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REVIEW
Europace (2016) 18, 332–339
doi:10.1093/europace/euv056
Dual atrioventricular nodal non-re-entrant
tachycardia
Christiane Peiker1,2,3, Christian Pott 4, Lars Eckardt 4, Malte Kelm 3, Dong-In Shin 3,
Stephan Willems 1,2, and Christian Meyer1,2,3*
1
Department of Cardiology – Electrophysiology, University Heart Centre, University Hospital Hamburg-Eppendorf, Martinistrasse 52, D-20246, Hamburg, Germany; 2DZHK (German
Centre for Cardiovascular Research), Partner site Hamburg, Kiel, Lübeck, Germany; 3Department of Cardiology, Pulmonology and Vascular Medicine, Medical Faculty, University Hospital
Duesseldorf, Germany; and 4Division of Electrophysiology, Department of Cardiovascular Medicine, University Hospital Muenster, Germany
Received 23 December 2014; accepted after revision 19 February 2015; online publish-ahead-of-print 16 April 2015
Dual atrioventricular nodal non-re-entrant tachycardia (DAVNNT), also known as ‘double fire’, has recently received more attention since it was
demonstrated to mimic more common arrhythmias such as atrial premature beats, atrial fibrillation, and ventricular tachycardia. This is important,
since mistaken differential diagnoses and the resulting therapeutic decisions have severe consequences for affected patients. DAVNNT is characterized by conduction characteristics of the atrioventricular (AV) node that leads to a double antegrade conduction of one sinoatrial nodal
activity via the slow and fast AV nodal pathways. As a result, the most significant hint from an electrocardiogram (ECG) is a P wave followed
by two narrow QRS complexes. Although DAVNNT is rather a rare arrhythmia, it now appears to be more common than previously
thought. To date, 68 cases including 3 small single-centre observational studies accumulated over the last 5 years have demonstrated the feasibility
and safety of radiofrequency catheter ablation for DAVNNT. Catheter ablation treats this arrhythmia effectively by modifying or eliminating slow
pathway function. Here, we review the current state of DAVNNT knowledge systematically and address current challenges presented by this
‘ECG chameleon from the AV node’.
----------------------------------------------------------------------------------------------------------------------------------------------------------Keywords
Ablation † Atrial fibrillation † AVNRT † DAVNNT † Double fire † Slow pathway
Introduction
Understanding of the anatomical and physiological properties of the
atrioventricular (AV) node as an integral part of the cardiac conduction system was important for the development of therapeutic concepts for bradycardia and tachycardia in the 20th century. It is now
well known that the AV node area can be functionally dissociated;
this may lead to pathways with different conduction characteristics,
namely a fast and a slow pathway.1 This dual physiology is the prerequisite for the most common supraventricular tachycardia, AV
nodal re-entrant tachycardia (AVNRT),2 where re-entry within
these two AV nodal pathways is present.3 – 6
In contrast, the related but rare form of relatively benign tachycardia, dual AV nodal non-re-entrant tachycardia (DAVNNT), is characterized by a sinus beat that leads to consecutive double antegrade
conduction via the fast and slow pathways, which results in two ventricular depolarizations.7
The phenomenon of dual fast and slow AV conduction of single
atrial beats, also termed ‘AV nodal double firing’ or simply ‘double
fire’, was first described in 1975.8 Since then the number of published
case reports and small case series has increased in each decade (see
references9 – 28 for those published in the last 5 years). It is now clear
that this relatively rare arrhythmia, which is not addressed in the
current guidelines of North American and European cardiology societies,29 may be more common than previously thought. We therefore review the current literature systematically and address the
diagnostic and therapeutic challenges of this ‘electrocardiogram
(ECG) chameleon from the AV node’.
Methods
The initial literature search was performed on 4 March 2014 and was
repeated periodically until 1 June 2014. We searched PubMed/
MEDLINE (1 January 1995 until 1 June 2014), EMBASE (1950 until July
2014), and the Cochrane Central Register of Controlled Trials
(CENTRAL—until June 2014) using the search terms ‘dual AV nodal nonreentrant tachycardia’ OR ‘DAVNNT’ OR ‘double fire’ OR ‘AV nodal
double firing’ OR ‘non-reentrant AV nodal tachycardia’ OR ‘nonreentrant AV nodal tachycardia’. We excluded references not published
in English unless an English version of the abstract was accessible. In an
* Corresponding author. Tel: +49 40 7410 52438; fax: +49 40 7410 55862, E-mail address: [email protected], [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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Dual atrioventricular nodal non-re-entrant tachycardia
attempt to access the grey literature, we searched the OpenGrey Database (http://www.opengrey.eu) and the online trial registry (www.
clinicaltrials.gov). We attempted to contact authors to clarify any areas
of uncertainty regarding study data. Potentially eligible studies were
assessed independently by two investigators (C.P. and C.M.). We
included all published case reports, case series, and studies that were
found with the specified search terms, as only 68 cases have been published so far. Because of well-documented weaknesses in the methodology, accuracy, and completeness of conference abstracts, we
excluded studies published only in abstract form. We supplemented
our database searches with manual searches of the reference lists of published studies and major review articles.
