CLINICAL RESEARCH
Europace (2016) 18, 1259–1264
doi:10.1093/europace/euv345
Cardiac electrophysiology
Novel electrophysiological characteristics
of atrioventricular nodal continuous conduction
curves in atrioventricular nodal re-entrant
tachycardia with concomitant cavotricuspid
isthmus-dependent atrial flutter
Chung-Hsing Lin 1,2,3, Yenn-Jiang Lin 1,2*, Shih-Lin Chang 1,2, Li-Wei Lo 1,2,
Hung-Kai Huang 1,4, Cheng-Hung Chiang 1,5, Suresh Allamsetty1,6, Jo-Nan Liao 1,2,
Fa-Po Chung 1,2, Yao-Ting Chang 1,2, Chin-Yu Lin 1,2, and Shih-Ann Chen 1,2
1
Division of Cardiology, Taipei Veterans General Hospital, 201, Sec. 2, Shih-Pai Road, Taipei, Taiwan; 2Faculty of Medicine, Institute of Clinical Medicine, and Cardiovascular Research
Institute, National Yang-Ming University, Taipei, Taiwan; 3Division of Cardiology, Taipei City Hospital, Ren-Ai Branch, Taipei, Taiwan; 4Division of Cardiology, Department of Medicine,
Changhua Christian Hospital, Changhua, Taiwan; 5Division of Cardiology, Department of Internal Medicine, Kaohsiung Veterans General Hospital, Kaohsiung, Taiwan; and 6Nizam’s
Institute of Medical Science, Hyderabad, India
Received 23 February 2015; accepted after revision 15 September 2015; online publish-ahead-of-print 26 November 2015
Aims
The detailed electrophysiological characteristics of patients with both atrioventricular nodal re-entrant tachycardia
(AVNRT) and atrial flutter (AFL) have not been clarified. This study investigated the related electrophysiological
differences in a large series of patients undergoing radiofrequency catheter ablation of AVNRT.
.....................................................................................................................................................................................
Methods and
A total of 1063 clinically documented AVNRT patients underwent catheter ablation were enrolled. Before the slow
pathway (SP) ablation, 61 patients (5.7%) had inducible sustained cavotricuspid isthmus (CTI)-dependent AFL (Group
results
1), and the others (94.3%) without inducible sustained CTI-dependent AFL were defined as Group 2. The electrophysiological characteristics of these two groups and effect of the SP ablation on the inducibility of AFL were assessed.
In Group 1, 36 patients (59%) had inducible/sustained AFL after the ablation of AVNRT and required a CTI ablation. The
Group 1 patients had more AVNRT with continuous atrioventricular (AV) node function curves (P , 0.001, odds
ratio ¼ 7.55 [3.70– 16.7], multivariate regression), and a younger age (P ¼ 0.02, odds ratio ¼ 1.02 [1.003 –1.03], multivariate regression) than Group 2. The other characteristics were comparable between the two groups. The long-term
follow-up (64.9 + 34.9 months) revealed that the recurrence of AFL/atrial fibrillation was similar between the two
groups (P . 0.05).
.....................................................................................................................................................................................
Conclusion
Atrioventricular nodal re-entrant tachycardia patients with concomitant CTI-dependent AFL had more continuous AV
node function curves. Forty-one per cent of these patients had non-inducible AFL after the SP ablation, indicating a slow
conduction isthmus in the triangle of Koch area.
----------------------------------------------------------------------------------------------------------------------------------------------------------Keywords
Ablation † Atrioventricular nodal re-entrant tachycardia † Atrial flutter † Cavotricuspid isthmus
Introduction
Cavotricuspid isthmus (CTI)-dependent atrial flutter (AFL) is a
macro-re-entrant tachyarrhythmia most often contained within
the right atrium (RA), and atrioventricular nodal re-entrant tachycardia (AVNRT) is the most common form of paroxysmal regular
supraventricular tachycardia in adults and accounts for 60% of these
tachycardias.1 In a previous study, AFL was induced in a greater
* Corresponding author. Tel: +886 2 2875 7156; fax: +886 2 2873 5656. E-mail address: [email protected]
Published on behalf of the European Society of Cardiology. All rights reserved. & The Author 2015. For permissions please email: [email protected].
