Europace (2006) 8, 2936

doi:10.1093/europace/euj010

REVIEW

Classication and differential diagnosis of

atrioventricular nodal re-entrant tachycardia
Demosthenes G. Katritsis1,2* and A. John Camm3
1

Department of Cardiology, Athens Euroclinic, 9 Athanassiadou Street, Athens 11521, Greece; 2 Cardiothoracic Centre, St Thomas
Hospital, London, UK; and 3 Department of Cardiological Sciences, St Georges Hospital Medical School, London, UK
Received 3 March 2005; accepted after revision 21 August 2005

KEYWORDS
Atrioventricular nodal
re-entrant tachycardia

Recent evidence on atrioventricular nodal re-entrant tachycardia has identied several types of this
common arrhythmia, with potential therapeutic implications. This article reviews the relevant new
information, discusses the differential diagnosis of atrioventricular nodal re-entrant tachycardia, and
summarizes the electrophysiological criteria for classication of the various forms of the arrhythmia.

* Corresponding author. Tel: 44 210 6416600; fax: 44 210 6416661/

6819779.
E-mail address: dkatrits@otenet.gr

Diagnostic problems
Dual atrioventricular nodal conduction
Following the initial description of Denes et al. in 1973,11
the presence of dual atrioventricular nodal pathways at electrophysiological study has been a time-honoured criterion for
the diagnosis of AVNRT. It is now known that discontinuous
refractory periodic curves may not be present in all patients
with AVNRT. Antegrade dual pathways are demonstrable in
75% of patients with tachycardia,12 and AVNRT may occur
in the presence of continuous AV nodal conduction
curves.1315 Conversely, antegrade dual pathways can be
demonstrated in subjects without tachycardia.1620
In patients with the fastslow variety of AVNRT, antegrade
conduction curves are mostly not discontinuous.21,22 Retrograde stimulation curves may demonstrate a jump if the
retrograde refractory period of the fast pathway exceeds
the retrograde refractory period of the slow one. The
pattern of conduction as well as the incessant nature seen
in patients with the fastslow form of AVNRT can also be
seen in atrioventricular re-entrant tachycardia (AVRT) due
to the presence of concealed septal accessory pathways
with decremental properties.23

Retrograde atrial activation sequence

AVNRT has been traditionally classied as slowfast or
typical AVNRT, and fastslow or atypical AVNRT, according
to the conventional description of dual AV junctional pathways. The fast pathway of the re-entry circuit runs superiorly and anteriorly in the triangle of Koch, whereas the
slow pathway runs inferiorly and posteriorly close to the

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Atrioventricular nodal re-entrant tachycardia (AVNRT) results

from re-entry in the region of the AV junction,1,2 i.e. the part
of the atrioventricular-specialized conducting system consisting of the transitional cell zone, the AV node and its extensions, and the penetrating part of the bundle of His.3 Although
AVNRT represents the most common paroxysmal supraventricular arrhythmia in the human,1,4 several questions
and obscure points remain. The old model of the re-entrant
circuit comprised two anatomically distinct limbs conned
to the AV node can provide explanations for many aspects of
the electrophysiological behaviour of these tachycardias.
However, these pathways have not been demonstrated histologically and, despite several attempts to provide a reasonable model based on anatomic or functional anisotropic
characteristics,510 the exact circuit responsible for the
re-entrant tachycardia is unknown. Furthermore, there is
no unanimously accepted scheme for the diagnosis and classication of various AVNRT forms. Recognition of the various
types of AVNRT, however, is of clinical importance because
an anatomically guided catheter ablation technique may
now offer quick eradication of the arrhythmia. In addition,
some forms of AVNRT are associated with an increased risk
of catheter ablation-induced AV block and special care is
needed to avoid such a complication. This review discusses
the differential diagnosis of AVNRT and summarizes the proposed electrophysiological criteria for classication of the
various forms of the arrhythmia.