Results
Clinical presentation
The currently reported age range of adult patients is broad, and varies
from 16 to 84 years (68 cases) with similar proportions of males and
females (Table 1).7,9 – 22,24 – 28,30 – 63 So far, only one case of a child (a
5-year-old boy) has been reported.23 Dual atrioventricular nodal
non-re-entrant tachycardia has been observed in patients with and
without structural heart disease, with no evidence of risk factors or
accumulating comorbidities.27,28 So far no relationship is evident
Table 1 Differential diagnosis of DAVNNT, reported as initial mistaken diagnosis in 48 of 68 cases
Differential diagnosis
Author
Sinus tachycardia
Arena, 1999
Bhatt, 2010
Wang, 2010
Kim, 1987
Nakao, 2001
Trajkov, 2006
Takahahi, 2012
Wang, 2013
Patients (n)
Age (range)
Sex: M/F (%)
3
16–46
66/33
5
5 –84
60/40
...............................................................................................................................................................................
Supraventricular premature beats
Non-specific supraventricular tachycardia
Elizari, 1991
Li, 1994
Anselme, 1996
Maury, 1999
Neumann, 2000
Labadet, 2001
Germano, 2005
Otsuka, 2005
Mofrad, 2007
Haman, 2009
Zimmermann, 2009
Barbato, 2010
Evertz, 2012
Mehairi, 2012
Pott, 2014
15
31–79
33/66
Atrial fibrillation
Sutton, 1983
Fraticelli, 1999
Sorbera, 1999
Mansour, 2003
Rostock, 2005
Dixit, 2006
Clementy, 2007
Silver, 2008
Jastrzebski, 2009
Dingh, 2010
Ozcan, 2013
Kirmanoglou, 2014
16
27–74
50/50
Junctional ectopic beats
Ventricular premature beats
Aasbo, 2009
Sutton, 1983
Madle, 1990
Maury, 2008
Li, 2011
Neuss, 1982
Karnik, 2014
Kirmanoglou, 2014
1
4
56
33–69
100/0
50/50
4
20–80
100/0
Ventricular tachycardia
Note that DAVNNT occurs equally in all ages and sexes. The most common misdiagnosis is atrial fibrillation.
F, female; M, male; n, number of patients.
334
C. Peiker et al.
common erroneous differential diagnosis.22,27,55 Other differential
diagnoses that mimic a DAVNNT are rare but might result in inappropriate implantation of a pacemaker or ICD in certain cases.17,24 – 26,47 In
an ECG, DAVNNT may be misinterpreted as ventricular tachycardia26,27,32 or ventricular premature beats.17,33,37,46,60 Functional
left15,23 or right22,27 bundle branch block during DAVNNT has been
reported in single cases and needs to be taken into consideration. In
these cases, differential diagnosis of ventricular tachycardia can be
guided by AV dissociation. The presence of unconventional AV association, which is characteristic of DAVNNT, needs to be evaluated
(Figure 3). Differential diagnosis can be especially challenging if only
standard monitoring documentation of an arrhythmia is available.
In cases with the unclear presence/morphology of P waves, additional
Holter electrode positions facilitate diagnosis. Apart from the risks of
misdiagnosis, the average delay of more than a year for correct
diagnosis7 may lead to tachycardia-induced cardiomyopathy, especially in relatively asymptomatic patients.15,17,24,42,52,57 A reduced
left ventricular ejection fraction has been diagnosed in some patients
who were ultimately diagnosed with DAVNNT and had a long history
of palpitations. Interestingly, the reduced ejection fraction often
returned to normal after successful treatment of DAVNNT, suggesting that left ventricular dysfunction was mainly induced by
tachycardia.15,17,24,42,52,57
with other cardiac pathologies (including those related to the cardiac
conduction system) apart from AVNRT. Patients diagnosed with
DAVNNT initially presented with various symptoms. The most commonly reported symptoms are palpitations.7 Less common unspecific symptoms include dyspnoea, syncope, dizziness, fatigue, and chest
pain.7 In two cases, ‘double fire’ resulted in inappropriate shocks from
an implantable cardioverter-defibrillator (ICD),26,27 since current
ICD discrimination algorithms are of limited value in differentiating
DAVNNT from ventricular tachycardia. One patient did not report
any symptoms, but a characteristic ECG was observed during
routine monitoring of his pacemaker.25
Diagnosis
The 12-lead surface ECG can be regarded as the ‘gold standard’ for detection of a suspected DAVNNT (Figure 1, left panel). The most significant hint from the ECG for diagnosis of DAVNNT is a P wave followed
by two narrow QRS complexes. There are several differential diagnoses for the characteristic (but not yet widely known) DAVNNT ECG
pattern (Figure 1, middle panel). Dual AV nodal conduction may be
intermittent, thus mimicking atrial premature beats or atrial fibrillation.
