Download Frequency of spontaneous and inducible atrioventricular nodal

Frequency of Spontaneous and Inducible
Atrioventricular Nodal Reentry Tachycardia in Patients
with Idiopathic Outflow Tract Ventricular Arrhythmias
IAN TOPILSKI, AHARON GLICK, SAMI VISKIN, and BERNARD BELHASSEN
From the Department of Cardiology, Tel-Aviv Sourasky Medical Center, and the Sackler School of Medicine,
Tel-Aviv University, Tel-Aviv, Israel
TOPILSKI, I., ET AL.: Frequency of Spontaneous and Inducible Atrioventricular Nodal Reentry Tachycardia in Patients with Idiopathic Outflow Tract Ventricular Arrhythmias. Objectives: We sought to assess
the frequency of spontaneous or inducible atrioventricular nodal reentry tachycardia (AVNRT) in patients
referred for radiofrequency ablation (RFA) of idiopathic outflow tract ventricular arrhythmias.
Background: In patients with no obvious heart disease, AVNRT and outflow tract ventricular tachycardia (VT) are the most frequently encountered supraventricular and ventricular tachycardias, respectively.
An increased coexistence of the two arrhythmias has been recently suggested.
Methods: In 68 consecutive patients referred for RFA of an idiopathic ventricular outflow tract arrhythmia, a stimulation protocol including repeated bursts of rapid atrial pacing, up to triple atrial extrastimuli
during sinus rhythm and rapid ventricular pacing was performed before and after isoproterenol infusion
following RFA of the ventricular arrhythmia. In patients with inducible AVNRT, RFA of the slow pathway
was performed.
Results: Of the 68 study patients, 17 (25%) had either spontaneous AVNRT documented prior to RFA
of the ventricular arrhythmia (n = 4) or inducible AVNRT at the time of RFA of the ventricular arrhythmia
(n = 13). AVNRT was induced by atrial pacing in 15 (88%) of 17 patients: in 3 patients without isoproterenol
and in 12 patients during isoproterenol infusion. Uncomplicated RFA of the slow pathway was successfully
achieved in all patients with inducible AVNRT.
Conclusion: Spontaneous or inducible AVNRT is relatively common in patients with idiopathic outflow
tract ventricular arrhythmias. Atrial stimulation, especially when performed after isoproterenol infusion
plays a major role in AVNRT inducibility. Although we performed RFA of the slow pathway in patients
with inducible AVNRT and no prior tachycardia documentation, the question whether this is mandatory
remains unsettled. (PACE 2006; 29:21–28)
AV nodal reentry tachycardia, outflow tract ventricular arrhythmias, radiofrequency ablation
Introduction
Early reports documented the rare coexistence
of supraventricular tachycardia and ventricular
tachycardia (VT) in the same patient, occurring
mainly in patients with organic heart disease and
digitalis toxicity.1–3 Later reports have suggested
such an association in patients with no obvious
heart disease4–10 where the most frequent combination consisted of atrioventricular nodal reentry tachycardia (AVNRT) and either right or left
outflow tract VT.7,9,10 In the present study, we assessed the prevalence of spontaneous or inducible
AVNRT in consecutive patients referred for radiofrequency ablation (RFA) of idiopathic outflow
tract ventricular arrhythmias.
Address for reprints: Bernard Belhassen, M.D., Department
of Cardiology, Tel-Aviv Sourasky Medical Center, Weizman
St, 6 Tel-Aviv 64239, Israel. Fax: 00-972-3-697-4418; e-mail:
[email protected]
Received August 16, 2005; revised September 27, 2005;
accepted September 27, 2005.
Patients and Methods
Patients
The study group consisted of 68 consecutive
patients referred for RFA of ventricular ectopy or
tachycardia originating from the right ventricular
(RV) or left ventricular (LV) outflow tract during
a 6-year period (1999–2004). None of the patients
had structural heart disease based on physical examination, resting ECG, and echocardiogram (the
existence of minimal segmental LV contraction abnormalities was tolerated).
Methods
The electrophysiologic studies were performed after informed consent by standard methods using two- or three-electrode catheters introduced through the right femoral vein. In patients with spontaneous ventricular arrhythmias
RFA was attempted first, using conventional mapping techniques. In patients without spontaneous
ventricular arrhythmias, induction of the ventricular arrhythmia was attempted with repeated bursts
of rapid right atrial pacing, atrial extrastimulation
C 2006, The Authors. Journal compilation C 2006, Blackwell Publishing, Inc.
