms in Group B (P , 0.05). There were no significant differences between
the groups in absolute LRACT or number of ablation lesions around the right pulmonary veins.
.....................................................................................................................................................................................
Conclusion
Right atrial flutter post-PVI is associated with prolongation of LRACTs. Ablation over the septal left atrium near the
posterior right atrium during isolation of the right pulmonary veins may cause conduction delays that can lead
to RAFL.
----------------------------------------------------------------------------------------------------------------------------------------------------------Keywords
Atrial flutter † Atrial fibrillation † Pulmonary vein isolation † Tricuspid valve isthmus
Introduction
Pulmonary vein isolation (PVI) as a therapy for atrial fibrillation
(AF) has become widespread given its greater efficacy compared
with drug therapy and improvement in safety record.1 – 5
However, recurrent atrial arrhythmias remain a significant issue
after PVI since they often require repeat procedures.6 – 8 Atrial
arrhythmias after PVI can be a recurrence of AF from incomplete
lesion sets, an unmasking of atrial flutter once AF is eliminated,
or the development of new atrial arrhythmias as a proarrhythmic
result of the lesion sets themselves. Although left atrial (LA)
flutter is a common arrhythmia after PVI and is most often felt
to be a result of the ablation lesions, isthmus-dependent right
atrial flutter (RAFL) is also quite common.9,10 It is unclear as
to whether RAFL is the proarrhythmic result of PVI or merely
a previously concealed mechanism unmasked by the elimination
of AF.
The purpose of this study is to examine low right atrial conduction times (LRACTs) before and after PVI in a group of patients
with no prior clinical RAFL. By correlating the LRACTs to the inducibility of RAFL, we hope to elucidate the relationship between PVI
and isthmus-dependent RAFL.
* Corresponding author. Tel: +1 914 428 3888; fax: +1 914 686 5366, Email: [email protected]
Published on behalf of the European Society of Cardiology. All rights reserved. & The Author 2011. For permissions please email: [email protected].
943
Low right atrial conduction times after pulmonary vein isolation
Methods
The study was approved by the Columbia University Institutional
Review Board. Patients scheduled for initial PVI for paroxysmal AF
with no history of atrial flutter and presenting in sinus rhythm were
candidates for the study. The absence of previous atrial flutter was
based on review of prior medical history, ECGs, Holter monitor, or
event recorder results. Patients taking amiodarone were excluded,
and other antiarrhythmic agents were discontinued for at least five
half-lives. Twenty consecutive patients who fulfilled the above criteria
were included in this analysis. Patients presented to the electrophysiology laboratory in the fasting state and were sedated and anaesthetized in standard fashion. A steerable octapolar catheter (CR Bard,
Inc., Murray Hill, NJ) was positioned within the coronary sinus with
the most proximal poles just within the os. A duodecapolar circular
catheter [(Halo, Biosense Webster, Inc., Diamond Bar, CA) 8 mm electrode spacing between bipoles] was positioned in the right atrium such
that the distal tip was close to or within the coronary sinus os and
atrial signals could be recorded across the tricuspid valve-inferior
vena cava (TV-IVC) isthmus and low right atrial (RA) lateral wall
(Figure 1). The proximal coronary sinus and distal Halo poles were
thus juxtaposed within 2– 3 cm, just posterior to the cavo-tricuspid
isthmus. This configuration was chosen in order to maximize stability
and maintain consistent position of the catheters.
Prior to PVI, atrial pacing was performed at the proximal coronary
sinus at 600 ms and twice capture threshold, and the timing from the
stimulus artefact to the low-lateral RA bipolar electrogram on the duodecapolar catheter was measured at 200 ms sweep speed using electronic calipers. The initial rapid deflection on the electrogram was
used as the measuring point, and consecutive beats were investigated
for reproducibility. This interval represents the clockwise LRACT
(CL-LRACT). Thereafter, the identical bipole in the low-lateral RA
from which the previous measurement was made was paced at
600 ms drive at twice capture threshold and the interval from the
stimulus artefact to the proximal coronary sinus electrogram was
measured (initial rapid deflection as measuring point). This interval
represents the counterclockwise LRACT (CC-LRACT). Pulmonary
vein isolation was then performed using a double transeptal approach,
which involved wide circumferential antral radiofrequency lesions with
an irrigated tip catheter around the left superior and inferior and right
Figure 1 Schematic of catheter positions and pacing locations.