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What’s new?
† Atrioventricular nodal re-entrant tachycardia patients associated with concomitant CTI-dependent AFL had a younger
age and more continuous AV node function curves.
† Radiofrequency ablation of the SP of the AVNRT circuit influences the inducibility of AFL.
percentage of patients with AVNRT, suggesting that there may be a
common area of the posteroseptal perinodal atrium participating in
the two-tachycardia circuits.2 On the basis of a post-mortem study,
Inoue and Becker3 reported that the human compact atrioventricular (AV) node contains rightward and leftward posterior extensions,
with the rightward extension close to the tricuspid annulus and CTI.
They concluded that these extensions are involved in ‘slow pathway’
conduction.
Percutaneous catheter mapping studies have shown that the AFL
re-entrant circuit may include an area of slow conduction bounded
on the lateral side by the septal leaflet of the tricuspid valve and the
inferior vena cava (lateral isthmus) and on the medial side by the Eustachian valve/ridge, septal leaflet of the tricuspid valve (medial isthmus), coronary sinus ostium, and septal leaflet of the tricuspid valve
(septal isthmus).4,5 Typical AVNRT usually has a dual AV nodal pathway physiology and can be cured by radiofrequency (RF) catheter ablation.6 The slow pathway (SP) is thought to have a predominantly
posterior-inferior location between the ostium of the coronary sinus
and septal leaflet of the tricuspid valve, and the fast pathway (FP) allegedly starts in the anterior-superior portion of the interatrial septum
(IAS).7 – 9 When an association between AVNRT and AFL was noted in
previous studies, it was logically attributed to the ‘shared pathway’ at
the low right atrial septum.10,11 Therefore, there should be an association between AFL and AVNRT. We hypothesized that AVNRT patients with concomitant AFL have different electrophysiology
characteristics from pure AVNRT patients. However, the previous
study used an aggressive pacing protocol to induce AFL,2 which might
not have reflected the true incidence of AFL in AVNRT patients.
In this study, first, we aimed to study the electrophysiological
characteristics in patients with and without inducible AFL, and the
AFL inducibility after an SP ablation in patients with an AVNRT ablation. Secondly, the electrophysiological properties in these patients with and without inducible AFL, immediately after the SP
ablation, and the long-term recurrence of AFL or atrial fibrillation
(AF) in these two groups were assessed.
Methods
Study population and electrophysiological
study
Between December 2004 and November 2013, a total of 1063 consecutive clinical documented AVNRT patients with catheter ablation
were enrolled in this study. All the patients had inducible AVNRT
(987 patients) or more than two AV re-entry echo beats (76 patients)
in the electrophysiological laboratory. No patients had any clinical documented and spontaneous AFL before the electrophysiological study
C.-H. Lin et al.
(EPS). All patients were referred to receive an EPS and RF catheter ablation in this institution.
As described previously, each patient underwent a baseline EPS in the
fasting, non-sedated state.12 – 14 All antiarrhythmic drugs were discontinued for a minimum of five drug half-lives before the procedure. A 7 F
decapolar catheter with a 2-mm interelectrode distance and 5-mm spacing between each electrode pair was placed in the coronary sinus. The
position of the proximal electrode pair at the ostium of the coronary
sinus was confirmed with a contrast injection. Three multipolar,
deflectable-tip, closely spaced (interelectrode spacing, 2 mm) electrode
catheters were placed in the high RA, His-bundle area, and right ventricle. At the beginning of the study, programmed electrical stimulation
consisting of atrial and ventricular incremental pacing and extrastimulation in 10-ms decrements was performed to ascertain the anterograde
and retrograde AV nodal conduction properties, and the inducibility of
AVNRT, till the atrial effective refractory period (ERP) and ventricular
ERP. Intravenous isoproterenol (at graded dosages from 1 to 4 mg/
min) was used to facilitate the induction of the tachycardia after attempting to induce it with pacing manoeuvres. If a tachycardia was
not inducible under an isoproterenol infusion, intravenous atropine
(0.5 – 1 mg) was used. If the AFL was induced and sustained (lasting
more than 30 s), with similar clinical documented symptoms, during
the study of AVNRT, we recorded it concomitantly. If any tachycardia
could not be induced, electrical pacing from the IAS, low right atrium
(LRA) near the crista terminalis, and coronary sinus (CS) pacing (eight