This might additionally make the diagnosis of DAVNNT difficult.24
Atypical presentation of supraventricular tachycardias such as atrial
fibrillation (Figure 2A and B)11,12,22,27,30,33,46,51,55,57,61,64 or atrial tachycardia10,14,15,20,21,28,38,42,48,53,54,58,60 is common erroneous differential
diagnoses (Table 1). Atypical sinus tachycardia,16,19,45 supraventricular
premature beats (Figure 2C and D),23,24,36,50,56 atrial bigeminy,11,61 and
atypical AVNRT with retrograde 2:1 block21 also need to be taken into
account. Furthermore, sporadic junctional extrasystoles9,21,23,45,46 or
parasystoles21 can mimic a ‘double fire’. Atrial fibrillation is the most
Therapy
Since 1994, all patients diagnosed with ‘double fire’ have been treated
with radiofrequency catheter ablation. As a consequence of the relevant AV nodal physiology, the therapeutic approach used for
DAVNNT is closely related to that used in most cases for the
Diagnosis
I
Anatomy
Physiology
V1
AF
II
Mechanism
Differential
12-lead ECG
V1
V2
SPB
Atrium
III
V3
SVT
AVR
AV
Node
V4
Ventricle
VPB
AVL
Conduction via fast pathway
V5
Conduction via slow pathway
AVF
VT
V6
Block in slow pathway
50 mm/s
Figure 1 Anatomical and physiological background of DAVNNT with ventricular ‘double fire’ following a single sinus node activity. Note the
regular PR intervals, with one P wave followed by two QRS complexes due to consecutive antegrade conduction via fast and slow pathways
from the AV node. In this example, due to early RS transition and a slurred upstroke resulting in a relatively broad QRS complex, finding the
correct diagnosis might be challenging. For details see text. Black arrows denote P waves. AF, atrial fibrillation; ECG, electrocardiogram; SPB, supraventricular premature beats; SVT, supraventricular tachycardia; VPB, ventricular premature beats; VT, ventricular tachycardia.
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Dual atrioventricular nodal non-re-entrant tachycardia
A
V1
50 mm/s
B
V1
HRA
HBE
RV
50 mm/s
C
V1
25 mm/s
D
avL
V1
V3
V6
CS 1–2
CS 3–4
CS 5–6
CS 7–8
25 mm/s
Figure 2 Electrocardiographic differential diagnosis of DAVNNT. Examples of DAVNNTs (A, B) and the relevant differential diagnosis of supraventricular premature beats (C, D) are presented. (A) Typical DAVNNT ECG pattern with biphasic P wave morphology in lead V1 consistent with
sinus rhythm followed by two QRS complexes. Despite the clear P wave, atrial fibrillation was initially misdiagnosed, which resulted in an oral anticoagulation regime. Searching for P waves in lead V1 might have minimized this misdiagnosis. (B) Atypical P waves in combination with ‘irregular’ RR
intervals often lead to the misdiagnosis of atrial fibrillation. Bundle branch block morphology may also delay correct diagnosis and here resulted in the
initial misdiagnosis of ventricular tachycardia. Note the ‘unconventional’ AV association characterizing DAVNNT. Also note the subtle QRS changes,
which might be explained by variable infra-His conduction.15 (C ) Frequent supraventricular premature beats with post extrasystolic pauses mimicking a DAVNNT. In this case, P waves occurring before each QRS complex within slight changes of T-wave morphology were detectable in
lead V1. Note the shorter PQ interval for supraventricular premature beats compared with sinus rhythm. (D) Dual atrioventricular nodal
non-re-entrant tachycardia-like morphology induced by frequent supraventricular premature beats exhibiting a typical ‘P on T’ pattern in a
patient undergoing pulmonary vein isolation. Atrial activity before each QRS complex is confirmed by the multipolar catheter located in the coronary
sinus (CS). Note that these supraventricular premature beats induce a QRS morphology change in lead V1. Black arrows denote P waves. HBE, his
bundle electrogram; HRA, high right atrium; RV, right ventricle.
treatment of AVNRT.65,66 Key differences are the approaches for the
final diagnosis as well as the procedural endpoint. The most widely
accepted procedural endpoint is non-inducibility of DAVNNT.7,46,51
For slow pathway modulation, radiofrequency energy is applied to
the well-described right atrial posteroseptal area until conduction differences of the remaining AV node occur.3,67 Ablation of the slow pathway
336
C. Peiker et al.
50 mm/s
AS
765
AS
765
VS
383
PVC
378
AS
765
VS
383
PVC
378
AS
765
VS
383
PVC
378
VS
383
PVC
378
Figure 3 Intracardiac recordings illustrating DAVNNT in a patient with a dual chamber ICD. Double ventricular activity was initially misdiagnosed as
ventricular tachycardia. Dual atrioventricular nodal non-re-entrant tachycardia was revealed by unconventional AV association and later confirmed in
an electrophysiological study. Importantly, isorhythmic dissociation needs to be ruled out. In this case, this was possible due to repetitive induction of an
ongoing tachycardia by programmed atrial stimulation. The upper signals denote atrial near-field intracardiac electrograms (IEGMs), the middle signals
are ventricular near-field IEGMs while the lower signals reflect far-field IEGMs. Coloured arrows denote antegrade conduction via fast and slow pathways. Marker channel: AS, atrial sensing; PVC, premature ventricular contraction; VS, ventricular sensing. Cycle lengths are annotated in milliseconds.
eliminates dual conduction.68 Cryoablation is possible, but has only been
reported in one patient.24 In this case, a second procedure using radiofrequency ablation was necessary due to recurrent DAVNNT.