30

VA conduction time
Traditionally, a VA interval measured from the onset of ventricular activation on surface ECG to the earliest deection
of the atrial activation in the His bundle electrogram
,60 ms, or a VA interval measured at the high right atrium
,95 ms,34 has been considered as diagnostic for the slow
fast form of AVNRT. Retrograde AV junctional pathways
have been characterized as fast (HA interval , 100 ms),
intermediate (100200 ms), or slow (.200 ms).28 Conduction times are sensitive to autonomic changes and
isoprenaline administration that is often used during diagnostic studies. However, a septal VA interval ,70 ms is
highly suggestive of slowfast AVNRT provided, of course,
that atrial tachycardia has been excluded.35,36

Lower common pathway

The lower common pathway is dened as the conduction
path between the distal turnaround point of the antegrade
and retrograde conduction pathways of the AVNRT circuit
and the His bundle. Its presence is indicated by demonstrating that the retrograde fast pathway as well as the conduction time over it are the same during ventricular pacing and
tachycardia and that the beginning of the antegrade His
bundle potential during tachycardia and the end of the
retrograde His bundle potential during ventricular pacing
represent activation at the same site.37,38 The conduction
time over the lower common pathway has been usually
estimated by subtracting the HA interval during tachycardia

from that during ventricular pacing at the same cycle

length and considered a measurable interval in the majority
of typical AVNRT cases.37 Studies utilizing para-Hisian
pacing, however, have failed to detect evidence of a lower
common pathway in typical slowfast AVNRT, as opposed
to fastslow or slowslow AVNRT, and have actually
used the demonstration of a lower common pathway in
order to categorize AVNRT as atypical (either fastslow
or slowslow).38,39 Application of this criterion requires
recording of a retrograde His bundle electrogram during
ventricular pacing, and this is not always feasible in the
electrophysiological laboratory.

AVNRT types
Heterogeneity of both fast and slow conduction patterns has
been well described and in certain patients all types of
AVNRT may be inducible.39,40 (Figure 1). A denitive diagnosis as well as the identication of a single AVNRT type may,
therefore, not always be possible. These observations could
be considered in the context of the inferior nodal extensions
model of the AVNRT circuit. The inferior nodal extensions
are basically part of the AV node and facilitate atrial
inputs that also contain transitional cells connecting atrial
myocardium with the nodal extensions. They have been proposed as the anatomic substrate of the slow pathway.9,42,43
Recently, we have shown that extrastimuli delivered at the
left inferoparaseptal area, close to the His bundle, may
reset the AVNRT probably by engaging the left inferior
nodal extension (Figure 2).43 Thus, various AVNRT types
could be explained on the basis of variable anatomical
characteristics and orientation of these extensions.
Observations on simultaneous recording of His bundle activation from both sites of the septum during slow pathway
ablation43 as well as reports of successful slow pathway
ablation from the left septum are also in support of this
hypothesis.44,45
Considering the published evidence so far, the following
diagnostic criteria and classication of AVNRT types can be
proposed (Table 1).

Typical AVNRT
Slowfast
In the slowfast form of AVNRT, the onset of atrial activation
appears early, at the onset or just after the QRS complex
thus maintaining an atrial-His/His-atrial ratio AH/HA . 1.
In particular, an AH/HA ratio .3,25 and a VA interval
measured from the onset of ventricular activation on
surface ECG to the earliest deection of the atrial activation
in the His bundle electrogram ,60 ms, or a VA interval
measured at the high right atrium ,95 ms34 are diagnostic
of the slowfast AVNRT type. Although, typically, the earliest retrograde atrial activation is being recorded at the
His bundle electrogram, cases of posterior retrograde fast
pathways, i.e. with the earliest retrograde atrial activation
at the CS os28 have been described.

Atypical AVNRT
Fastslow
In the fastslow form of AVNRT (510% of all AVNRT cases),
retrograde atrial electrograms begin well after ventricular
activation with an AH/HA ratio ,1, indicating that

