CLINICAL RESEARCH
Europace (2015) 17, 1099–1106
doi:10.1093/europace/euu387
Cardiac electrophysiology
Atypical atrioventricular nodal reentrant
tachycardia: prevalence, electrophysiologic
characteristics, and tachycardia circuit
Demosthenes G. Katritsis1*, Ali Sepahpour 2, Joseph E. Marine 3, George D. Katritsis 4,
Tanyanan Tanawuttiwat 3, Hugh Calkins 3, Edward Rowland 2, and Mark E. Josephson 5
1
Athens Euroclinic, Athens, Greece; 2The Heart Hospital, London, UK; 3Johns Hopkins Hospital, Baltimore, MD, USA; 4The Oxford University Clinical Academic Graduate School,
Oxford, UK; and 5Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA, USA
Received 28 September 2014; accepted after revision 3 December 2014; online publish-ahead-of-print 2 February 2015
Aims
This study aimed at assessing the prevalence, electrophysiologic characteristics, and mechanism of atypical atrioventricular nodal reentrant tachycardia (AVNRT).
.....................................................................................................................................................................................
Methods
We studied 925 consecutive patients with AVNRT. Atrial-His (AH) and His-atrial (HA) intervals were measured during
atypical AVNRT (HA . 70 ms), and compared with measurements in 34 patients with typical (slow-fast) AVNRT.
and results
Assuming that conduction velocity over the fast pathway is similar in the anterograde and retrograde directions, the
AH interval during the fast –slow form should be smaller than the HA during slow–fast. Atypical AVNRT was diagnosed
in 59 patients (6.4%), median age 50 years (range 19–79 years), and 37 (59.7%) of them female. Fast–slow AVNRT was
diagnosed in 44 patients (74.5%), and slow–slow AVNRT in 9 patients (15.2%). The remaining six patients (10.2%) could
not be reliably classified due to inconsistent AH, and HA/AH patterns or variable intervals. Tachycardia induction with
anterograde conduction jumps was seen in two patients with the fast–slow, and in three patients with slow–slow or
intermediate forms. Atrial-His in the fast–slow group was significantly longer than HA in the slow–fast group,
99.7 + 40.5 ms vs. 45.8 + 7.7 ms, P , 0.001. Tachycardia cycle length was longer in fast–slow compared with slow–
fast, 379.1 + 68.5 ms vs. 317.1 + 42.8 ms, P , 0.001.
.....................................................................................................................................................................................
Conclusion
Of AVNRT cases, 6.4% are atypical and may display patterns that do not necessarily correspond to the fast–slow
or slow–slow conventional types. Atypical fast– slow and typical AVNRT do not appear to utilize the same limb for
fast conduction.
----------------------------------------------------------------------------------------------------------------------------------------------------------Keywords
Atypical atrioventricular nodal tachycardia † Fast-slow tachycardia † Slow– slow tachycardia † Nodal extensions
Introduction
Atypical atrioventricular nodal reentrant tachycardia (AVNRT) has
not been extensively studied. Published reports have presented a
limited number of cases, and no universal scheme for the definition
and classification of forms of atypical AVNRT exists, with various criteria used by different investigators.1 The tachycardia mechanism of
atypical, as well as typical, AVNRT also remains elusive.2 The longitudinally dissociated dual atrioventricular (AV) nodal pathways have
not been demonstrated histologically, and the exact circuit responsible for the reentrant tachycardia is unknown. Attempts to
provide a reasonable hypothesis have been made by reference to
contextual considerations, such as the anisotropic conduction properties of the transitional area between the atria and the AV node.3 – 7
In addition, there has been electrophysiologic evidence that the right
and left inferior extensions of the human AV node and the atrio-nodal
inputs they facilitate, which have been identified histologically, might
provide the anatomic substrate of the slow pathway.8 – 11 However,
data indicating the potential anatomic site of the fast pathway are virtually non-existent. There has been histologic and electrophysiologic
evidence of multiple superior atrial inputs to the AV node,12 – 16 and of
variability in the space constant of tissue and poor gap junction
* Corresponding author. Tel: +30 210 6416600; fax: +30 210 6722535; E-mail address: dgkatr@otenet.gr; dkatritsis@euroclinic.gr
Published on behalf of the European Society of Cardiology. All rights reserved. & The Author 2015. For permissions please email: journals.permissions@oup.com.
1100
What’s new?