Recurrence of reduced symptoms has only been reported in three
patients treated with modulation/ablation of the slow pathway.24,28 In
one of these patients, DAVNNT was not inducible during an electrophysiological studyand slow pathway modulation was undertaken empirically, so that in retrospect it is not clear that the diagnosis of DAVNNT
was appropriate in this case.28 Another patient was successfully treated
by adjusting his ICD settings. The lower rate limit was increased from
40 to 70 b.p.m. to suppress slow pathway conduction, and the AV
delay was increased to 300 ms to ensure intrinsic conduction.24
To date, the success rate of slow pathway modulation/ablation for
DAVNNT treatment seems to be comparable but slightly lower than
for AVNRT. This might be explained by the small number of reported
cases. In our experience with .10 cases from three centres27,28
(n ¼ 8 published of 68 reported cases worldwide), no AV block or
other complications were observed. Treatment with antiarrhythmic
medications was only successful in the long term in one of the 68
patients, who was successfully treated with flecainide in 1987.36
Short-term successful treatment with medication has been described
in two other patients. One of these did not give consent for slow
pathway ablation and was treated with propafenone,25 which was
successful at the 1-day follow-up but could not be evaluated later.
The remaining patient was initially treated successfully with amiodarone,37 but medication had to be discontinued due to side effects.
Electrophysiological characteristics of
dual atrioventricular nodal non-re-entrant
tachycardia
Well-established dual AV node physiology is verified if programmed
decremental atrial stimulation induces a ‘jump’, defined as a
conduction delay of 50 ms.2,3,27,69 This ‘jump’ is not reported for all
patients with DAVNNT. This might be explained in part by the difficulty of performing diagnostic stimulation manoeuvres during frequent ventricular ‘double firing’ where this ‘jump’ is already
clinically manifest.19,22,31,41,46,50 Thus, dual AV nodal antegrade conduction in DAVNNT can also be characterized by discontinuous AV
conduction, or it may be implied by a single atrial complex followed by
two His and two related ventricular complexes (Figure 1, right
panel).7,37
A DAVNNT is further defined by a fixed interval between His and
ventricular activation,7,22,59 although slight variations in the R1R2
interval (interval between the first and second R wave) may occur
due to fluctuations in AV nodal conduction velocity.70 In addition,
slight changes in QRS morphology may be manifest (Figure 2B). Variability in slow and fast pathway conductions influences infra-His conduction as a form of gap phenomenon, leading to these changes in
QRS morphology.17 Diagnosis is confirmed if modulation/ablation
of the slow pathway terminates this ‘double firing’.7,46,51
The temporal delay between fast and slow pathway conductions is
measured as the interval between His bundle activities induced by
conduction in fast and slow pathways, both of which follow the
same atrial complex. Conduction delay between the fast and the
slow pathways needs to be relatively long and ranges from 265 to
520 ms with a mean + standard deviation of 359 + 46 ms for all
reported cases.7,28,36,48 For a DAVNNT to occur, it is crucial that
the effective refractory period of the His-Purkinje system is shorter
than the interval between fast and slow pathway conductions.42,51,58,60 Retrograde conduction from the ventricle to the
atrium is usually absent or weak.7,42,51,55,58,60 Moreover, His bundle
ectopies followed by ventricular depolarization, which may also
cause double ventricular responses, can be differentiated from
DAVNNT by their irregular interval between both His complexes.7,28 Dual atrioventricular nodal non-re-entrant tachycardia
337
Dual atrioventricular nodal non-re-entrant tachycardia
and junctional extrasystoles can be differentiated by administering
atropine, which should suppress DAVNNT and intensify junctional
activity.36
Discussion
The major findings of this systematic review are: (i) DAVNNT seems
to be more common than previously thought; (ii) since misdiagnosis
can have severe consequences for patients, DAVNNT needs to be
considered as a differential diagnosis for tachycardias involving suspected but atypical ECG patterns of atrial fibrillation and ventricular
tachycardia; and (iii) ECG analysis allows instant visual diagnosis,
which can be verified and successfully treated in an electrophysiological study with subsequent radiofrequency catheter ablation.
The presence of slow and fast pathways within the AV node is the
prerequisite for both the re-entry tachycardias such as the three commonly seen forms of slow–fast, fast –slow, and slow–slow AVNRT,
as well as the non-re-entry tachycardia DAVNNT.27,69 Dual atrioventricular nodal non-re-entrant tachycardia can also initiate or convert
into AVNRT.20 The true co-incidence of these arrhythmias is currently unknown. An international multicentre registry might be
useful to determine the prevalence of DAVNNT. This might result
in first recommendations regarding this rare arrhythmia in future
guidelines of North American and European cardiology societies.
Patient characteristics and clinical presentation are not helpful in
discriminating between DAVNNT and more common arrhythmias.
As outlined, DAVNNT may mimic clinical signs of AF or ventricular
tachycardia, while ECG documentation is key for differential diagnosis. The general concept of diagnosing a DAVNNT based on the occurrence of a P wave followed by two narrow QRS complexes may be
complicated by bundle branch block or intraventricular conduction
disturbances (Figure 2B). It is worth noting that although the interval
between the two QRS complexes is fixed in most episodes, marginal
changes in the R1R2 interval may occur. Furthermore, the fibrosis
that accompanies ageing and cardiovascular disease increases the
extent and heterogeneity of structural discontinuity, which can
affect QRS complex morphology.71 This might explain the minimal
differences between conducted QRS complexes in surface ECG
recordings that have been described in a significant number of
patients (Figure 2B).17,63 Asynchronous activation spread via ventricular myocardium and heterogeneous repolarization might also affect
QRS morphology in DAVNNT.