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coronary sinus ostium.6 Indeed, in the majority of slowfast

cases of AVNRT, the site of the earliest atrial activation is
close to the apex of Kochs triangle, near the AV node-His
bundle junction, i.e. anterior to the AV node.24,25 In the
fastslow form, the site of the earliest atrial activation is
usually recorded posterior to the AV node near the orice
of the coronary sinus.21,22
The recognition of the fact that AVNRT may present with
atypical retrograde atrial activation has made diagnosis of
the arrhythmia as well as classication attempts more
complicated. Previous studies have reported on a posterior
(or type B) variety of presumed slowfast AVNRT, with long
ventriculoatrial (VA) intervals and the earliest retrograde
atrial activation near the coronary sinus ostium.26,27
Posterior fast pathways have been reported in up to 6% of
patients with AVNRT28,29 and require special attention for
the avoidance of AV block when delivering radiofrequency
energy at the anatomical site of the slow pathway. These
observations should be considered in the context of the
documented multiple, heterogeneous sites of early atrial
activation, rather than a focal breakthrough site, during
the arrhythmia in the majority of patients with AVNRT.30
Eccentric retrograde atrial activation of the fastslow31,32
as well as the slowslow31,32 forms has also been reported. It
is now becoming evident that fastslow AVNRT may be of the
(usual) posterior, anterior, and middle type according to the
mapped location of the retrograde slow pathway.32 In
certain cases of fastslow or slowslow AVNRT, retrograde
activation is even suggestive of a left lateral accessory
pathway.31,33 Appropriate diagnosis in this setting is of
importance for the avoidance of prolonged procedures
with high uoroscopy times and unnecessary radiofrequency
lesions.

D.G. Katritsis and A.J. Camm

Classication and differential diagnosis of AVNRT

31

retrograde conduction is slower than antegrade conduction.22 The VA interval measured from the onset of ventricular activation on surface ECG to the earliest deection of
the atrial activation in the His bundle electrogram is
.60 ms, and in the high right atrium .100 ms.46 In the
majority of fastslow cases, the site of the earliest atrial
activation is posterior to the AV node near the orice of
the coronary sinus.47,48 However, anterior and mid-forms
of fastslow AVNRT have also been described.32
Slowslow
In the slowslow form, the AH/HA ratio is .1 but the VA
interval is .60 ms, suggesting that two slow pathways are
utilized for both anterograde and retrograde activations.31,49
Usually, but not always, the earliest atrial activation is at the
posterior septum (coronary sinus ostium).32,33 The so-called
posterior or type B AVNRT has been demonstrated in 2%
of patients with the anterior form of slowfast AVNRT.26 In
posterior tachycardia, the VA times (as measured from the
onset of ventricular activity to the onset of atrial activity
by whichever electrode recorded the earliest interval) may
be prolonged, ranging from 76 to 168 ms.26 The atrial-His/
His-atrial ratio, however, remains more than 1. It seems
that the reported cases of posterior slowfast AV junctional
re-entry tachycardia (AVJRT) may actually represent the
slowslow form.2,28

Differential diagnosis
In the presence of a narrow-QRS tachycardia, AVNRT should
be differentiated from atrial tachycardia or orthodromic
atrioventricular re-entrant tachycardia (AVRT) due to an
accessory pathway. When a wide-QRS tachycardia is encountered, antidromic AVRT should be differentiated from AVNRT
with a bystanding accessory pathway and the possibilities of
AVNRT or atrial tachycardia with aberrant conduction due to
bundle branch block should also be considered.

AVNRT vs. atrial tachycardia

Demonstration of change in AA interval when a ventricular
extrastimulus is delivered during tachycardia, tachycardia
termination by a ventricular extrastimulus that did not
conduct to the atrium, constant His-atrial interval of the
return cycle after introduction of a premature atrial
impulse with a wide range of coupling intervals during
tachycardia, and demonstration of ventricle to atrium to
His sequence during retrograde initiation of tachycardia
indicate aetiology other than atrial tachycardia.5052 In
particular, the atrial response upon cessation of ventricular
pacing associated with 1:1 VA conduction during tachycardia
can distinguish between atrial tachycardia and AVNRT or
AVRT. Atrial tachycardia is associated with an A-A-V response
whereas AVNRT or AVRT produce an A-V response.52 This rule

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Figure 1 Anterior slowfast AVNRT (left) and slowslow AVNRT (right) with alternating retrograde conduction intervals. This recording was obtained during slow
pathway ablation and indicates AVNRT circuits alternatively using two different pathways in the retrograde direction. Reproduced from Katritsis et al. 41 with kind
permission. V1: ECG lead, HRA: high right atrium, His: His bundle, Pol: ablating catheter, DCS: distal coronary sinus, PCS: proximal coronary sinus.