beats, followed by bursts) were performed. The methods of tachycardia
induction included (i) baseline pacing (eight-beat drive, twice the diastolic threshold) with single and double premature stimuli at three different
cycle lengths (CLs; 600, 500, and 400 ms) and (ii) burst pacing (20 beats,
twice the diastolic threshold or up to 10 mA) at progressively shorter
CLs until 2:1 atrial capture from the LRA and CS ostium (CSo).15
Definitions
The details of the diagnostic EPS and diagnostic criteria of AVNRT have
been well-described previously.12 – 14 In brief, dual AV nodal pathway
curves were characterized by a jump (≥50 ms) in the H1 – H2 interval
at a critical range of A1 – A2 coupling intervals (10 ms decrements), resulting in a discontinuity between the portion of the curve to the right of
the jump in the H1 – H2 interval (FP conduction) and the portion of the
curve to the left of the jump (SP conduction). A continuous AV nodal
function curve was defined by no atrio-His (AH) jump during the basic
EPS. Cavotricuspid isthmus-dependent AFL was defined as either counterclockwise or clockwise activation around the tricuspid annulus in the
RA and concealed entrainment was observed with pacing from the septal or lateral CTI.15
Mapping and ablation technique
The method used for the mapping and ablation of AVNRT has been previously described.12 – 14 To determine the possible anatomic site of the
SP, the mapping and ablation catheter tip was initially positioned in the
posterior region, then the medial region, and finally the anterior region,
if necessary. The presumed ablation site was considered optimal if the
bipolar electrograms obtained from the distal electrode exhibited an atrial/ventricular electrogram amplitude ratio of 0.1 – 0.5, with a multicomponent or a putative SP potential. Catheter ablation was
performed (40 – 50 W, 50 – 608C, and 20 – 60 s) using a 4-mm tip nonirrigated ablation catheter. Radiofrequency energy was delivered from
a generator (EPT-1000, Boston Scientific Co., Natick, MA, USA), and
if junctional rhythm did not appear during the first 10 s, the energy delivery was terminated and another ablation site was selected. The energy
delivery was also terminated immediately in the event of an increase in
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AVNRT associated with concomitant CTI-dependent atrial flutter
the impedance, dislocation of the catheter, prolongation of the PR interval, or occurrence of AV block. An attempt to induce AVNRT with the
evaluation of the AV nodal conduction properties was conducted
immediately after each application of RF energy. The endpoint of the
procedure was the elimination of the anterograde SP with noninducibility of AVNRT or a modification of the anterograde SP with
only one residual echo beat with an intravenous infusion of isoproterenol. After the AVNRT ablation, we did the same programmed
electrical stimulation protocol as that before ablation, to study the
anterograde and retrograde AV nodal physiology and observe if any
tachycardia was inducible.
After the SP ablation, the reproducibility of sustained AFL was confirmed with the identical protocols which used before the SP ablation.
We performed and recorded the ablation of sustained AFL (.30 s), if
patients were under similar documented symptoms clinically. Radiofrequency energy was delivered with an 8-mm tip catheter (Blazer II XP
ablation catheter, 8mm, Boston Scientific, MA, USA) to achieve a tip –
tissue interface temperature of 708C during sinus rhythm with pacing
from the CS ostium. The pre-set duration of each RF pulse was 120 s.
A continuous application of RF energy during a pullback of the ablation
catheter from the right ventricle towards the inferior vena cava was used
to create linear lesions of the cavotricuspid isthmus. Successful ablation
was defined as an achievement of bidirectional isthmus conduction
block without induction of typical or atypical AFL.14
Complete electrocardiograms were performed on the second day
and 1 week after the ablation. Holter recordings and further complete
electrocardiograms were also performed in the outpatient departments
according to the clinical symptoms. We reviewed those records for AFL
recurrence by the end of December 2014.
Statistical analyses
The continuous variables were presented as the mean + SD. The comparisons of the continuous variables were performed using a Student’s
t-test and Mann – Whitney test, and the nominal variables were compared by a x 2 analysis with a Yates correction or Fisher’s exact test. Univariate and multivariate regression analyses were performed where
indicated. A P value of ,0.05 indicated statistical significance. All statistical analyses were performed using commercial statistical SPSS Version
20.0 software (SPSS, Chicago, IL, USA).