† Atypical atrioventricular nodal reentrant tachycardia (AVNRT)
may display patterns that do not necessarily correspond to the
conventional fast–slow or slow–slow paradigms.
† The term ‘fast–slow AVNRT’ is ambiguous and probably
should be abandoned in favour of the term ‘atypical AVNRT’
for all subtypes.
† Atypical AVNRT of the fast –slow type and typical AVNRT do
not appear to utilize the same pathway for fast conduction.
† Atypical AVNRT may involve the left and right inferior nodal
extensions, regardless of the atrial-His/His-atrial relationship.
D.G. Katritsis et al.
defined by delayed retrograde atrial activation with HA . 70 ms. If the
AH was ,200 ms and the AH , HA, the atypical form was characterized
as fast– slow. If AH . 200 m and AH . HA, the atypical form was considered slow– slow. Tachycardias with a prolonged AH interval .200 ms
but AH , HA, or with AH , 200 ms and AH . HA, or with variable
intervals during the same or different episodes, were classified as indeterminate. Retrograde atrial activation sequence may be variable in all forms
of AVNRT, typical or atypical,1,8 and was not considered as a criterion for
classification of AVNRT types. Similarly, the demonstration of a lower
common pathway was not employed as a reliable criterion for differential
diagnosis of AVNRT types.1
Measurements
Atypical atrioventricular nodal reentrant tachycardia
connectivity due to differential expression of connexin isoforms in
the nodal area,17 – 19 that could explain the multiple, heterogeneous
sites of early atrial activation during the arrhythmia on both sides of
the septum during typical AVNRT.8,20 However, several questions
remain about the nature of fast pathway conduction, especially in
fast–slow atypical tachycardias. It is not known whether the ‘fast
pathway’ component of the circuit in the fast – slow form represents
conduction through the same fast pathway used retrogradely by
typical slow–fast AVNRT, or uses alternative limbs, such as the
short, left-sided inferior nodal extension.21,22
We hypothesized that conduction times such as the atrial-His
(AH) and His-atrial (HA) intervals during tachycardia can be used
to provide data on the conduction characteristics of the fast and
slow circuit limbs. We further hypothesized that by comparing
these intervals in typical and atypical tachycardia, we could derive information regarding the nature of the anterograde and retrograde
pathways involved in atypical AVNRT, and particularly the fast–
slow form. This study, therefore, examined the prevalence of atypical
AVNRT, the electrophysiologic characteristics of the arrhythmia, and
the nature of the fast component of the tachycardia circuit during
atypical AVNRT with characteristics compatible with the fast–slow
form.
Methods
Patients
Data from consecutive adult patients with AVNRT undergoing catheter
ablation at four centres, Athens Euroclinic, Greece (2007 – 2014); Beth
Israel Deaconess Medical Center, Boston, MA, USA (2009 – 2013); The
Heart Hospital, London, UK (2009 – 2013); and The Johns Hopkins
Hospital, Baltimore, MD, USA (2011 – 2014), were analysed. All patients
were studied in the post-absorptive state, under mild sedation, and after
all antiarrhythmic agents had been discontinued for more than 5 days.
No patient had received amiodarone for the preceding three months.
The study received approval from our institutional review boards.
Definitions
Atrioventricular nodal reentrant tachycardia was diagnosed by fulfillment
of established criteria during detailed atrial and ventricular pacing maneuvers,1,2 and subsequent abolition of the tachycardia by anatomic ablation
of the slow-pathway. Typical (slow– fast) AVNRT was defined by an AH/
His-atrial ratio . 1, and HA interval ≤70 ms. Atypical AVNRT was
The AH interval during tachycardia was measured from the latest rapid
deflection of the atrial activation to the earliest deflection of the His
bundle activation on the His bundle electrogram (Figure 1). The HA interval during tachycardia was measured from the end of the His bundle activation to the earliest rapid deflection of the atrial activation in the His
bundle electrogram (Figure 1). Data are presented in Table 1.
Typical atrioventricular nodal reentrant tachycardia
For comparative purposes, patients with typical, slow-fast AVNRT, and in
whom proper identification of the retrograde atrial and His bundle activation during tachycardia could be achieved, were also considered.
During typical AVNRT, precise identification of earliest atrial activation
may be difficult. Thus, techniques for separation of atrial and ventricular
activity were employed as previously described.8 Identification of atrial
electrograms was verified by observations on spontaneous, pharmacologic or pacing-induced termination of tachycardia as well as by producing
separation of ventricular and atrial electrograms by atrial or ventricular
extrastimuli. Details of our methodology have been discussed and presented elsewhere.8 Atrial-His and HA intervals were measured as previously described. Data on typical AVNRT represent measurements
from consecutive, consenting patients studied with this methodology
at Athens Euroclinic (Table 1).