32

D.G. Katritsis and A.J. Camm

Table 1 Classication of AVNRT types

Typical AVNRT
Slowfast
Atypical AVNRT
Fastslow
Slowslow

AH/HA

VA (His) (ms)

Usual ERAAa

.1

,60

His

Finally, the difference of the post-pacing interval and the

tachycardia cycle length (PPITCL interval) as described by
Michaud et al.,46 may also be of help.

AVNRT vs. AVRT due to septal accessory pathways

,1
.1

.60
.60

CS os/LRAS
CS os/LRAS

AH, atrial to His interval; HA, His to atrium interval; VA, interval
measured from the onset of ventricular activation on surface ECG to
the earliest deection of the atrial activation in the His bundle electrogram; ERAA, earliest retrograde atrial activation; CS os, ostium of the
coronary sinus.
a
Variable earliest retrograde atrial activation has been described for all
types.

does not always hold in the presence of a long HV interval.53

The His deection should also be considered in this respect,
since a late V electrogram might give an apparent AAV
response that is actually AH/AV response in the presence
AVNRT or AVRT, as opposed to an AA/HV one in the presence
of atrial tachycardia.53,54 The difference in the AH interval
between atrial pacing and the tachycardia may also allow
differentiation of atypical AVNRT from other types of long
RP tachycardias. A DAH . 40 ms indicates AVNRT, whereas
in patients with AVRT due to septal pathways or atrial tachycardia these differences are ,20 and 10 ms, respectively.50

The eccentric retrograde atrial activation during ventricular

stimulation or tachycardia and the demonstration of continuous AV or VA conduction curves usually characterizing
non-septal concealed accessory pathways differentiate this
form of atrioventricular re-entry from AVNRT. However,
AVNRT is now known to occur with eccentric atrial activation
and, in addition, decremental septal pathways may mimic
AVNRT especially of the fastslow or slowslow forms.
Septal pathways may have the property of decremental conduction and normal atrial retrograde activation during
tachycardia.55

ECG criteria
In case of relatively delayed retrograde conduction that
allows the identication of retrograde P waves, ECG criteria
can be applied for diagnosis. The presence of a pseudo-r0
wave in lead V1 or a pseudo-S wave in leads II, III, and aVF
has been reported to indicate anterior AVNRT with an accuracy of 100%. A difference of .20 ms in RP intervals in leads
V1 and III was indicative of posterior AVNRT rather than AVRT
due to a posteroseptal pathway.56

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Figure 2 Resetting of slowfast AVNRT. The tachycardia cycle length is 370 ms. An atrial extrastimuli is delivered from the left inferoparaseptal area very close
to the His area, 360 ms following the His bundle activation, and results in resetting of the next His bundle and RIPS electrograms by 20 ms. I and II: ECG leads,
LIPS: left inferoparaseptal area, RIPS: right inferoparaseptal area, His: His bundle, CS: coronary sinus.

Classication and differential diagnosis of AVNRT

Development of AV block or bundle branch block

The documentation of pre-excited beats as well as AV dissociation and the induction of bundle branch block during
tachycardia may assist the differential diagnosis. The demonstration of AV block or AV dissociation during tachycardia
is characteristic of AVNRT excluding the presence of an
accessory pathway.57,58 Similarly, the development of
bundle branch block either spontaneously or after introduction of ventricular extrastimuli during AVNRT does not
change the AA or HH intervals. A signicant change in the
VA interval with the development of bundle branch block
is diagnostic of orthodromic AVRT and localizes the
pathway to the same side as the block.59

preceded atrial activation, but such a coincidence is rare.