The underlying mechanisms of AV nodal and consecutive ventricular activation are not fully understood. Early findings indicated that
slow conduction involves impulse transmission to the compact AV
node from regions inferior to the coronary sinus through transitional
cells (posterior input), whereas fast regions involve direct input to
the AV node from septal and left-sided inputs.63,65 In 2013, this
concept was extended by the observation that two distinct patterns
of pathway conduction may be present in patients with DAVNNT.64
Using novel mathematical techniques, the authors found that functional interaction between the slow and fast pathways may be
present in some patients, whereas others might display largely independent activation of the ventricle. Unification of both individual
pathways into one common pathway (equivalent to a lower
common pathway in AVNRT) before activation of the His bundle
and downstream structures has been suggested.64 Characterization
of the 3D geometry in combination with computerized mapping
models of the cardiac conduction system or analysis of its components at the cellular level might also improve our understanding of
AV nodal function.71 This is supported by a model that incorporates
atrial myocardium, inferior nodal extension, penetrating bundle, His
bundle, and ventricular myocardium based on connexin 43 and neurofilament expression.72 This 3D reconstruction has been used to investigate the structural and functional bases of re-entry in the AV
node.72 The related electrophysiological properties of myocardial
and conduction system tissue are partly but not entirely influenced
by autonomic control on a beat-to-beat basis.73 It is therefore not
surprising that pharmacological beta-adrenergic and muscarinergic
modulation has proved to be useful for diagnosis but not for
therapy in patients with DAVNNT. Optical mapping techniques including optical coherence tomography (with a spatial resolution
down to 1–2 mm) or microelectrodes addressing cells with different
morphologic and molecular characteristics might be useful in analysing the neuro-myocardial interplay in AV nodal physiology in more
detail.
Slow pathway ablation for AVNRT is reported to have an immediate success rate of .95% with a risk of permanent AV block of
,1%.65 Whether these results can be extrapolated to DAVNNT is
yet not known but indicated by published cases and our experience.
Modulation or ablation of the slow pathway should be considered as a
long-term remedy for this ‘ECG chameleon from the AV node’.
Funding
This work was supported by a research grant from the Forschungskommission of the University of Duesseldorf. C.M. is also supported by a grant
from the DZHK (German Centre for Cardiovascular Research).
Conflict of interest: none declared.
References
1. Moe G, Preston J, Burlington H. Physiologic evidence for a dual A-V transmission
system. Circ Res 1956;4:357 –75.
2. Denes P, Wu D, Dhingra R, Chuquimia R, Rosen K. Demonstration of dual A-V nodal
pathways in patients with paroxysmal supraventricular tachycardia. Circulation 1973;
48:549–55.
3. Jackman W, Beckman K, McClelland J, Wang X, Friday K, Roman C 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.
4. Link M. Clinical practice. Evaluation and initial treatment of supraventricular tachycardia. N Engl J Med 2012;367:1438 –48.
5. Katritsis DG, Sepahpour A, Marine JE, Katritsis GD, Tanawuttiwat T, Calkins H et al.
Atypical atrioventricular nodal reentrant tachycardia: prevalence, electrophysiologic characteristics, and tachycardia circuit. Europace 2015;17:1099 –106.
6. Nakatani Y, Mizumaki K, Nishida K, Sakamoto T, Yamaguchi Y, Kataoka N et al. Electrophysiological and anatomical differences of the slow pathway between the
fast-slow form and slow-slow form of atrioventricular nodal reentrant tachycardia.
Europace 2014;16:551 –7.
7. Wang N. Dual atrioventricular nodal nonreentrant tachycardia: a systematic review.
Pacing Clin Electrophysiol 2011;34:1671 – 81.
8. Wu D, Denes P, Dhingra R, Pietras R, Rosen K. New manifestations of dual A-V nodal
pathways. Eur J Cardiol 1975;2:459 – 66.
9. Aasbo J, Prasertwitayakij N, Morady F, Jongnarangsin K. Nonreentrant dual atrioventricular nodal tachycardia in a patient with atrioventricular nodal conduction abnormality. Heart Rhythm 2009;6:1504 –6.
10. Haman L, Praus R, Parizek P. Non-re-entrant atrioventricular nodal tachycardia. Mil
Med 2009;174:866 –8.
11. Jastrzebski M, Kukla P. Tachycardia caused by a double fire – simultaneous double
atrioventricular nodal conduction: a rare or underdiagnosed arrhythmia? Spectrum of electrocardiographic pictures in three patients. Kardiol Pol 2009;67:
77 – 86.
338
12. Singh S, Barrett C, Das S. Pseudo-atrial fibrillation due to non-reentrant AV nodal
tachycardia. Europace 2009;12:36.
13. Zhong-qun Z, Chong-quan W, Shu-yi D. Double ventricular response via dual atrioventricular nodal pathways resulting in sustained supraventricular nonreentrant
tachycardia. J Electrocardiol 2009;42:232.
14. Zimmermann M, Testuz A, Schmutz M, Burri H. Narrow-complex tachycardia with
cycle length alternans: What is the mechanism? Heart Rhythm 2009;6:1238 – 9.