Results
Patient characteristics
The study population consisted of 1063 clinical documented
AVNRT patients (mean age: 49.2 + 17.2 years old) whom underwent catheter ablation. Before the SP ablation, only 61 patients
(5.7%) had inducible sustained CTI-dependent AFL (Group 1) during the EPS, and the others (94.3%) without inducible sustained CTIdependent AFL were defined as Group 2 (Table 1, Figure 1).
In Group 1 patients, 4 of 61 Group 1 patients (6.6%) were noted
with clinical documented, sustained AF, and 3 patients (4.9%) with
clinical documented, sustained AFL during the EPS. All these seven
patients were not excluded because of the positive inducibility for
AFL. Twenty-one (34%) of Group 1 patients had inducible AF after
anterograde SP ablation. Six (28.5%) of these 21 patients had sustained AF and AFL, and electrical cardioversion was needed to restore the sinus rhythm, for facilitating the CTI ablation.
For the induction mode, eight patients (13%) were induced by RA
burst pacing, and two of these eight patients (25%) were under
isoproterenol infusion. The other 45 patients (73.7%) were induced
during diagnostic EPS for AVNRT, and 11 of these 45 patients
(24.4%) were under isoproterenol infusion.
A total of 36 of the 61 patients (59%) had inducible and sustained AFL after the ablation of the anterograde SP of the AV
node and required a CTI ablation (Group 1a), and the other 25 patients (41%) did not require a CTI ablation (Group 1b). The baseline characteristics showed that Group 1 patients were significantly
younger than Group 2 patients (42.2 + 16.7 vs. 47.6 + 16.9 years,
P ¼ 0.02). The other characteristics were similar between the two
groups.
Electrophysiological characteristics in the
patients with and without atrial flutter
Table 1 shows the electrophysiologic characteristics of the Group 1
and Group 2 patients. The AH intervals, ERP and functional
Table 1 Baseline and electrophysiological characteristics in the AVNRT patients with and without AFL
Variables
AVNRT with AFL
(Group 1) (n 5 61)
AVNRT without AFL
(Group 2) (n 5 1002)
Univariate
Multivariate
...................................
.....................................
OR
95% CI
P-Value
OR
95% CI
P-Value
...............................................................................................................................................................................
Age (mean + SD)a
Sex (male, n, %)
42.2 + 16.7
29 (47.5)
47.6 + 16.9
370 (36.9)
1.02
0.64
1.00– 1.03
0.38– 1.08
0.01
0.12
1.02
1.003–1.03
0.02
Continuous curve (n, %)a
15 (24.6)
39 (3.9)
8.06
4.15– 15.6
,0.001
0.13
0.06–0.27
,0.001
AH interval (ms)
Atrial ERP (ms)
87.6 + 23.7
219.2 + 64.6
85.0 + 21.9
221.8 + 36.2
0.99
1
0.98– 1.00
0.99– 1.01
0.17
0.37
Atrial FRP (ms)
248.1 + 66.8
257.5 + 44.0
1
0.99– 1.01
0.38
1
0.99–1.00
0.08
Anterograde conduction
Fast pathway ERP (ms)
327.0 + 85.5
340.4 + 86.0
1
0.99– 1.00
0.28
Fast pathway FRP (ms)
398.8 + 66.5
417.4 + 83.2
1
0.99– 1.00
0.06
AVNRT cycle length (ms)
341.3 + 68.6
354.5 + 70.3
0.99
0.99– 1.00
0.16
AH, atrio-His; ERP, effective refractory period; FRP, functional refractory period; AVNRT, atrioventricular nodal re-entrant tachycardia.
a
Indicate the risk of AFL per decrement of age per year, and the presence of continuous curve.
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C.-H. Lin et al.
Figure 1 Flow chart of the study patients and the difference of electrophysiologic characteristics of AVNRT patinets with and without AFL.