All measurements were performed at a speed of 200 mm/s using an
on-line automated caliper system. Measurements were analysed by
two different investigators at separate time intervals to assess interobserver reproducibility. To assess temporal reproducibility, all measurements were made during repeated episodes of tachycardia and
right ventricular pacing.
Study rationale: theoretical considerations
During AVNRT, the tachycardia circuit is confined within the AV node
territory, and activation of the atrium takes place following activation of
the retrograde pathway. Thus, during typical, slow – fast AVNRT, the
HA interval represents the time difference between activation of the
His bundle and activation of the atrium, this is HA ¼ Fretro + A 2 H,
where Fretro is the time the impulse goes retrogradely along the fast
pathway, A is the time the impulse travels from the AV node to right
atrium as recorded by the electrode positioned on the His bundle,
and H is the time the impulse travels from the AV node to the His
bundle (Figure 2). Similarly, the AH interval represents the time difference
between activation of the right atrium as recorded by the electrode positioned on the His bundle, and the next activation of the His bundle, this is
AH ¼ Sante + H 2 A, where Sante is the anterograde conduction along
the slow pathway (probably one of the inferior nodal extensions), H is
the time the impulse travels from the AV node to the His bundle, and A
the time the impulse travels from the AV node to right atrium. During
atypical, fast– slow AVNRT, HA ¼ Sretro + A 2 H, where Sretro is the
1101
Atypical atrioventricular nodal reentrant tachycardia
I
aVF
V1
V5
HRA
HAHis = 140 ms
His 5–6
Tachy CL = 317 ms
AH = 157 ms
His 3–4
His 1–2
HACS = 151 ms
CS 5–6
CS 3–4
CS 1–2
RV 1–2
200 mm/s
Figure 1 Methodology of measurement of AH and HA intervals during atypical AVNRT. HAHis indicates HA interval measured by considering
the retrograde A at the His bundle, and HACS the retrograde A at the CS. I, aVF, V1, V5: leads I, aVF, V1, V5 of the surface ECG; HRA, high right
atrium; His, His bundle recording electrode; CS, coronary sinus; RV, right ventricle.
Table 1 Tachycardia types and conduction intervals
AVNRT
type
n
Age
Sex (F/M)
CL (ms)
AH (His)
activation
HA (His)
activation
HA (pCS)
activation
Earliest retrograde
atrial activation
...............................................................................................................................................................................
Fast –slow
44
50.7 + 19.3
23/21
379.1 + 68.5
99.7 + 40.5
251.7 + 76.4
251.5 + 77.2
pCS (59%)
Slow– slow
Intermediate
9
6
45.6 + 20.0
52.5 + 13.7
7/2
4/2
476.4 + 137.9
395.8 + 105.5
286.0 + 83.2
197.0 + 31.1
163.3 + 60.5
176.0 + 72.9
171.0 + 60.9
173.8 + 66.7
His (67%)
His/pCS (50%)
Slow– fast
34
39.0 + 7.5
22/12
331.1 + 46.8
270.4 + 44.3
45.8 + 7.7
51.4 + 7.5
His (85%)
Fast–slow type: AH , 200 ms and AH , HA; slow–slow type: AH . 200 ms and AH . HA; intermediate: all other patterns.
CL, tachycardia cycle length; AH tachy, atrial to His interval during tachycardia; HA tachy, His to right atrium interval during tachycardia.
time the impulse goes retrogradely along the slow pathway, A is the time
the impulse travels from the AV node to the right atrium, and H is the time
the impulse travels from the AV node to the His bundle. AH ¼ ‘F’ante + H
2 A, where Fante is the anterograde conduction along the ‘fast’ pathway, H
is the time the impulse travels from the AV node to the His bundle, and A
the time the impulse travels from the AV node to right atrium. Atrial-His
and HA intervals during slow–slow tachycardia that utilizes two slow
pathways (probably the two inferior nodal extensions), are also depicted
in Figure 2. Assuming that conduction velocity over the fast pathway is
similar in the anterograde and retrograde direction, and that A ≥ H
(because His bundle activation always precedes atrial activation, thus
F + A . H, and F by definition should be a minimum quantity), the AH
interval during fast– slow tachycardia should be smaller or equal than
the HA interval during slow– fast, since (H 2 A) ≤ (A 2 H ), if these
two tachycardia types use the same ‘fast’ pathway component in their circuits. We therefore compared intervals in a series of atypical AVNRT
with those derived by patients with typical, slow– fast AVNRT in whom
measurements could be accomplished as described.