15. Barbato G, Carinci V, Badhwar N. Tachycardia-induced cardiomyopathy. Card Electrophysiol Clin 2010;2:209 –12.
16. Bhatt AG, Monahan K. Nonreentrant supraventricular tachycardia misdiagnosed as
inappropriate sinus tachycardia. Pacing Clin Electrophysiol 2011;34:e70.
17. Li V, Mallick A, Concannon C, Li V. Wide complex tachycardia causing congestive
heart failure. Pacing Clin Electrophysiol 2011;34:1154 –7.
18. Burri H, Hoffmann J, Zimmermann M. Double fire tachycardia. Heart 2012;98:958.
19. Wang N, Razak E, Jain S, Saba S. Isoproterenol facilitation of slow pathway ablation in
incessant dual atrioventricular nodal nonreentrant tachycardia. Pacing Clin Electrophysiol 2012;35:e31.
20. Al Mehairi M, Al Ghamdi S, Dagriri K, Al Fagih A. Simultaneous antegrade dual AV
node conduction initiates AV nodal re-entrant tachycardia (a rare initiation mechanism). J Saudi Heart Assoc 2013;25:35 –7.
21. Evertz R, Merschón F, Berruezo A, Mont L. Dual ventricular response: another road
to supraventricular tachycardia in dual atrioventricular nodal physiology. Rev Esp
Cardiol 2013;66:145 – 6.
22. Ozcan E, Szeplaki G, Merkely B, Geller L. Non-reentrant atrioventricular nodal
tachycardia. Clin Res Cardiol 2013;102:383–6.
23. Takahashi K, Nakayashiro M, Ganaha H. Dual atrioventricular nodal non-reentrant
tachycardia in a child undergoing repair of ventricular septal defect. Pediatr Cardiol
2013;34:715 –8.
24. Wang N, Shah H, Jain S, Saba S. Dual atrioventricular nodal nonreentrant tachycardia
with alternating 1:1 and 1:2 AV conduction: mechanistic hypotheses and total suppression using right atrial pacing. Ann Noninvasive Electrocardiol 2013;18:199 – 203.
25. Kaczmarek K, Ruta J, Wranicz J, Ptaszynski P. A new type of dual atrioventricular
nodal nonreentrant tachycardia. Ann Noninvasive Electrocardiol 2014;19:501 –3.
26. Karnik A, Hematpour K, Bhatt A, Mazzini M. Dual AV nodal nonreentrant tachycardia
resulting in inappropriate ICD therapy in a patient with cardiac sarcoidosis. Indian
Pacing Electrophysiol J 2014;14:44– 8.
27. Kirmanoglou K, Peiker C, Clasen L, Shin D, Kelm M, Meyer C. Duale AV-nodale
nicht-reentry-tachykardie. Herzschrittmacherther Elektrophysiol 2014;25:109–15.
28. Pott C, Wegner F, Bögeholz N, Frommeyer G, Dechering D, Zellerhoff S et al. A
patient series of dual atrioventricular nodal nonreentrant tachycardia (DAVNNT)
— an often overlooked diagnosis? Int J Cardiol 2014;172:e9.
29. Blomström-Lundqvist C, Scheinman M, Aliot E, Alpert J, Calkins H, Camm A et al.
ACC/AHA/ESC guidelines for the management of patients with supraventricular
arrhythmias--executive summary. a report of the American college of cardiology/
American heart association task force on practice guidelines and the European
society of cardiology committee for practice guidelines (writing committee to
develop guidelines for the management of patients with supraventricular arrhythmias) developed in collaboration with NASPE-Heart Rhythm Society. J Am Coll
Cardiol 2003;42:1493 –531.
30. Rostock T, Sanders P, Rotter M, Haı̈ssaguerre M. Sinus rhythm mimicking atrial fibrillation recurrence. Heart Rhythm 2005;2:1158.
31. Csapo G. Paroxysmal nonreentrant tachycardias due to simultaneous conduction in
dual atrioventricular nodal pathways. Am J Cardiol 1979;43:1033 –45.
32. Neuss H, Buss J, Schlepper M, Mitrović V. Double ventricular response in dual AV
nodal pathways mimicking supraventricular as well as ventricular tachycardia. Eur
Heart J 1982;3:146 –54.
33. Sutton F, Lee Y. Supraventricular nonreentrant tachycardia due to simultaneous
conduction through dual atrioventricular nodal pathways. Am J Cardiol 1983;51:
897 –900.
34. Buss J, Kraatz J, Stegaru B, Neuss H, Heene D. Unusual mechanism of PR interval variation and nonreentrant supraventricular tachycardia as manifestation of simultaneous anterograde fast and slow conduction through dual atrioventricular nodal
pathways. Pacing Clin Electrophysiol 1985;8:235 – 41.
35. Sutton F, Lee Y. Paroxysmal nonreentrant tachycardia due to simultaneous conduction via dual atrioventricular nodal pathways. Am Heart J 1985;109:157 –9.
36. Kim S, Lal R, Ruffy R. Paroxysmal nonreentrant supraventricular tachycardia due to
simultaneous fast and slow pathway conduction in dual atrioventricular node pathways. J Am Coll Cardiol 1987;10:456–61.