AVNRT, atrioventricular nodal reentrant tachycardia; AFL, atrial flutter; CTI, cavotricuspid isthmus; AVN, atrioventricular node; SP, slow pathway.
refractory period (FRP) of the RA, effective refractory period of the
anterograde FP, and AVNRT CL were comparable between the two
groups. The Group 1 patients had a higher incidence of continuous
AV node function curves (24.6 vs. 3.9%, P , 0.001, odds ratio ¼
7.55 [3.70 – 16.7], multivariate regression). The atrial FRP was
borderline shorter Group 1 patients than the control group Group 2
patients (398.8 + 66.5 vs. 417.4 + 83.2 ms, P ¼ 0.06, univariate
regression).
Catheter ablation and follow-up results
During a follow-up of 64.9 + 34.9 months, the recurrence of clinically documented AFL in the Group 1a and 1b patients was 8.3% (3 in
36) and 8.0% (2 in 25, P ¼ 0.963), respectively. None of those patients received a secondary procedure for atrial arrhythmias.
Discussion
Major findings
Electrophysiological characteristics in
patients with and without atrial flutter
after slow pathway ablation
Table 2 shows the electrophysiological characteristics of the Group
1a (with AFL after SP ablation) and Group 1b (without AFL after SP
ablation) patients. The AH intervals, effective refractory period of
the RA, ERP and FRP of the anterograde FP, and AVNRT CL did
not differ between these two groups of patients. However, the
FRP of the RA was borderline shorter (207.2 + 45.9 vs. 236.1 +
82.9 ms, P ¼ 0.06) in the Group 1a patients.
For the anatomical position of SP ablation, there were 41.7% (15
of 36) patients in Group 1a had SP ablation in the posterior projection of AV nodal SP, i.e. near or inside the CS ostium, and 29.2% (7 of
25) patients in Group 1b (P ¼ 0.67). Regarding the position of CTI
ablation in Group 1a patients, 86% (31 of 36) were in the middle
CTI, 8% (3 of 36) were in paraseptal CTI, and 6% (2 of 36) were
in the lateral CTI.
The major findings of this study were the following: first, AFL was
induced in a limited (5.7%) number of patients with AVNRT. A
younger age and more continuous AV node function curves in the
AVNRT patients were associated with concomitant CTI-dependent
AFL. Secondly, RF ablation of the SP of the AVNRT circuit may have
affected the inducibility of AFL in patients who had simultaneous
inducible CTI-dependent AFL. Overall 41% of those patients had
non-inducible AFL after the SP ablation, and the patients who had
a tendency for a longer refractory period of the RA may have had
a lesser inducibility of CTI-dependent AFL after the SP ablation
for AVNRT.
Compared with previous studies
A previous study reported by Kalbfleisch et al. 11 showed that AFL
was more inducible in patients with AVNRT (37 of 42 patients,
88%) and in those with a history of AFL (92%) than in the control
patients (36%). They also reported that the incidence of AFL was
similar before and after the SP ablation. The difference between
1263
AVNRT associated with concomitant CTI-dependent atrial flutter
Table 2 Electrophysiological differences in the patients with inducible or non-inducible AFL after AVNRT ablation
Variables
AFL inducible
(Group 1a) (n 5 36)
AFL non-inducible
(Group 1b) (n 5 25)
Univariate analysis
Multivariate analysis
....................................
....................................
OR
95% CI
P-Value
OR
95% CI
P-Value
1.01
2.35
0.98– 1.04
0.83– 6.69
0.38
0.17
0.99
0.97–1.00
0.09
...............................................................................................................................................................................
Age (mean + SD)
Sex (male, n, %)
43.8 + 16.8
14 (38.9%)
40.0 + 16.6
15 (60.0%)
Continuous curve (n, %)
8 (22.2%)
7 (28.0%)
1.36
0.42– 4.40
0.83
AH (ms)
HV (ms)
81.6 + 36.1
41.3 + 16.9
85.8 + 18.3
46.3 + 8.7
0.99
0.97
0.97– 1.01
0.92– 1.01
0.55
0.19
Atrial ERP (ms)
207.2 + 45.9
236.1 + 82.9
0.99
0.98– 1.00
0.16
Atrial FRP (ms)
Anterograde conduction
232.0 + 55.8
272.2 + 76.3
0.98
0.97– 1.00
0.06
Fast pathway ERP (ms)
323.4 + 81.6
332.1 + 92.8
0.99
0.99– 1.00
0.72
Fast pathway FRP (ms)
AVNRT cycle length (ms)
395.5 + 54.4
348.4 + 63.4
403.0 + 80.6
329.8 + 71.8
0.99
1
0.99– 1.00
0.99– 1.01
0.7
0.29
AVNRT, atrioventricular nodal re-entrant tachycardia; AFL inducible, atrial flutter inducible after AVNRT ablation, and also ablated; AFL non-inducible, atrial flutter non-inducible
after AVNRT ablation and not ablated; AH, atrio-His; HV, His-ventricular; ERP, effective refractory period; FRP, functional refractory period.