In addition, at the time of His bundle activation the accessory pathway may be refractory and resetting by ventricular
extrastimuli may not be seen. Thus, resetting or termination
of the tachycardia with His-refractory ventricular extrastimuli is specic but not a highly sensitive criterion for
differential diagnosis.
AH conduction
The difference in the AH interval between atrial pacing and
the tachycardia may allow differentiation of atypical AVNRT
from other types of long RP0 tachycardias. A DAH . 40 ms
has been reported to indicate AVNRT, whereas in patients
with AVRT due to septal pathways or atrial tachycardia
these differences were ,20 and 10 ms, respectively.50
VA conduction indices
Using ventricular-induced atrial pre-excitation, Miles
et al. 62 devised a pre-excitation index for the differentiation of AVNRT and AVRT using an accessory pathway.
Progressively premature right ventricular extrastimuli
were introduced during tachycardia and the difference
between the TCL and the longest stimulation interval at
which atrial pre-excitation occurred dened the preexcitation index. A pre-excitation index of 100 ms or
greater characterized AVJRT, whereas an index less than
45 ms characterized AVRT using a septal pathway. In
another report of 16 patients with AVNRT and 23 patients

Figure 3 Absence of resetting of slowfast AVNRT by His-synchronous ventricular extrastimuli. The tachycardia cycle length is 424 ms. At 380 ms following the
His bundle electrogram, a ventricular extrastimulus is delivered at a time when the His bundle is expected to be refractory and fails to reset the next atrial
electrogram. I and II: ECG leads, LRA: low right atrium, His: His bundle, CS: coronary sinus.

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His-synchronous ventricular extrastimulation

In the presence of septal decremental pathways, ventricular
extrastimuli introduced whereas the His bundle is refractory
during tachycardia (i.e. delivered coincident with the His
potential or up to 50 ms before this) may advance or delay
subsequent atrial activation (extranodal capture).60 In
AVNRT, atrial activity is not perturbed with His-synchronous
ventricular extrastimulation (Figure 3). Failure to reset the
atria suggests, but does not prove, that an accessory
pathway is not present or that it is relatively far from the
site of premature stimulation.61 Theoretically, it is possible that resetting of the atrium might be a result of an
increase in conduction time over such a pathway of a magnitude equal to the interval by which the extrastimulus

33

34

with AVRT studied at St Georges Hospital in London, the

ratio between the minimum VA interval during tachycardia
and ventricular pacing was 0.320.27 in AVNRT, 0.911.08
in AVRT using a posteroseptal pathway, and 0.941.29 in
AVRT using an anteroseptal pathway.35 A difference in the
VA interval during tachycardia and right apical ventricular
pacing .90 ms has also been reported to differentiate
patients with AVNRT from those with AVRT.63 The difference
between the VA interval obtained during apical pacing and
that obtained during posterobasal pacing (VA index) can
also discriminate between patients with posteroseptal
pathways (.10 ms) and patients with nodal retrograde
conduction (,5 ms).64

Tachycardia resetting criteria

Right apical stimulation is relatively close to the insertion of
a septal accessory pathway as opposed to the AV junction.
Thus, ventricular fusion during resetting or entrainment of
tachycardia has been reported to occur in patients with
AVRT due to septal pathways but not with AVNRT.67
Michaud et al. 46 have proposed two additional criteria for
differential diagnosis. The VA interval and total cycle
length (TCL) were measured during tachycardia, and
entrainment of the tachycardia was accomplished with
right apical ventricular pacing. The intervals between the
last ventricular pacing stimulus and the last entrained
atrial depolarization during tachycardia (SA) as well as the
PPI were considered. All patients with AVNRT had SAVA
intervals .85 ms and PPITCL intervals .114 ms.46
It should be noted that in clinical practice, pacing or other
manoeuvres cannot be applied to all cases and multiple criteria have to be used for the differential diagnosis of narrow
complex tachycardias with atypical characteristics.36

AVNRT with bystanding accessory pathway vs.

antidromic AVRT
Antidromic AVRT, i.e. tachycardia using the accessory
pathway for antegrade conduction and the AV node for
retrograde conduction, may be induced in 6% of patients
with accessory pathways located in the left or right free
wall, or the anterior septum at an adequate distance from

the AV node.68 In some cases, atrioventricular junctional

re-entry may be the underlying mechanism of the preexcited tachycardia and the possibility of AVJRT conducting
over a bystanding accessory pathway should be considered
in the presence of transition from narrow to wide
complex tachycardia of a similar cycle length and without
disturbing the HH intervals.69 In this case, atrial extrastimuli fail to induce advancement of the following preexcited QRS complex, the next retrograde His bundle
deection where apparent, and the subsequent atrial
deection, as may happen in the presence of a macro-reentrant loop.70