The bipole on the Halo catheter in the low-lateral right atrial
location and the proximal bipole on the steerable octapolar catheter within the os of the coronary sinus were used for pacing.
superior and inferior pulmonary veins separately. Pulmonary vein isolation, which was the endpoint for the catheter ablation procedure, was
confirmed by elimination of recorded potentials by a circular mapping
catheter (Lasso, Biosense Webster, Inc.) positioned within each vein.
Following PVI, with the patient still under sedation, the CL-LRACT
and CC-LRACT were re-measured, taking care to ensure that the duodecapolar and coronary sinus catheters were positioned as prior to
PVI under biplane fluoroscopy. Figure 2 is an example of the
CL-LRACT (A) and CC-LRACT (B) before and after PVI for one
patient. Trains of atrial stimuli were delivered, starting at a pacing
cycle length of 300 ms and proceeding with 10 ms decrements from
the high RA and the distal coronary sinus until 200 ms was reached;
one-to-one capture was lost; or AF or flutter was induced. Sustained
AF or flutter was defined as lasting .2 min. If atrial flutter was
induced, activation sequence in the duodecapolar catheter and entrainment from within the cavo-tricuspid isthmus was performed to determine whether the atrial flutter was isthmus dependent (Figure 3,
example of RAFL from one patient). All patients with inducible
isthmus-dependent RAFL underwent ablation of the TV-IVC isthmus
as part of their procedure, with demonstration of bidirectional block
across the isthmus. As per our current laboratory policy, inducible atypical atrial flutter is not ablated at initial PVI of paroxysmal AF patients.
Similarly, no additional lesions are delivered for inducible AF after confirming that the pulmonary veins are isolated.
Statistical analysis
The absolute values and differences between the pre- and post-PVI
LRACTs were tabulated. These and other continuous variables were
compared between the patients who had and did not have inducible
RAFL using an unpaired two-tailed Student’s t-test. A P-value of
,0.05 was considered significant.
Results
Table 1 lists the individual CL-LRACT and CC-LRACT for the 20
patients, both before and after PVI, separated by the fact
whether RAFL was inducible or not. Six patients had inducible
sustained RAFL post-PVI, and 14 patients did not. Non-sustained
AF was the only arrhythmia induced in 10 patients and no atrial
arrhythmia was induced in 4 patients. Table 2 lists the characteristics of the patients grouped by inducibility of RAFL. None of
the patients had structural heart disease defined as abnormal
LV or RV function or more than mild atrial dilation or mitral
regurgitation. There were no significant differences in age
between the patients with or without inducible RAFL. In
addition, there were no significant differences between the two
groups in the number of ablation lesions applied around the
right pulmonary veins.
Table 3 lists the average absolute LRACTs post-PVI and the
average LRACT differences between pre- and post-PVI, according
to whether RAFL was inducible or not. There were no significant
differences in the absolute value of the LRACTs between the two
groups. However, the post-PVI prolongation of the CL-LRACT and
CC-LRACT was significantly greater in the group with inducible
RAFL. The range of the LRACTs was wider for the inducible
group of patients. Analysis of the timing of the intracardiac electrograms during pacing in the patients with post-PVI prolongation of
LRACTs suggested that the area of conduction delay was within
the posteroseptal RA.
944
J. Dizon et al.
Figure 2 (A) Example of clockwise low right atrial conduction times. Left panel, proximal coronary sinus pacing pre-pulmonary vein isolation.