our study results and those of Kalbfleisch et al. may be related to the
more aggressive pacing protocols used by Kalbfleisch et al. who
paced down to a CL of 100 ms and the difference in the patients’
histories. Takagi et al. 2 reported that the incidence of AVNRT
with concomitant AFL was higher (38 of 71 patients, 53%), and
that there was no difference in the inducibility of AFL before and
after the SP ablation. In our study, in 41% of the AVNRT patients
with inducible CTI-dependent AFL, it was not possible to induce
AFL after the ablation of the AV node. The difference between
our study results and those of Takagi et al. was related to the different pacing protocols and pacing positions before and after the RF
ablation. They paced from different sites, including the RA appendage, low lateral RA, and CS ostium starting from a CL of 300 ms in
decreasing increments of 20 ms until achievement of 2:1 atrial capture. Further, we had a greater patient number than the previous
studies, which might have revealed the true incidence of inducible
AFL in AVNRT patients.
However, another previous study revealed that ablation of the SP of
the AV node allowed for a reduction in the ventricular rate during AFL
or AF.16 In patients with a dual AV nodal pathway physiology, the AV
node Wenckebach CL and maximal AH interval during RA pacing
were significantly longer after the RF ablation of the CTI. This suggested that there might be a common area of perinodal atrium participating in the two-tachycardia circuits. The AV node properties differed
in the patients with associated AFL. The atrial musculature in the CTI
significantly contributed to the slow AV node conduction.15
There was also study regarding the CSo myocardium. In their four
patients with atrial tachycardia (AT) from CSo, Huo et al. 17 did
three-dimensional entrainment mapping, activation mapping, to localize the re-entrant circuit or differentiate a localized re-entrant AT
from macro-re-entant AT, and also confirmed re-entry as an underlying mechanism of AT by evaluating consistency of return cycles
after entrainment at multiple sites in both atria. They found fragmented and/or double potentials recorded in the CSo with prominent
prolonged electrogram duration compared with those during sinus
rhythm, and a significant conduction delay within the CS. The CSo
myocardium was suggested as a part of the critical isthmus within
the re-entrant circuit, and also could be a part of AFL isthmus where
SP is also successfully ablated.17
Possible mechanisms of the continuous
atrioventricular nodal function curve
Failure to demonstrate anterograde AV node dual pathways, i.e. a
continuous AV node function curve, in the AVNRT patients in response to atrial extrastimuli, is usually due to one of the three factors. (i) The refractory periods of SP and FP may be similar. (ii) A
long atrial FRP limits the prematurity of with which atrial extrasimuli
can reach the AV node, which renders the extrastimuli incapable of
dissociating FP and SP. (iii) Block in the FP already occurs during the
basal drive. Thus, conduction always proceeds over the SP.18 It is
also well known in the electrophysiology laboratory that discontinuous AV node conduction curves may become continuous during an
isoproterenol infusion, because the refractory period of the FP
could be abbreviated to the extent that the SP conduction could
not be achieved with single or even double atrial extrastimuli or
with incremental atrial pacing.18 Multiple drive CLs, multiple extrastimuli, and even more drugs, such as calcium channel blockers, beta
blockers, and even digoxin, may be necessary to dissociate the SP
and FP for our study patients, and more concomitant CTIdependent AFL might be discovered.19 However, it could also be
explained by higher functional block on isthmus that facilitates the
conduction block which lead easier to re-entry arrhythmias.20
Autonomic tone
A change in autonomic tone has been considered an important factor in the initiation of flutter, and enhanced sympathetic modulation,
or decreased vagal tone in AVNRT patients may also involve the
genesis of inducible AFL. Another study found that the inducibility
of AFL in AVNRT patients (38%) in whom the electrophysiological
1264
testing was only performed during the baseline state for the clinical
arrhythmia induction was not lower than that in the patients (32%)
who underwent electrophysiological testing both during the baseline state and the use of isoproterenol. This observation may indicate that the sympathetic tone is higher in patients in whom the
AV nodal re-entrant tachycardia could be induced during the baseline state.21 Atrioventricular nodal re-entrant tachycardia patients
have an unbalanced sympathovagal tone compared with controls.22
The younger people had a stronger sympathetic tone. This could be
one possible mechanism of the age difference in this study.