1102
D.G. Katritsis et al.
Slow-fast AVNRT
Slow-slow AVNRT
Slow-fast AVNRT
Fast-slow AVNRT
A
A
A
AH
HA
A
H
Sante
Fretro
Sante
Fretro
Sretro
Sante
“F”ante
A
Sretro
“Fast”-slow AVNRT
H
H
His
His
H
His
A
AH
HA
HA = Fretro+A–H
HA = sretro+A–H
HA = sretro+A–H
AH= Sante+H–A
AH= Sante+H–A
AH= “F”ante+H–A
H
“F”ante
A
Sretro
Figure 2 Left panel: Depiction of conduction and resultant AH and HA during typical and atypical AVNRT types (see text for details). F, retrograde
conduction over the fast pathway; ‘F’, anterograde conduction over the fast pathway that is utilized by the fast-slow form; S, conduction over the slow
pathway (anterogradely or retrogradely); A, conduction from the AVN node to right atrium as recorded by the electrode positioned on the His
bundle; H, conduction from the AVN to His bundle; HA, time difference between activation of the His bundle and right atrium; AH, time difference
between activation of right atrium and the next His. Right panel: Schematic representation of conduction times during slow– fast AVNRT (upper
panel). With these relationships the AH interval is approximately 5 times larger than the HA, as derived from our data. If the fast– slow form
(lower panel) utilizes the same fast pathway for anterograde conduction, the AH during fast– slow should be less than the HA during slow– fast.
Abbreviations as in Figure 1.
Statistical analysis
Data normality was analysed using the Kolmogorov– Smirnov test. In all
cases the examined variables followed the normal distribution and Student’s t-test was used to analyse difference between two groups and
the one-way analysis of variance test to analyse differences between
more than two groups. All reported P values were based on two-sided
tests and were compared with a significant level of 5%. All statistical calculations were performed on SPSS for Windows version 13.0 (SPSS, Inc).
Results
Prevalence
In total, 925 consecutive patients with AVNRT were studied in
Athens Euroclinic, Greece (n ¼ 287), Beth Israel Deaconess
Medical Center, Boston, MA, USA (n ¼ 188), the Heart Hospital,
London, UK (n ¼ 179), and the Johns Hopkins Hospital, Baltimore,
MD, USA (n ¼ 271). Using the criteria mentioned above, 59 patients
(6.4%) had atypical AVNRT. Of these, 44 patients (74.5%) had fast –
slow AVNRT according to both the AH , HA and AH , 200 ms,
and 9 patients (15.2%) had slow– slow AVNRT. The remaining six
patients (10.2%) could not be reliably classified due to inconsistent
AH and HA/AH patterns or variable intervals. Patient characteristics
and conduction intervals during tachycardia are shown in Table 1.
Median age of all patients was 50 years (range 19 –79 years), and 37
patients (59.7%) were female. Patient age and tachycardia cycle
lengths in the atypical AVNRT group were significantly higher than
in the slow–fast group, 50.1 + 18.7 vs. 39.0 + 7.5 years (P ¼
0.002), and 395.7 + 91.0 vs. 331.1 + 46.8 ms (P , 0.001), respectively. There was no significant difference in age between atypical
AVNRT groups (P ¼ 0.721).
Mode of induction and earliest atrial
retrograde activation
Tachycardia induction during atrial pacing with anterograde conduction jumps was seen in two patients with the fast– slow form, and in
three patients with slow– slow or intermediate forms and variable
AH/HA intervals (Figure 3). Variable AH/HA intervals were seen in
six patients (Figure 4, left panel). During tachycardia, induction by ventricular pacing descrete retrograde jumps were difficult to define,
mainly due to inability to record reliably a retrograde His bundle electrogram. Seven patients (11.9%) had also typical AVNRT induced,
either spontaneously or following autonomic manipulation with atropine or isoproterenol (Figure 4, right panel, and Figures 5 and 6).
One patient had transient 2 : 1 infrahisian block during tachycardia.