37. Mádle A. A nonreentrant arrhythmia due to a dual atrioventricular nodal pathway. Int
J Cardiol 1990;26:217 –9.
38. Elizari M, Sanchez R, Chiale P. Manifest fast and slow pathway conduction patterns
and reentry in a patient with dual AV nodal physiology. J Cardiovasc Electrophysiol
1991;2:98 –102.
C. Peiker et al.
39. Li H, Klein G, Natale A, Thakur R, Yee R. Nonreentrant supraventricular tachycardia
due to simultaneous conduction over fast and slow AV node pathways: successful
treatment with radiofrequency ablation. Pacing Clin Electrophysiol 1994;17:1186 –93.
40. Goutner C, Dechandol A, Bourguet J, Donzeau J. Tachycardie supraventriculaire due
à une conduction simultanée dans la voie nodale rapide et lente. Traitement par ablation de la voie lente. Arch Mal Coeur Vaiss 1995;88:1651 – 5.
41. Ajiki K, Murakawa Y, Yamashita T, Oikawa N, Sezaki K, Kotsuka Y et al. Nonreentrant
supraventricular tachycardia due to double ventricular response via dual atrioventricular nodal pathways. J Electrocardiol 1996;29:155–60.
42. Anselme F, Frederiks J, Boyle N, Papageorgiou P, Josephson M. An unusual cause of
tachycardia-induced myopathy. Pacing Clin Electrophysiol 1996;19:115 –9.
43. Verdino R, Iuliano S, Tracy C. Successful ablation of a nonreentrant dual atrioventricular nodal tachycardia. J Interv Card Electrophysiol 1997;1:159 –61.
44. Glotz de Lima G, Roy D, Talajic M, Dubuc M. One-to-two atrioventricular conduction causing nonreentrant tachycardia: successful treatment with radiofrequency ablation. Pacing Clin Electrophysiol 1998;21:1152 – 4.
45. Arena G, Bongiorni M, Soldati E, Gherarducci G, Mariani M. Incessant nonreentrant
atrioventricular nodal tachycardia due to multiple nodal pathways treated by radiofrequency ablation of the slow pathways. J Cardiovasc Electrophysiol 1999;10:1636 –
42.
46. Fraticelli A, Saccomanno G, Pappone C, Oreto G. Paroxysmal supraventricular
tachycardia caused by 1:2 atrioventricular conduction in the presence of dual atrioventricular nodal pathways. J Electrocardiol 1999;32:347–54.
47. Sorbera C, Cohen M, Dhakam S, Fazio J. Symptomatic atrioventricular dual pathway
double responses: a role for slow pathway ablation. Pacing Clin Electrophysiol 1999;22:
958 –61.
48. Neumann T, Schulte B, Pitschner H, Neuss H, Hamm C, Neuzner J. Doppelte Ventrikelerregung bei dualer AV-Knoten-Leitungsphysiologie: Katheterablation des
langsamen Leitungsweges des dualen AV-Knotens. Z Kardiol 2000;89:1014 –8.
49. Labadet C, Di Villamil A, Tommaso F, Maurice MF, Prieto N. Double atrioventricular
conduction during sinus rhythm. Rev Argent Cardiol 2001;69:281 –3.
50. Nakao K, Hayano M, Iliev I, Doi Y, Fukae S, Matsuo K et al. Double ventricular response via dual atrioventricular nodal pathways resulting with nonreentrant supraventricular tachycardia and successfully treated with radiofrequency catheter
ablation. J Electrocardiol 2001;34:59–63.
51. Mansour M, Marrouche N, Ruskin J, Natale A, Keane D. Incessant nonreentrant
tachycardia due to simultaneous conduction over dual atrioventricular nodal pathways mimicking atrial fibrillation in patients referred for pulmonary vein isolation.
J Cardiovasc Electrophysiol 2003;14:752–5.
52. Gaba D, Pavri B, Greenspon A, Ho R. Dual antegrade response tachycardia induced
cardiomyopathy. Pacing Clin Electrophysiol 2004;27:533 – 6.
53. Germano J, Essebag V, Papageorgiou P, Josephson M. Concealed and manifest 1:2
tachycardia and atrioventricular nodal reentrant tachycardia: manifestations of
dual atrioventricular nodal physiology. Heart Rhythm 2005;2:536 –9.
54. Otsuka T, Igarashi M, Fujino N, Nakanishi R, Takamura K, Kobayashi K et al. Successful
radiofrequency catheter ablation of nonreentrant supraventricular tachycardia due
to simultaneous conduction through dual atrioventricular nodal pathways. Europace
2005;7:37.
55. Dixit S, Callans D, Gerstenfeld E, Marchlinski E. Reentrant and nonreentrant forms of
atrio-ventricular nodal tachycardia mimicking atrial fibrillation. J Cardiovasc Electrophysiol 2006;17:312 –6.
56. Trajkov I, Kovacevic D, Boskov V, Poposka L, Gjorgov N. Induction of atrioventricular node reentry by simultaneous anterograde conduction over the fast and slow
pathways. Prilozi 2006;27:113 –20.
57. Clementy N, Casset-Senon D, Giraudeau C, Cosnay P. Tachycardiomyopathy secondary to nonreentrant atrioventricular nodal tachycardia: recovery after slow
pathway ablation. Pacing Clin Electrophysiol 2007;30:925 – 8.