Study limitations
First, this was a single-centre retrospective study from a tertiary
arrhythmia centre. The autonomous activity was not evaluated
systemically. Therefore, it was unclear to what extent the electrophysiological differences observed among the different patient groups
could be attributed to the differences in the autonomous tone. Secondly, detailed mapping of the tachycardia circuits within Koch’s triangle was not yet available. Evaluating the electrophysiological
properties involved in AVNRT in the deeper layers of Koch’s triangle
is a challenge with the endocardial technique. The incidence of clinically documented AFL during the electrophysiology study was only
three patients (4.9% of Group 1). The data of this study were mostly
based on induction, rather than spontaneous occurrence of AFL, and
the data remain speculative. Thirdly, there might also be electrophysiological difference between AVNRT patients with ‘concomitant
spontaneous’ AFL and ‘inducible’ AFL. We could not recognize if the
clinical symptoms were from AVNRT, AFL, or AF. The incidence of
spontaneous AF, AFL might be underestimated. Finally, we did not
routinely evaluate the effect of different dosage of intravenous
isoproterenol on the inducible tachycardia. Further investigation is
required for the lower limit of dosage of isoproterenol.
Conclusion
Cavotricuspid isthmus-dependent AFL was induced in 5.7% of the
patients with AVNRT without previous documented AFL, was dominant in the younger age groups, and had a higher incidence of continuous AV function curves. Radiofrequency ablation of the SP of the
AVNRT circuit influenced the inducibility of AFL. About 41% of
these patients had non-inducible AFL after the SP ablation, suggesting that there may be a common area of posteroseptal perinodal
atrium participating in these two tachycardias.
Funding
This work was supported by Ministry of Science and Technology of
Taiwan support for the Center for Dynamical Biomarkers and Translational Medicine, National Central University, National Yang-Ming University, and Taipei Veterans General Hospital (MOST 103-2911-I-008-001,
103-2314-B-010-048-MY3, 102-2314-B-010-056-MY2); grant of Taipei
Veterans General Hospital (V103E7-003); joint foundation of Taipei
Veterans General Hospital and National Taiwan University Hospital
(VN103-04).
Conflict of interest: none declared.
C.-H. Lin et al.
References
1. Elvas L, Gursoy S, Brugada J, Andries E, Brugada P. Atrioventricular nodal reentrant
tachycardia: a review. Can J Cardiol 1994;10:342 –8.
2. Takagi Y, Watanabe I, Okumura Y, Okubo K, Ashino S, Kofune M et al. Inducibility
of atrial flutter in patients with atrioventricular nodal reentrant tachycardia. Circ J
2006;70:1133 –7.
3. Inoue S, Becker AE. Posterior extensions of the human compact atrioventricular
node: a neglected anatomic feature of potential clinical significance. Circulation
1998;97:188 –93.
4. Kalman JM, Olgin JE, Saxon LA, Fisher WG, Lee RJ, Lesh MD. Activation and entrainment mapping defines the tricuspid annulus as the anterior barrier in typical
atrial flutter. Circulation 1996;94:398 –406.
5. Nakagawa H, Lazzara R, Khastgir T, Beckman KJ, McClelland JH, Imai S et al. Role of
the tricuspid annulus and the Eustachian valve/ridge on atrial flutter. Relevance to
catheter ablation of the septal isthmus and a new technique for rapid identification
of ablation success. Circulation 1996;94:407 – 24.
6. Katritsis DG, Josephson ME. Classification of electrophysiological types of atrioventricular nodal re-entrant tachycardia: a reappraisal. Europace 2013;15:1231 –40.