Earliest atrial retrograde activation was variable, but most often
recorded at the proximal coronary sinus electrogram (57%), especially in the fast–slow form (Table 1).
Conduction intervals
The AH interval in the fast –slow group was significantly longer than
HA in the slow–fast group, 99.7 + 40.5 vs. 45.8 + 7.7 ms, P , 0.001,
and tachycardia cycle length was also longer (379.1 + 68.5 vs.
331.1 + 46.8, P , 0.001), respectively. The HA interval during
fast– slow was not different that the AH during slow–fast
(251.7 + 76.4 vs. 270.4 + 44.3, P ¼ 0.2), respectively. In Figure 4
(right panel), the HA during slow–fast (55 ms) is completely different
from both the AH and HA during atypical AVNRT. The AH in slow–
slow is shorter than the AH during slow–fast (260 vs. 340 ms), with
the difference probably due to shorter tachycardia cycle length as
well as fast retrograde activation that results in delayed conduction
1103
Atypical atrioventricular nodal reentrant tachycardia
II
I
III
aVF
V1
V1
HRA
V6
AH 618
AH 170
HRA
HA = 240 ms
HA = 252 ms
HA = 252 ms
His
His 2
His 1
A1-H1 = 84 ms A2-H2 = 204 ms
AH = 140 ms
AH = 122 ms
AH = 122 ms
CS 5
CS 5
CS 4
CS 4
CS 3
CS 3
CS 2
CS 2
CS 1
CS 1
RV
RV
Figure 3 Left panel: Induction of fast– slow AVNRT by atrial pacing and anterograde conduction jump. Right panel: Induction of slow– slow
AVNRT by atrial pacing and anterograde conduction jump. Abbreviations as in Figure 1.
05
II
06
07
I
V1
II
V6
HA 264
HA 335
HA 375
V1
HRA
HRA
His1–2
AH 535
AH 665
AH 500
HA = 180 ms
AH 515
HA = 65 ms
HA = 55 ms
HA = 55 ms
His3–4
AH = 260 ms
CS9–10
His1–2
CS7–8
CS9–10
HH = 480 ms
CS5–6
AH = 260 ms
AH = 340 ms
HH = 450 ms
AH = 340 ms
HH = 440 ms
CS7–8
CS5–6
CS3–4
CS3–4
CS1–2
CS1–2
RVAp
RV
HH 635
HH 770
HH 840
100 mm/s
Figure 4 Left panel: Variable conduction intervals during atypical AVNRT. Right panel: Spontaneous transition from atypical to typical AVNRT.
Abbreviations as in Figure 1.
in the slow pathway or the AV nodal–His interval. In Figure 5 the HA
during slow– fast (left panel) is shorter (45 ms) than the AH during
fast–slow (67 ms, right panel).
Discussion
There are four main findings of our study. First, the prevalence of atypical AVNRT is lower than previously reported. Second, atypical AVNRT
may display patterns that do not necessarily correspond to the fast–
slow or slow–slow conventional types. Third, earliest retrograde
activation during atypical AVNRT is variable and not always eccentric.
Fourth, atypical AVNRT of the fast–slow type, and typical AVNRT
most probably do not utilize the same limb for fast pathway conduction.
In our series, AVNRT with prolonged HA intervals was identified
in 6% of all AVNRT cases. We believe that the reason for a higher
prevalence reported by other groups is the characterization as slow–
slow atypical AVNRT what are actually typical AVNRT cases, mainly
due to eccentric retrograde activation or identification of a lower
1104
D.G. Katritsis et al.
I
II
III
V1
HRA
His1–2
CS9–10
CS7–8
CS5–6
CS3–4
CS1–2
RVA p
100 mm/s
100 mm/s
Figure 5 Induction of typical AVNRT by atrial pacing (left panel), and atypical AVNRT by ventricular pacing (right panel) in the same patient.
A
C
B
I
III
aVR
aVF
V1
V5
His 3–4
AVNRT CL = 262 ms
AVNRT CL = 294 ms
A–H = 248 ms
HA = 294 ms
His 1–2
CS 5–6
CS 3–4
CS 1–2
100 mm/s
Figure 6 (A) Typical AVNRT with 2:1 suprahisisan conduction block. Following aventricular ectopic beat (arrow), there is restoration of 1:1 conduction. The tachycardia cycle length is stable and the same (262 ms) in both atrial and ventricular electrograms. (B) Same patient. Dissociation of
atria (atrial fibrillation) and ventricles during AVNRT (stable His and V cycle length of 294 ms). (C) Same patient. Spontaneous initiation of atypical
AVNRT.