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TOPILSKI, ET AL.
using up to triple extrastimuli during sinus rhythm
and bursts of rapid RV pacing, first in the baseline state and then (in noninducible patients) during isoproterenol infusion. After ablation of the
ventricular arrhythmia, the previously described
pacing protocol was repeated (with and without isoproterenol) to induce AVNRT. Whenever
AVNRT was induced, ablation of the slow AV
nodal pathway was performed using conventional
techniques. In patients who had easily inducible
AVNRT that interfered with ablation of the ventricular arrhythmia, RFA of the slow pathway was
performed first.
Definitions
An arrhythmia was defined as sustained if it
lasted ≥30 seconds, and nonsustained if it lasted
>6 beats but <30 seconds.
Statistical Analysis
Values were expressed as mean ± standard
deviation. A Student’s t-test was used to compare
parametric data. The χ 2 test was used to compare
nonparametric data. P value <0.05 was considered
statistically significant.
Results
Overall Results
Of the 68 patients who underwent RFA of their
outflow tract ventricular arrhythmias, 17 (25%)
had either spontaneous AVNRT documented prior
to ablation of the ventricular arrhythmia or inducible AVNRT during the stimulation protocol.
Clinical Characteristics of the Patients with
“Double Arrhythmia”
There were 12 women and 5 men, aged 18–74
years (mean 46.5 ± 16). Most patients (n = 16) suffered from recurrent palpitations felt to have different rates by 1 patient (#7). One patient (#16) was
asymptomatic and had his ventricular arrhythmia
diagnosed during routine exercise test. Symptoms
duration ranged from a few weeks to 20 years
(mean 58 ± 67 months) (Table I).
Spontaneous Ventricular Arrhythmias
The clinically documented ventricular arrhythmia was sustained VT in 3 patients, nonsustained VT in 8 patients (including a repetitive
form in 3) and only couplets and triplets in the
remaining 6 patients. In 9 patients the ventricular
TABLE I.
Baseline Symptoms and Clinical Tachycardia
Patient
1
2
3*
4
5
6†
7
8†
9
10
11
12
13
14
15
16
17*
Gender
Age
Symptoms
Spontaneous Arrhythmias
(rate in beats/min)
M
M
F
F
M
F
F
F
F
F
M
F
F
F
F
M
F
64
53
29
52
72
56
40
30
55
25
38
57
74
51
49
18
28
Palpitations
Palpitations
Palpitations + syncope (pregnant)
Palpitations
Palpitations
Palpitations + syncope
Palpitations of two types
Palpitations
Palpitations
Palpitations
Palpitations
Palpitations
Palpitations + chest pain
Palpitations
Palpitations + dizziness
Asymptomatic
Palpitations
LVOT-HGVA
RVOT-NSVT (repetitive) (EET)
RVOT-SUVT + AVNRT(250)
RVOT-NSVT
LVOT-HGVA
RVOT-SUVT +AVNRT (220)
RVOT-HGVA
RVOT-NSVT (repetitive)† AVNRT(260)
RVOT-HGVA
RVOT-SUVT
RVOT-HGVA
RVOT-SUVT
RVOT-NSVT
RVOT-NSVT (repetitive)
RVOT-NSVT
RVOT-NSVT
RVOT-HGVA + AVNRT
VT Rate
(beats/min)
200
190
230
220–260
240
250
230
150
160
170
150
AVNRT = atrioventricular nodal reentry tachycardia; ET = exercise test; F = female; HGVA = high-grade ventricular arrhythmias;
LVOT = left ventricular outflow tract; M = male; NSVT = nonsustained VT; RVOT= right ventricular outflow tract; SUVT = sustained VT.
*Patients #3 and #17 had documented and inducible AVNRT during radiofrequency ablation of the slow pathway performed 4 years (#3)
and 14 months (#17) prior to ablation of the ventricular arrhythmia.
† Patients #6 and #8 had spontaneously documented and inducible AVNRT at the time of radiofrequency ablation of the ventricular
arrhythmia.
22
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AVNRT AND OUTFLOW TRACT VENTRICULAR ARRHYTHMIAS
arrhythmia occurred without any obvious precipitating cause while in 8 patients it was precipitated
by exercise or stress. The spontaneous VT rate
ranged from 150 to 260 (mean 201 ± 39) beats/min.