58. Mofrad P, Hsia H. An unusual cause of incessant tachycardia. Pacing Clin Electrophysiol
2007;30:418 –20.
59. Laszlo R, Weig H, Weretka S, Schreieck J. Narrow complex tachycardia with alternating R-R intervals during physical stress: double ventricular excitation. Indian Pacing
Electrophysiol J 2008;8:129 –32.
60. Maury P, Hebrard A, Duparc A, Fontan A, Adegnon K, Delay M. Incessant nonreentrant supraventricular tachycardia interrupted by apparent simultaneous
wenckebach sequences along both nodal pathways. Pacing Clin Electrophysiol 2008;
31:757 – 60.
61. Silver J, Smith B, John R. Regularly irregular narrow complex tachycardia: what is the
mechanism? Heart Rhythm 2008;5:487–8.
62. Katritsis D, Josephson M. Classification of electrophysiological types of atrioventricular nodal re-entrant tachycardia: a reappraisal. Europace 2013;15:1231 – 40.
63. Mendenhall GS, Voigt A, Saba S. Insights into atrioventricular nodal function from
patients displaying dual conduction properties: interactive and orthogonal pathways.
Circ Arrhythm Electrophysiol 2013;6:364 –70.
64. Meyer C, Pürerfellner H. Continuous heart rhythm monitoring to detect and quantify atrial fibrillation. Expert Rev Cardiovasc Ther 2010;8:889 –90.
339
Dual atrioventricular nodal non-re-entrant tachycardia
65. Nakagawa H, Jackman W. Catheter ablation of paroxysmal supraventricular tachycardia. Circulation 2007;116:2465 – 78.
66. Insulander P, Bastani H, Braunschweig F, Drca N, Gudmundsson K, Kennebäck G
et al. Cryoablation of substrates adjacent to the atrioventricular node: acute and
long-term safety of 1303 ablation procedures. Europace 2014;16:271–6.
67. 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.
68. Posan E, Gula L, Skanes A, Krahn A, Yee R, Petrellis B et al. Characteristics of slow
pathway conduction after successful AVNRT ablation. J Cardiovasc Electrophysiol
2006;17:847 –51.
69. Eickholt C, Boring Y, Kelm M, Shin D, Meyer C. Nonfluoroscopic catheter ablation of
a double-loop re-entry tachycardia guided by real-time contact force information.
Can J Cardiol 2013;29:254.e9– 254.e11.
70. Amasyali B, Kilic A. Dual atrioventricular nodal nonreentrant tachycardia: The rarest
aspect of the structure causing the most frequent PSVT. Int J Cardiol 2014;173:550.
71. Smaill BH, Zhao J, Trew ML. Three-dimensional impulse propagation in myocardium:
arrhythmogenic mechanisms at the tissue level. Circ Res 2013;112:834–48.
72. Li J, Greener ID, Inada S, Nikolski VP, Yamamoto M, Hancox JC et al. Computer
three-dimensional reconstruction of the atrioventricular node. Circ Res 2008;102:
975 –85.
73. Appel ML, Berger RD, Saul JP, Smith JM, Cohen RJ. Beat to beat variability in cardiovascular variables: noise or music? J Am Coll Cardiol 1989;14:1139 –48.
EP CASE EXPRESS
doi:10.1093/europace/euv428
Online publish-ahead-of-print 6 February 2016
.............................................................................................................................................................................
Catheter ablation of multiple accessory pathways in Ebstein anomaly guided
by intracardiac echocardiography
Mihailo Vukmirović, Petr Peichl*, and Josef Kautzner
Department of cardiology, Institute for Clinical and Experimental Medicine, Vı́den̆ská 1958/9, Prague 140 21, Czech Republic
* Corresponding author. E-mail address: [email protected]
A 24-year-old-female with Ebstein anomaly and preexcitation (ECG#1) was referred for catheter ablation. The procedure was guided by fluoroscopy,
electroanatomical mapping system (CARTO 3TM ,
Biosense-Webster), and intracardiac echocardiography (ICE) (Acunav, Siemens). At first, ICE (upper
Panel) was used to define the true location of tricuspid annulus (TA) by course of the right coronary
artery (RCA). Both anatomical and functional insertions of the tricuspid valve were then annotated
(lower Panel shows right atrium in left anterior
oblique and caudal view). Subsequently, the earliest
ventricular activity during sinus rhythm was mapped
to the posterolateral portion of TA. After delivery of
radiofrequency (RF) current at that site, a small
change in pre-excitation pattern (ECG#2) was
noted and the earliest ventricular activation shifted
more septally. Further RF lesions (dark red points
in lower Panel) were deployed along the posterior
and subsequently towards posteroseptal part of
the TA, leading to gradual elimination of conduction
(ECG#3) via the wide/multiple accessory pathways
(APs).
It has been recognized that catheter ablation in
Ebstein anomaly should optimally target anatomical
and not functional TA. In this case, ICE enabled easy identification of the true TA by displaying the course of RCA and guided successfully
ablation despite complex anatomy.
Funding
This work was supported by MH CZ - DRO (Institute for Clinical and Experimental Medicine – IKEM, IN 00023001)
Conflict of interest: none declared.
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