1105
Atypical atrioventricular nodal reentrant tachycardia
common pathway.1 Our results demonstrate that the electrophysiologic characteristics of the ‘fast’ component of the tachycardia circuit
in the fast–slow form are not similar to those of the fast conduction
pathway during typical, slow–fast AVNRT. Our measurements are in
keeping with data provided by other investigators who have reported
on atypical AVNRT. Atrial-His and HA intervals during fast– slow
tachycardia were 135 + 32 and 250 + 89 ms,21 107 + 29 ms and
222 + 67 ms,23 109 + 31 ms and 261 + 69 ms,24 77 + 21 ms and
321 + 61, 112 + 8 ms and 230 + 30 ms, 120 + 38 ms and 282 +
120 ms,25 respectively. For typical AVNRT, reported AH and HA
intervals during tachycardia were 364 + 71 and 45 + 15 ms, respectively,21 although reliable identification of the atrial electrogram
without specific maneuvers as described, may not be possible in
typical AVNRT where atrial and ventricular activation may be simultaneous. Induction of fast –slow AVNRT with an AV conduction jump
indicates involvement of a ‘slow’ pathway in anterograde conduction,
and measured intervals suggest that ‘fast’ conduction properties
during fast – slow tachycardia resemble those displayed during retrograde conduction of slow–slow AVNRT. It is therefore probable that
re-entry may involve the left and right inferior extensions in all forms
of atypical AVNRT, including the fast-slow variety, as proposed by
Heidbüchel and Jackman21 and Lockwood et al.22 Depending on
the relative lengths and conduction properties of the left and right
inferior extensions, AH and HA relationship may vary, and this
explains the indeterminate forms that cannot be classified according
to conventional criteria, as well as the disagreement about classification and definitions of forms of atypical AVNRT. For example,
fast–slow AVNRT has been defined by means of an AH interval
,185 ms22 or AH , 200 ms,21 or by means of the AH/HA pattern
only,25 – 27 by different investigators.
Different HA times during slow–fast and fast–slow AVNRT could
be explained by different H intervals in the two types of tachycardia.
A long H interval during slow–fast AVNRT (Figure 2) could explain
the short HA and long AH intervals, whereas a short H interval
during fast –slow AVNRT could explain the long HA and relatively
short AH interval. However, the demonstration of both types of
tachycardia in the same patient, argues against such an explanation.
Data on ventricular pacing at the tachycardia cycle length and the
derived ‘lower common pathway’ were not used in our study. During
ventricular pacing, the HA time is HA ¼ Hretro + AVN + A, where
Hretro is the time the impulse travels retrogradely from the His
bundle to the AV node, AVN is conduction through the compact
AV node and either of the AV nodal pathways, and A the time the
impulse travels from the exit of the AV node to right atrium. Thus,
it is fundamentally different that the HA time with which it is compared with derive the lower common pathway. Conduction during
ventricular pacing may also not be relevant to activation sequence,
and intervals, during AVNRT. We have previously shown that the
breakthrough of atrial activation is discordant from that observed
during ventricular pacing in up to 43% of patients with AVNRT.8
Similarly, the difficulty in using earliest atrial activation sites to guide
classification of AVNRT is well documented,1,11 and the pattern of
earliest activation was not considered to be of diagnostic significance
in our study.
In Figure 7 we propose a hypothetical model of the AVNRT tachycardia circuits based on the concept of nodal extensions. Both
described superior atrial inputs to the AV node and the anisotropic,
Typical AVNRT
S/AAT
LI
FO
RI
CS
Atypical AVNRT
TV
Figure 7 (central illustration). Proposed circuit of AVNRT.
During typical AVNRT (slow– fast), right- or left-sided circuits
may occur with antegrade conduction through the inferior inputs
and retrograde conduction through the superior inputs (S) or the
anisotropic atrionodal transitional area (AAT). In atypical AVNRT
conduction occurs anterogradely through one of the inferior
inputs, left (LI) or right (RI) and retrogradely through the other
one. Depending on the orientation of the circuit we may record
the so-called ‘fast – slow’ or ‘slow– slow’ types. FO, foramen
ovale; CS, coronary sinus; TV, tricuspid valve.
transitional atrionodal area could serve as the fast limb of typical
AVNRT. In atypical AVNRT, re-entry involves the inferior nodal
extensions and this is probably why this tachycardia displays different
electrophysiologic behaviour than typical AVNRT. The AH/HA relationship depends on the length and conduction properties of the
right and left (usually shorter) extensions. The AH interval also
can be variable and any threshold used for characterization of the
arrhythmia type is arbitrary.