Previously Documented AVNRT
Four of the above 17 patients (#3, #6, #8,
#17) had spontaneous AVNRT documented prior
to RFA of the ventricular arrhythmia. Two of these
patients (#3, #17) underwent successful RFA of
AVNRT 4 years and 14 months, prior to RFA
of the ventricular arrhythmia. In the other 2 patients (#6 and #8) spontaneous double tachycardia (VT and AVNRT) was documented. In patient
#6, VT (220–260/min) and AVNRT (220/min) were
documented during exercise testing with AVNRT
following termination of VT (Fig. 1). In patient
#8 both spontaneous VT (240–260/min) initiating
AVNRT (220/min) as well as initiation of AVNRT
during VT were documented during symptomatic
episodes (Fig. 2). The remaining 13 patients had
AVNRT documented only during the electrophysiologic study for RFA of their ventricular arrhythmias.
There was no correlation between the symptoms, type of clinical tachycardia, and rate of
tachycardia. In the single patient (#7) who complained of two types of palpitations, only one
type of tachycardia (VT) was spontaneously documented.
Electrophysiological Results
AVNRT was induced before isoproterenol infusion in 3 patients: in 2 patients (#5, #6) with
atrial pacing, and in 1 patient (#16) with both atrial
and ventricular pacing (Fig. 3). In the remaining
14 patients AVNRT was induced after isoproterenol infusion: in 12 patients during atrial pacing
and in 2 during ventricular pacing (Table II).
Induced AVNRT was sustained in 15 patients
(88%) and nonsustained (but lasting ≥15 seconds)
in 2 (12%). AVNRT rate ranged from 150 to 260
(mean 200 ± 34) beats/min but was not correlated
with the induced (r = 0.46, P = NS) or spontaneous
VT rate (r = 0.45, P = NS). In 1 patient (#8), nonsustained RV outflow tract tachycardia was documented during AVNRT induced with atrial and
ventricular pacing during isoproterenol (Fig. 4).
Figure 1. Patient #6. A 56-year-old woman with double tachycardia induced during exercise testing. During the
immediate recovery phase, VT (260/min) was initiated and terminated 20 seconds later after a slight rate slowing
(220/min). At VT termination, a sustained AVNRT was observed (220/min). No fusion beats were observed during VT
or AVNRT.
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Figure 2. Patient #8. A 30-year-old woman with spontaneously documented double tachycardia
at admission to the hospital for palpitations. Standard ECG leads are shown. Rapid VT (260/min)
occurred during sinus rhythm and terminated 4.5 seconds later after slight slowing (240/min) of
the tachycardia rate; a few beats of AVNRT (220/min) then followed. A similar sequence of events
was subsequently observed while VT and AVNRT rates were similar (220/min). Several fusion
beats were observed suggesting that both tachycardias were occurring simultaneously.
Results of Catheter Ablation
Ventricular Arrhythmias
In 2 (12%) patients (#1, #5) in whom the origin of the ventricular arrhythmia was felt to be in
the LV outflow tract or a coronary cusp, RFA was
not attempted. Catheter ablation of the ventricular
arrhythmia was acutely successful in all the other
15 (88%) patients. The successful ablation sites in
the RV outflow tract were located at the anteroseptal area (7 patients), posteroseptal area (4 patients),
and midseptal area (4 patients).
AVNRT
Ablation of the slow AV nodal pathway was
successfully performed without complications in
all 17 patients with inducible AVNRT. In addition
to the 2 patients (#3, #17) who underwent ablation of AVNRT 4 years and 14 months before the
ablation of the ventricular arrhythmia, 7 patients
underwent slow pathway ablation before ablation
of the ventricular arrhythmia while the remaining
8 patients underwent slow pathway ablation after
ablation of the ventricular arrhythmia.
Discussion
Association Idiopathic VT-AVNRT
The association between idiopathic VT and
AVNRT was first described by our group more
than 20 years ago.4 Both arrhythmias were induced during electrophysiologic study but only
VT (originating from the LV) had been clinically
documented before study. Four other case reports
24
have documented the association of idiopathic VT
and AVNRT: VT originated from the LV in 2 patients5,6 and in the RV outflow tract in the other
2 patients.7,9 In 2 cases, VT was the only clinically documented arrhythmia6,9 while in the 2 others both VT and AVNRT were documented.5,7 Induction of both tachycardias was observed during
electrophysiologic study in all 4 patients. Recently
Kautzner et al.10 reported the first systematic study
assessing the induction of AVNRT in patients with
idiopathic outflow tract VT (most originating in
the RV). They found that 7 (15%) of 46 patients
with VT developed reproducible AVNRT during
electrophysiologic study. However, none of these
7 patients had documented prior AVNRT.