7. Haissaguerre M, Gaita F, Fischer B, Commenges D, Montserrat P, d’Ivernois C et al.
Elimination of atrioventricular nodal reentrant tachycardia using discrete slow potentials to guide application of radiofrequency energy. Circulation 1992;85:
2162 –75.
8. Jackman WM, Beckman KJ, McClelland JH, Wang X, Friday KJ, Roman CA et al.
Treatment of supraventricular tachycardia due to atrioventricular nodal reentry,
by radiofrequency catheter ablation of slow-pathway conduction. N Engl J Med
1992;327:313–8.
9. Jazayeri MR, Hempe SL, Sra JS, Dhala AA, Blanck Z, Deshpande SS et al. Selective
transcatheter ablation of the fast and slow pathways using radiofrequency energy in
patients with atrioventricular nodal reentrant tachycardia. Circulation 1992;85:
1318 –28.
10. Interian A Jr, Cox MM, Jimenez RA, Duran A, Levin E, Garcia O et al. A shared pathway in atrioventricular nodal reentrant tachycardia and atrial flutter: implications
for pathophysiology and therapy. Am J Cardiol 1993;71:297 –303.
11. Kalbfleisch SJ, el-Atassi R, Calkins H, Langberg JJ, Morady F. Association between
atrioventricular node reentrant tachycardia and inducible atrial flutter. J Am Coll
Cardiol 1993;22:80 –4.
12. Chen SA, Chiang CE, Tsang WP, Hsia CP, Wang DC, Yeh HI et al. Selective radiofrequency catheter ablation of fast and slow pathways in 100 patients with atrioventricular nodal reentrant tachycardia. Am Heart J 1993;125:1 –10.
13. Tai CT, Chen SA, Chiang CE, Lee SH, Chiou CW, Ueng KC et al. Multiple anterograde atrioventricular node pathways in patients with atrioventricular node reentrant tachycardia. J Am Coll Cardiol 1996;28:725–31.
14. Tai CT, Chen SA, Chiang CE, Lee SH, Wen ZC, Chiou CW et al. Complex
electrophysiological characteristics in atrioventricular nodal reentrant tachycardia
with continuous atrioventricular node function curves. Circulation 1997;95:
2541 –7.
15. Tai CT, Tsai CF, Hsieh MH, Lin WS, Lin YK, Lee SH et al. Effects of cavotricuspid
isthmus ablation on atrioventricular node electrophysiology in patients with typical
atrial flutter. Circulation 2001;104:1501 – 5.
16. Della Bella P, Carbucicchio C, Tondo C, Riva S. Modulation of atrioventricular
conduction by ablation of the “slow” atrioventricular node pathway in
patients with drug-refractory atrial fibrillation or flutter. J Am Coll Cardiol 1995;
25:39 –46.
17. Huo Y, Arya A, Gaspar T, Richter S, Schoenbauer R, Sommer P et al. Role of the
coronary sinus ostium musculature in reentrant formation. Herzschrittmacherther
Elektrophysiol 2012;23:121 – 7.
18. Josephson ME. Clinical Cardiac Electrophysiology: Techniques and Interpretations.
Philadelphia, USA: Lippincott Williams & Wilkins; 2008.
19. Kuo CT, Lin KH, Cheng NJ, Chu PH, Hsu TS, Chiang CW et al. Characterization of
atrioventricular nodal reentry with continuous atrioventricular node conduction
curve by double atrial extrastimulation. Circulation 1999;99:659 – 65.
20. Brembilla-Perrot B, Burger G, Beurrier D, Houriez P, Nippert M, Miljoen H et al.
Influence of age on atrial fibrillation inducibility. Pacing Clin Electrophysiol 2004;27:
287 –92.
21. Wen ZC, Chen SA, Tai CT, Chiang CE, Chiou CW, Chang MS. Electrophysiological
mechanisms and determinants of vagal maneuvers for termination of paroxysmal
supraventricular tachycardia. Circulation 1998;98:2716 – 23.
22. Liu S, Yuan S, Hertervig E, Kongstad O, Ljungstrom E, Bertil Olsson S. Electrophysiology of inducible atrial flutter in patients with atrioventricular nodal reentrant
tachycardia. Clinical physiology and functional imaging 2004;24:19– 24.