Clinical implications
Atrioventricular nodal reentrant tachycardia with prolonged retrograde atrial activation (HA . 70 ms) represents an atypical form regardless of the site of earliest retrograde atrial activation. Further
classification into fast–slow or slow–slow types has no validity.
Attempts at establishing the presence of a lower common pathway
are also of no practical significance, and may result in unnecessarily
prolonged procedures. Since atypical AVNRT most likely utilizes
the two inferior nodal extensions for its circuit, ablation should be
directed only towards the anatomic position of the slow pathway. If
right septal attempts are unsuccessful, the left septal side should be
tried.28 Ablation targeting earliest atrial activation sites during
typical AVNRT or the fast pathway, is not justified.
Study limitations
Our study has several limitations. The theoretical models of the three
types of AVNRT accept similar A and H times, an A interval longer
than H, and similar anterograde and retrograde conduction velocities
of the fast and slow AV nodal pathways, but these assumptions cannot
be deduced from our data. Retrograde atrial activation, in particular,
may not take similar paths in all forms of AVNRT, thus disputing the
1106
significance of our calculations. However, induction via a jump, and
consistently longer tachycardia cycles in fast –slow, do suggest a
different circuit of this tachycardia, rather than an ‘inverse’ slow–
fast form.
Conclusions
Acknowledging these limitations, we conclude that atypical AVNRT
may display patterns that do not necessarily correspond to the conventional fast–slow or slow–slow paradigms. Atypical AVNRT of the
fast–slow type and typical AVNRT do not utilize the same pathway
for fast conduction. The term ‘fast – slow AVNRT’ is ambiguous and
probably should be abandoned in favour of the term ‘atypical
AVNRT’ for all subtypes. Atypical AVNRT probably may involve
the left and right inferior nodal extensions, regardless of the AH/
HA relationship.
Conflict of interest: none declared.
References
1. Katritsis DG, Josephson ME. Classification of electrophysiological types of atrioventricular nodal re-entrant tachycardia: a reappraisal. Europace 2013;15:1231 –40.
2. Katritsis DG, Camm AJ. Atrioventricular nodal reentrant tachycardia. Circulation
2010;122:831 –40.
3. Spach MS, Josephson ME. Initiating reentry: The role of nonuniform anisotropy in
small circuits. J Cardiovasc Electrophysiol 1994;5:182 –209.
4. Mazgalev TN, Ho SY, Anderson RH. Anatomic-electrophysiological correlations
concerning the pathways for atrioventricular conduction. Circulation 2001;103:
2660 –7.
5. Keim S, Werner P, Jazayeri M, Akhtar M, Tchou P. Localization of the fast and slow
pathways in atrioventricular nodal re-entrant tachycardia by intraoperative ice
mapping. Circulation 1992;86:919 –25.
6. Wu D, Yeh SJ, Wang CC, Wen MS, Lin FC. Double loop figure-of-8 reentry as the
mechanism of multiple atrioventricular node reentry tachycardias. Am Heart J
1994;127:83 –95.
7. Patterson E, Scherlag BJ. Decremental conduction in the posterior and anterior AV
nodal inputs. J Interv Card Electrophysiol 2002;7:137 –48.
8. Katritsis DG, Ellenbogen KA, Becker AE. Atrial activation during atrioventricular
nodal reentrant tachycardia: studies on retrograde fast pathway conduction. Heart
Rhythm 2006;3:993 – 1000.
9. Katritsis DEK, Becker A, Camm AJ. Retrograde slow pathway conduction in patients
with atrioventricular nodal reentrant tachycardia. Europace 2007;9:458 –65.
10. Katritsis DG, Becker AE, Ellenbogen KA, Giazitzoglou E, Korovesis S, Camm AJ.
Effect of slow pathway ablation in atrioventricular nodal reentrant tachycardia
on the electrophysiologic characteristics of the inferior atrial inputs to the human
atrioventricular node. Am J Cardiol 2006;97:860 –86.
11. Katritsis DG, Becker A. The atrioventricular nodal reentrant tachycardia circuit:
A proposal. Heart Rhythm 2007;4:1354 –60.
D.G. Katritsis et al.