In the present study, we found a higher incidence (25%) of inducible AVNRT in a series of
68 consecutive patients referred for ablation of an
idiopathic ventricular outflow tract arrhythmia.
Interestingly, 4 (23.5%) of the 17 patients with
inducible AVNRT also had the same arrhythmia
clinically documented.
Dual AV nodal pathways are frequently observed during electrophysiologic evaluation of patients without spontaneous AVNRT, especially in
heavily sedated patients.11 However, AVNRT is
rarely induced in such patients, even after administration of isoproterenol and atropine. We also
reviewed our data (1999–2004) on AVNRT induction in a group of 252 consecutive patients with no
heart disease after successful RFA of an accessory
pathway. The stimulation protocol was similar to
that of the present study including rapid atrial
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AVNRT AND OUTFLOW TRACT VENTRICULAR ARRHYTHMIAS
Figure 3. Patient #16. An 18-year-old man with asymptomatic spontaneous catecholamine sensitive VT. During baseline electrophysiologic study, no ventricular arrhythmias were observed; however, AVNRT (170/min) was easily induced with atrial stimulation and therefore RFA of slow pathway was performed first. After slow pathway ablation, and
during isoproterenol infusion, sustained VT (150/min) spontaneously occurred and was ablated at the posteroseptal
area of the RV outflow tract (note that the early R/S transition in V2 rather suggests a VT origin in the LV outflow tract
or a coronary cusp). After VT ablation, extensive atrial and ventricular pacing before and after isoproterenol failed to
induce any type of tachycardia.
pacing, atrial extrastimulation and rapid ventricular pacing before and after isoproterenol infusion.
We induced AVNRT in 17 (6.7%) of the 252 patients ( P < 0.005 as compared to the induction rate
in the present study). Josephson reported a similar inducibility rate of AVNRT (8–10%) in patients
with concealed or manifest accessory pathways.12
In contrast the induction rate of AVNRT in our
patients with idiopathic outflow tract ventricular
arrhythmias was much higher, yet reports of this
association are scanty. This discrepancy could be
explained by the relatively aggressive protocol of
atrial stimulation used in our study (that included
repeated bursts of rapid right atrial pacing and
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the application of up to triple atrial extrastimuli,
before and after isoproterenol infusion). Indeed,
AVNRT could be induced in 15 of 17 patients with
atrial pacing, in most cases (13/15) during isoproterenol infusion.
Possible Mechanisms for the AVNRT-VT
Coexistence
There are several possible explanations for the
frequent association of these two arrhythmias as
observed in our study. The first is a random coexistence of these two frequently encountered arrhythmias. However, the 25% incidence of AVNRT
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TABLE II.
EPS and RF Ablation Results
Patient VT Characteristics
1
2
3*
4
5
6†
7
8†
9
10
11
12
13
14
15
16
17*
SUVT
NSVT
HGVA
NSVT
HGVA
HGVA
Noninducible
NSVT
HGVA
HGVA
HGVA
NSVT
NSVT
NSVT
NSVT
NSVT
HGVA
AVNRT Induction
AVNRT Rate (beats/min) First Ablated Arrhythmia
RA pacing + isoproterenol
RA pacing + isoproterenol
RA pacing + isoproterenol
RV pacing + isoproterenol
RA pacing
RA pacing
RA pacing + isoproterenol
RA & RV pacing + isoproterenol
RA pacing + isoproterenol
RV pacing + isoproterenol
RA pacing + isoproterenol
RA pacing + isoproterenol
RA pacing + isoproterenol
RA pacing + isoproterenol
RA pacing + isoproterenol
RA pacing + RV pacing
RA pacing + isoproterenol
170
180
240
190
150
150
200
230
250
200
260
230
210
220
160
170
190
AVNRT (VA not ablated)
VA
AVNRT
VA
AVNRT (VA not ablated)
AVNRT
AVNRT
AVNRT
VA
AVNRT
VA
VA
VA
VA
VA
AVNRT
AVNRT
RA = right atrium; RV = right ventricle; VA = ventricular arrhythmia; other abbreviations as in Table I.
found in our VT patient population as compared
to the 6.7% incidence found in patients undergoing accessory pathway ablation argues against
such a mere random coexistence. A second possible explanation is that VT is induced by AVNRT.