Right panel, proximal coronary sinus pacing post-pulmonary vein isolation. Surface leads I, II, AVF, and V1 followed by low-lateral right atrial and
proximal coronary sinus electrograms. Note the increase in low right atrial conduction time post-pulmonary vein isolation. (B) Example of
counterclockwise low right atrial conduction times in the same patient. Left panel, low-lateral right atrial pacing pre-pulmonary vein isolation.
Right panel, low-lateral right atrial pacing post-pulmonary vein isolation. Surface leads and intracardiac channels as in (A). Note increase in low
right atrial conduction time post-pulmonary vein isolation.
Discussion
Post-PVI atrial arrhythmias are problematic since they require
additional time or extra procedures to eliminate, and sometimes
cause more disturbing symptoms than the AF that originally led
to PVI. While LA flutters are generally believed to be an iatrogenic
result of LA ablation,6,8,11 the mechanism of post-PVI typical RAFL
in patients with no prior history of typical RAFL is less clear.
The results of this study show that LRACTs may be prolonged
by PVI in a subgroup of patients and that the extent of lengthening
945
Low right atrial conduction times after pulmonary vein isolation
Figure 3 Example of entrainment of isthmus-dependent right atrial flutter induced after pulmonary vein isolation. Cycle length 223 ms.
Surface leads I, II, AVF followed by group of electrograms on circular catheter, mapping catheter, and stimulus channel. Atrial flutter has
counterclockwise activation and post-pacing return is close to tachycardia cycle length.
correlates with the inducibility of isthmus-dependent RAFL. This
observation suggests that PVI may play a causal role in the induction of RAFL after LA ablation.
Mechanistically, one might postulate that the delivery of ablation
lesions to the septal left atrium could reach the septal RA wall
during right-sided PVI, which could result in conduction delays
that could promote typical RAFL (Figures 4 and 5). This is plausible
given that the typical RAFL circuit may involve these areas.12,13 In
our study, we noted that the area of conduction delay was
between the proximal coronary sinus and distal duodecapolar
catheter electrograms, consistent with the conduction delay
being on the posterior-septal side of the RA. However, the absolute value of the LRACTs post-PVI did not correlate with the inducibility of RAFL, nor did the number of radiofrequency lesions
applied to the right-sided pulmonary veins. In addition, two
patients who had inducible RAFL did not have prolongation of
the LRACTs after PVI (Table 1). These observations suggest that
there are factors beyond mere conduction delay or extent of
radiofrequency current delivery that contribute to the milieu
which allows for the development of post-PVI RAFL. For
example, Waldo et al. have proposed that a necessary component
for the induction of RAFL is functional or anatomic block between
the venae cavae, which would effectively prevent short circuiting of
the flutter circuit.14,15 It is possible that such conduction block is
occurring during ablation of the LA septum during isolation of
the right-sided pulmonary veins, which manifested as low RA conduction delay in some of our patients with inducible RAFL, but not
all of the patients. We cannot be certain as to whether prolongation
of LRACTs has primacy in the induction of RAFL or is merely a
marker of the milieu which supports RAFL. Further studies with
more intricate mapping may be able to elucidate this issue.
Limitations
This study is limited by the small number of patients, which was
a result of the inclusion criteria requiring the patients to be in
sinus rhythm and off all antiarrhythmic agents. Therefore, our
findings need to be confirmed in a larger series of patients. A
procedural limitation is the possible small displacement of the
coronary sinus or duodecapolar catheter, potentially affecting
the LRACT measurements, although care was taken to maintain
position by biplane fluoroscopy. We did not place additional
catheters in the RA or LA to better delineate the areas of conduction delay after PVI, as we wanted to make use of our standard configuration of catheters for ablation of AF. As to the
absence of clinical RAFL, we ascertained as best possible that
all available recorded tachyarrhythmias in all patients were AF
and not atrial flutter. Since our policy is to first isolate the pulmonary veins during sinus rhythm in paroxysmal AF patients, we
did not perform programmed stimulation prior to PVI in order
946
J. Dizon et al.
Table 1 Individual low right atrial conduction times and inducibility of right atrial flutter post-pulmonary vein isolation
Patient
Pre-CL-LRACT
Post-CL-LRACT
Pre-CC-LRACT
Post-CC-LRACT
...............................................................................................................................................................................