12. Wu J, Wu J, Olgin J, Miller JM, Zipes DP. Mechanisms underlying the reentrant
circuit of atrioventricular nodal re-entrant tachycardia in isolated canine atrioventricular nodal preparation using optical mapping. Circ Res 2001;88:1189 –95.
13. Antz M, Scherlag BJ, Otomo K, Pitha J, Tondo C, Patterson E et al. Evidence for multiple atrio-AV nodal inputs in the normal dog heart. J Cardiovasc Electrophysiol 1998;9:
395 –408.
14. Hirao K, Scherlag BJ, Poty H, Otomo K, Tondo C, Antz M et al. Electrophysiology of
the atrio-AV nodal inputs and exits in the normal dog heart: radiofrequency ablation
using an epicardial approach. J Cardiovasc Electrophysiol 1997;8:904 –15.
15. Toshida N, Hirao K, Yamamoto N, Tanaka M, Suzuki F, Isobe M. Ventricular echo
beats and retrograde atrioventricular nodal exits in the dog heart: multiplicity in
their electrophysiologic and anatomic characteristics. J Cardiovasc Electrophysiol
2001;12:1256 –64.
16. Gonzalez MD, Contreras LJ, Cardona F, Klugewicz CJ, Conti JB, Curtis AB et al. Demonstration of a left atrial input to the atrioventricular node in humans. Circulation
2002;106:2930 –4.
17. Loh P, Ho SY, Kawara T, Hauer RN, Janse MJ, Breithardt G et al. Reentrant circuits in
the canine atrioventricular node during atrial and ventricular echoes: electrophysiological and histological correlation. Circulation 2003;108:231 –8.
18. Hucker WJ, McCain ML, Laughner JI, Iaizzo PA, Efimov IR. Connexin 43 expression
delineates two discrete pathways in the human atrioventricular junction. Anat Rec
(Hoboken) 2008;291:204 –15.
19. Nikolaidou T, Aslanidi OV, Zhang H, Efimov IR. Structure-function relationship in the
sinus and atrioventricular nodes. Pediatr Cardiol 2012;33:890 –9.
20. Anselme F, Hook B, Monahan K, Frederiks J, Callans D, Zardini M et al. Heterogeneity
of retrograde fast-pathway conduction pattern in patients with atrioventricular
nodal reentry tachycardia: observations by simultaneous multisite catheter
mapping of Koch’s triangle. Circulation 1996;93:960 –8.
21. Heidbüchel H, Jackman WM. Characterization of subforms of AV nodal reentrant
tachycardia. Europace 2004;6:316 – 29.
22. Lockwood DJ, Otomo C, Wang Z, Foresti S, Nakagawa H, Beckman K et al. Electrophysiological characteristics of atrioventricular reentrant tachycardia: implications
for the reentrant circuits. In Zipes DP, Jalife J (eds). Cardiac Electrophysiology. From
Cell to Bedside. Elsevier; 2004. pp. 537 –57.
23. 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.
24. Yamabe H, Shimasaki Y, Honda O, Kimura Y, Hokamura Y. Demonstration of the
exact anatomic tachycardia circuit in the fast-slow form of atrioventricular nodal
reentrant tachycardia. Circulation 2001;104:1268 –73.
25. Nawata H, Yamamoto N, Hirao K, Miyasaka N, Kawara T, Hiejima KF et al. Heterogeneity of anterograde fast-pathway and retrograde slow-pathway conduction patterns in patients with the fast-slow form of atrioventricular nodal reentrant
tachycardia: electrophysiologic and electrocardiographic considerations. J Am Coll
Cardiol 1998;32:1731 –40.
26. Nam G-B, Rhee K-S, Kim J, Choi K-J, Kim Y-H. Left atrionodal connections in typical
and atypical atrioventricular nodal re-entrant tachycardias: activation sequence in
the coronary sinus and results of radiofrequency catheter ablation. J Cardiovasc
Electrophysiol 2006;17:1 –7.
27. Hwang CMD, Goodman JS, Gang ES, Mandel WJ, Swerdlow CD, Peter CT et al.
Atypical atrioventricular node reciprocating tachycardia masquerading as tachycardia using a left-sided accessory pathway. J Am Coll Cardiol 1997;30:218 –25.
28. Katritsis DG, Giazitzoglou E, Zografos T, Ellenbogen KA, Camm AJ. An approach to
left septal slow pathway ablation. J Interv Card Electrophysiol 2011;30:73 –9.