This was observed in one patient (#8) both spontaneously (Fig. 2) and at electrophysiologic study
during isoproterenol infusion (Fig. 4). One may
suspect that this patient had outflow tract VT due
to c-AMP-mediated triggered activity that could
be induced by rapid heart rhythm resulting from
AVNRT in the presence of adrenergic stimulation.
Kautzner et al.10 reported 3 patients with a similar mode of induction. The fact that the ventricular arrhythmia could be induced only at rapid,
narrow ranges of AVNRT rates (230–260/min) as
well as the similar VT and AVNRT rates further
support that mechanism. A third possible explanation of our results is that AVNRT is induced by
VT. This was observed in 2 patients (#6, #8) either
spontaneously or during exercise testing (Figs. 1
and 2). The fact that a similar induction of AVNRT
was achieved following rapid ventricular pacing
in 2 other patients (#4, #10) gives further support
to that explanation. This implies retrograde conduction in the fast pathway during the ventricular
rhythm just before AVNRT initiation. Similar cases
were previously reported.7,9,10 Finally, the fourth
possible explanation was raised by Kautzner et
al.10 who hypothesized that patients with coexistent outflow tract ventricular arrhythmias and
26
AVNRT may have more abundant specialized myocytes both in the perinodal area and in the outflow
tract.13,14 In any case, sympathetic stimulation
seemed to play an important role both in facilitating delayed afterdepolarization-mediated triggered activity (assumed to be responsible for
outflow tract ventricular arrhythmias) and conduction in the antegrade and retrograde limbs of the
AV nodal circuit.
Study Limitations
Our study does not answer the interesting
question whether AVNRT should be ablated in
patients without previous clinical documentation
since we ablated the slow pathway in all our
17 patients with inducible AVNRT, including the
13 patients who did not have spontaneous documentation of this tachycardia. We elected to ablate
the slow pathway for two main reasons: (a) AVNRT
is rarely induced in patients who do not exhibit
this arrhythmia clinically, and (b) RFA ablation of
slow pathway is associated with a high success
rate. However, we recognize that a conservative
attitude could also have been justifiable, deferring
RFA to the occasional patient who later develops
symptomatic tachycardia, because: (a) the prognostic clinical significance of inducible AVNRT in
patients without previously documented tachycardias is uncertain; (b) RFA of slow pathway is associated with a minimal but definite risk of complications such as AV block; (c) it may be difficult to
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AVNRT AND OUTFLOW TRACT VENTRICULAR ARRHYTHMIAS
Figure 4. Same patient as in Figure 2. Nonsustained VT occurred during AVNRT previously induced with rapid atrial
pacing during isoproterenol infusion. Note the similarity of the cycle lengths of AVNRT and VT and the presence of
several fusion beats. His = His bundle electrogram activity; HRA = high right atrial electrogram.
obtain a “true” informed patient consent for ablation of slow pathway during the course of RFA of a
ventricular arrhythmia though this study suggests
that such a minimum consent should be obtained
in most patients. Only a randomized study can answer the question if patients who underwent slow
pathway ablation will have a benefit from the additional ablation of this undocumented (and perhaps
not clinical) tachycardia or not.
Conclusion
Our study describes an unexpected high incidence of the coexistence of spontaneous or induced AVNRT and idiopathic ventricular outflow
tract arrhythmias and this mandates a search for
AVNRT in patients undergoing electrophysiologic
assessment of outflow tract ventricular arrhythmias. The stimulation protocol including atrial
stimulation before and after isoproterenol infusion
plays a major role in AVNRT inducibility. Physicians should be aware of the frequent coexistence
of outflow ventricular arrhythmias and AVNRT
and therefore be careful before attributing palpitations occurring after a successful VT ablation to
arrhythmia recurrence. Although we elected to ablate the slow pathway in patients with inducible
but not previously documented AVNRT, the question whether this is mandatory remains unsettled.
Acknowledgment: We thank Serge Barold, M.D., for his
helpful comments.
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