Non-inducible RAFL
1.
2.
73
71
77
61
72
60
71
58
3.
87
90
80
80
4.
5.
70
52
72
72
55
74
71
75
6.
102
99
105
100
7.
8.
80
138
90
135
50
140
45
144
9.
102
91
110
105
10.
11.
76
80
90
90
90
110
97
109
12.
85
80
95
89
13.
14.
77
116
67
99
75
127
82
117
1.
2.
70
64
100
90
63
72
135
90
3.
74
108
90
130
4.
5.
33
44
44
74
47
48
43
85
6.
93
81
104
95
Inducible RAFL
PVI, pulmonary vein isolation; LRACT, low right atrial conduction time; CL, clockwise; CC, counterclockwise; RAFL, isthmus-dependent right atrial flutter.
Table 2 Group characteristics
Age
Sex (male/female)
Structural heart disease
Number of radiofrequency
lesions to right pulmonary veins
...............................................................................................................................................................................
Inducible RAFL, n ¼ 6
65.0 + 9.5
6/0
None
78 + 22
Non-inducible RAFL, n ¼ 14
55.3 + 11.3
11/3
None
76 + 26
RAFL, isthmus-dependent right atrial flutter.
Table 3 Low right atrial conduction times
DLRACT range (ms)
clockwise/
counterclockwise
Absolute
clockwise
LRACT (ms)
Absolute
counterclockwise
LRACT (ms)
Clockwise
DLRACT
post-PVI (ms)
Counterclockwise
DLRACT post-PVI (ms)
82.8 + 22.7
96.3 + 33.6
19.8 + 17.5*
25.7 + 30.4*
212 to 34/29 to 72
86.6 + 18.2
88.8 + 25.6
0.3 + 10.7*
0.0 + 6.7*
217 to 20/210 to 16
...............................................................................................................................................................................
Inducible RAFL,
n¼6
Non-inducible
RAFL, n ¼ 14
LRACT, low right atrial conduction times; RAFL, isthmus-dependent right atrial flutter.
*P , 0.05.
947
Low right atrial conduction times after pulmonary vein isolation
Figure 4 Electroanatomic map in right anterior oblique view
showing right atrium (transparent light blue-green with extensions showing superior vena cava and inferior vena cava) overlying left atrium (light grey). The ablation lesions (red) around
the right pulmonary veins (dark grey) are shown directly posterior to the right atrium. The coronary sinus catheter (light
blue with numbers), approximate position of the coronary
sinus os (dark blue oval), and mapping catheter (green tip) with
sample ablation points in tricuspid valve isthmus (light blue
points) are shown for reference.
Figure 5 Identical electroanatomic map in left anterior oblique
view showing the left atrium posterior to the right atrium and the
separate septal walls of the left atrium and right atrium.
Conflict of interest: none declared.
Funding
There are no applicable grants or funding to report for this study.
References
to avoid the induction of AF. We therefore cannot tell whether
the atrial substrate for typical RAFL preceded PVI in these
patients. Finally, this study did not address whether prolonged
LRACTs after PVI predict future clinical RAFL.
Conclusion
Prolongation of LRACTs after PVI is associated with inducibility of
RAFL. This observation suggests that conduction delay, possibly
related to radiofrequency lesions on the LA septum close to the
posterior-septal RA during right-sided PVI, predisposes to RAFL
and is a proarrhythmic result of PVI. Further studies are needed
to confirm these mechanisms, and to assess their predictive
value for post-PVI RAFL.