AVNRT vs. non-paroxysmal AV junctional

tachycardia and focal junctional tachycardia
Non-paroxysmal junctional tachycardia was frequently diagnosed in the past as a junctional rhythm of gradual onset and
termination with a rate between 70 and 130 b.p.m., and was
considered a typical example of digitalis-induced arrhythmias.71 It may also occur in patients with underlying heart
disease such as myocardial infarction, or after open heart
surgery, and, very rarely, even in apparently normal
persons.72,73 Although these tachycardias can be induced
by atrial ectopics or atrial pacing, they are not re-entrant;
most cases, especially the digitalis-induced, are caused by
delayed after-depolarizations and triggered activity in the
AV node.74
Focal junctional tachycardia, also called automatic
junctional tachycardia, junctional ectopic tachycardias,
and His bundle tachycardia, may occur as a congenital
arrhythmia or early after infant open heart surgery.75,76
Diagnosis is made on the ECG which shows a narrow QRS
tachycardia with slower and dissociated P waves. At electrophysiological study, there are normal HV intervals and
normal AV conduction curves.77,78 In adult patients, this
tachycardia is associated with a structurally normal heart
and the prognosis is usually benign.79 The usual electrocardiographic nding is a narrow QRS tachycardia with AV dissociation. Occasionally, the tachycardia might be irregular
thus resembling atrial brillation. In the electrophysiological laboratory, the arrhythmia is not inducible by
programmed electrical stimulation but is sensitive to isoprenaline administration, and in some cases, rapid atrial
or ventricular pacing may result in tachycardia induction.
During tachycardia, there is a normal or increased HV
interval with atrioventricular dissociation that is interrupted
by frequent episodes of VA conduction with the earliest
atrial activation in the posteroseptal, anteroseptal, or midseptal regions. At times, the mode of tachycardia induction
resembles a double AV nodal response that is characteristic
of AVNRT.75

Conclusions
(i) Recent evidence has identied several types of AVNRT
which is the most common paroxysmal supraventricular arrhythmia in the human.
(ii) AVNRT types are classied as typical (slowfast) and
atypical (fastslow and slowslow), according to the
ratio of atrial-His/His-atrial intervals, the VA interval
measured on the His bundle and high right atrial electrograms, and the site of the earliest retrograde

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Retrograde conduction (HA)

Miller et al. 65 found the His to atrial (HA) intervals to offer
more precise discrimination. Their criterion is the difference
between His to atrial intervals during pacing and during
tachycardia (DHA). In 84 patients, a retrograde His was
present in 93% of them and the DHA was .0 ms in AVNRT
and ,227 ms in orthodromic AVRT incorporating a septal
accessory pathway. Thus an intermediate value of
DHA 210 ms had 100% sensitivity, specicity, and predictive accuracy in differentiating the two forms of tachycardia. Para-Hisian pacing and the change in timing and
sequence of retrograde atrial activation between His and
proximal right bundle branch capture and non-capture
have also been used for differentiation between AV nodal
and septal pathway retrograde conductions.66 The response
is considered extranodal when the retrograde atrial
activation during His bundle capture is the same as during
ventricular capture without His bundle capture. These techniques, however, require recording of both antegrade and
retrograde His bundle activations.

D.G. Katritsis and A.J. Camm

Classication and differential diagnosis of AVNRT

atrial activation. However, variable sites of retrograde

atrial activation have been described for all types of
this arrhythmia.
(iii) Several electrocardiographic and electrophysiological
criteria have been used for differential diagnosis of
AVNRT vs. atrial tachycardia, AVNRT vs. AVRT due to
a septal accessory pathway, AVNRT with bystanding
accessory pathway vs. antidromic AVRT, and AVNRT
vs. non-paroxysmal junctional tachycardia and focal
junctional tachycardia. In clinical practice, not all
proposed manoeuvres can be universally applied and
multiple criteria have to be used for the differential
diagnosis of narrow complex tachycardias with
atypical characteristics.

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