1. Piccini JP, Lopes RD, Kong MH, Hasselblad V, Jackson K, Al-Khatib SM. Pulmonary
vein isolation for the maintenance of sinus rhythm in patients with atrial fibrillation: a meta-analysis of randomized, controlled trials. Circ Arrhythm Electrophysiol
2009;2:626 –33.
2. Calkins H, Reynolds MR, Spector P, Sondhi M, Xu Y, Martin A et al. Treatment of
atrial fibrillation with antiarrhythmic drugs or radiofrequency ablation: two systematic literature reviews and meta-analysis. Circ Arrhythm Electrophysiol 2009;2:
349 –61.
3. Bonanno C, Paccanaro M, La Vecchia L, Ometto R, Fontanelli A. Efficacy and
safety of catheter ablation versus antiarrhythmic drugs for atrial fibrillation: a
meta-analysis of randomized trials. J Cardiovasc Med 2010;11:408–18.
4. Cappato R, Calkins H, Chen SA, Davies W, Iesaka Y, Kalman J et al. Up-dated
worldwide survey on the methods, efficacy and safety of catheter ablation for
human atrial fibrillation. Circ Arrythm Electrophysiol 2010;3:32 –8.
5. Bunch T.J., Weiss J.P., Crandall B.G., May H.T., Bair T.L., Osborn J.S. et al. Longterm clinical efficacy and risk of catheter ablation for atrial fibrillation in octogenarians. Pacing Clin Electrophysiol 2010;33:146 – 52.
6. Morady F, Oral H, Chugh A. Diagnosis and ablation of atypical atrial tachycardia
and flutter complicating atrial fibrillation ablation. Heart Rhythm 2009;6(suppl.):
S29 – 32.
948
7. Deisenhofer I, Estner H, Zrenner B, Schreieck J, Weyerbrock S, Hessling G et al.
Left atrial tachycardia after circumferential pulmonary vein ablation for atrial fibrillation: incidence, electrophysiological characteristics, and results of radiofrequency ablation. Europace 2006;8:573 –82.
8. Ouyang F, Antz M, Ernst S, Hachiya H, Mavrakis H, Deger FT et al. Recovered pulmonary vein conduction as a dominant factor for recurrent atrial tachyarrhythmias after complete circular isolation of the pulmonary veins: lessons from
double Lasso technique. Circulation 2005;111:127 –35.
9. Scharf C, Veerareddy S, Ozaydin M, Chugh A, Hall B, Cheung P et al. Clinical significance of inducible atrial flutter during pulmonary vein isolation in patients with
atrial fibrillation. J Am Coll Cardiol 2004;43:2057 –62.
10. Lim HE, Pak H, Lee HS, Hwang C, Ro YM, Kim Y. Significance of atrial flutter after
catheter ablation of atrial fibrillation: impact of the different ablation techniques.
Heart Rhythm 2005;2(suppl 1):S273.
J. Dizon et al.
11. Magnano AR, Argenziano M, Dizon JM, Vigilance D, Williams M, Yegen H et al.
Mechanisms of atrial tachyarrhythmias following surgical atrial fibrillation ablation.
J Cardiovasc Electrophysiol 2006;17:366 –73.
12. Rodriguez L, Timmermans C, Nabar A, Hofstra L, Wellens HJJ. Biatrial activation
in isthmus-dependent atrial flutter. Circulation 2001;104:2545 –50.
13. Shah DC, Jais P, Haissaguerre M, Chouairi S, Takhashi A, Hocini M et al. Threedimensional mapping of the common atrial flutter circuit in the right atrium.
Circulation 1997;96:3904 –12.
14. Waldo AL, Feld GK. Inter-relationships of atrial fibrillation and atrial
flutter mechanisms and clinical implications. J Am Coll Cardiol 2008;51:
779 –86.
15. Bui HM, Khrestian CM, Ryu K, Sahadevan J, Waldo AL. Fixed intercaval block in
the setting of atrial fibrillation promotes the development of atrial flutter. Heart
Rhythm 2008;5:1753 –4.