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    REVIEW

    Classification and differential diagnosis of

    atrioventricular nodal re-entrant tachycardia

    Demosthenes G. Katritsis1,2*and A. John Camm3

    1Department of Cardiology, AthensEuroclinic, 9 AthanassiadouStreet,Athens 11521,Greece;2 Cardiothoracic Centre, St Thomas

    Hospital, London, UK; and 3Department of Cardiological Sciences, St Georges Hospital Medical School, London, UK

    Received 3 March 2005; accepted after revision 21 August 2005

    Recent evidence on atrioventricular nodal re-entrant tachycardia has identified several types of thiscommon arrhythmia, with potential therapeutic implications. This article reviews the relevant newinformation, discusses the differential diagnosis of atrioventricular nodal re-entrant tachycardia, andsummarizes the electrophysiological criteria for classification of the various forms of the arrhythmia.

    KEYWORDSAtrioventricular nodal

    re-entrant tachycardia

    Atrioventricular nodal re-entrant tachycardia (AVNRT) resultsfrom re-entry in the region of the AV junction,1,2 i.e. the partof the atrioventricular-specialized conducting system con-sisting of the transitional cell zone, the AV node and its exten-sions,and thepenetrating part of thebundle of His.3 Although

    AVNRT represents the most common paroxysmal supra-ventricular arrhythmia in the human,1,4 several questionsand obscure points remain. The old model of the re-entrantcircuit comprised two anatomically distinct limbs confinedto the AV node can provide explanations for many aspects ofthe electrophysiological behaviour of these tachycardias.However, these pathways have not been demonstrated histo-logically and, despite several attempts to provide a reason-able model based on anatomic or functional anisotropiccharacteristics,510 the exact circuit responsible for there-entrant tachycardia is unknown. Furthermore, there isno unanimously accepted scheme for the diagnosis and clas-sification of various AVNRT forms. Recognition of the varioustypes of AVNRT, however, is of clinical importance because

    an anatomically guided catheter ablation technique maynow offer quick eradication of the arrhythmia. In addition,some forms of AVNRT are associated with an increased riskof catheter ablation-induced AV block and special care isneeded to avoid such a complication. This review discussesthe differential diagnosis of AVNRT and summarizes the pro-posed electrophysiological criteria for classification of thevarious forms of the arrhythmia.

    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 elec-

    trophysiological study has been a time-honoured criterion forthe diagnosis of AVNRT. It is now known that discontinuousrefractory periodic curves may not be present in all patientswith AVNRT. Antegrade dual pathways are demonstrable in75% of patients with tachycardia,12 and AVNRT may occurin the presence of continuous AV nodal conductioncurves.1315 Conversely, antegrade dual pathways can bedemonstrated in subjects without tachycardia.1620

    In patients with the fastslow variety of AVNRT, antegradeconduction curves are mostly not discontinuous.21,22 Retro-grade stimulation curves may demonstrate a jump if theretrograde refractory period of the fast pathway exceedsthe retrograde refractory period of the slow one. Thepattern of conduction as well as the incessant nature seen

    in patients with the fast

    slow form of AVNRT can also beseen in atrioventricular re-entrant tachycardia (AVRT) dueto the presence of concealed septal accessory pathwayswith decremental properties.23

    Retrograde atrial activation sequence

    AVNRT has been traditionally classified as slowfast ortypical AVNRT, and fastslow or atypical AVNRT, accordingto the conventional description of dual AV junctional path-ways. The fast pathway of the re-entry circuit runs super-iorly and anteriorly in the triangle of Koch, whereas theslow pathway runs inferiorly and posteriorly close to the

    & The European Society of Cardiology 2006. All rights reserved. For Permissions, please e-mail: [email protected]

    * Corresponding author. Tel: 44 210 6416600; fax: 44 210 6416661/6819779.

    E-mail address: [email protected]

    Europace (2006) 8, 2936

    doi:10.1093/europace/euj010

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    coronary sinus ostium.6 Indeed, in the majority of slowfastcases of AVNRT, the site of the earliest atrial activation isclose to the apex of Kochs triangle, near the AV node-Hisbundle junction, i.e. anterior to the AV node.24,25 In thefastslow form, the site of the earliest atrial activation isusually recorded posterior to the AV node near the orificeof the coronary sinus.21,22

    The recognition of the fact that AVNRT may present with

    atypical retrograde atrial activation has made diagnosis ofthe arrhythmia as well as classification attempts morecomplicated. Previous studies have reported on a posterior(or type B) variety of presumed slowfast AVNRT, with longventriculoatrial (VA) intervals and the earliest retrogradeatrial activation near the coronary sinus ostium.26,27

    Posterior fast pathways have been reported in up to 6% ofpatients with AVNRT28,29 and require special attention forthe avoidance of AV block when delivering radiofrequencyenergy at the anatomical site of the slow pathway. Theseobservations should be considered in the context of thedocumented multiple, heterogeneous sites of early atrialactivation, 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. Itis now becoming evident that fastslow AVNRT may be of the(usual) posterior, anterior, and middle type according to themapped location of the retrograde slow pathway.32 Incertain cases of fastslow or slowslow AVNRT, retrogradeactivation is even suggestive of a left lateral accessorypathway.31,33 Appropriate diagnosis in this setting is ofimportance for the avoidance of prolonged procedureswith high fluoroscopy times and unnecessary radiofrequencylesions.

    VA conduction time

    Traditionally, a VA interval measured from the onset of ven-tricular activation on surface ECG to the earliest deflectionof 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 slowfast form of AVNRT. Retrograde AV junctional pathwayshave been characterized as fast (HA interval , 100 ms),intermediate (100200 ms), or slow (.200 ms).28 Con-duction times are sensitive to autonomic changes andisoprenaline administration that is often used during diag-nostic studies. However, a septal VA interval ,70 ms ishighly suggestive of slowfast AVNRT provided, of course,that atrial tachycardia has been excluded.35,36

    Lower common pathway

    The lower common pathway is defined as the conductionpath between the distal turnaround point of the antegradeand retrograde conduction pathways of the AVNRT circuitand the His bundle. Its presence is indicated by demonstrat-ing that the retrograde fast pathway as well as the conduc-tion time over it are the same during ventricular pacing andtachycardia and that the beginning of the antegrade Hisbundle potential during tachycardia and the end of theretrograde His bundle potential during ventricular pacingrepresent activation at the same site.37,38 The conductiontime over the lower common pathway has been usually

    estimated by subtracting the HA interval during tachycardia

    from that during ventricular pacing at the same cyclelength and considered a measurable interval in the majorityof typical AVNRT cases.37 Studies utilizing para-Hisianpacing, however, have failed to detect evidence of a lowercommon pathway in typical slowfast AVNRT, as opposedto fastslow or slowslow AVNRT, and have actuallyused the demonstration of a lower common pathway inorder to categorize AVNRT as atypical (either fastslow

    or slow

    slow).38,39 Application of this criterion requiresrecording of a retrograde His bundle electrogram duringventricular pacing, and this is not always feasible in theelectrophysiological laboratory.

    AVNRT types

    Heterogeneity of both fast and slow conduction patterns hasbeen well described and in certain patients all types ofAVNRT may be inducible.39,40 (Figure 1). A definitive diagno-sis as well as the identification of a single AVNRT type may,therefore, not always be possible. These observations couldbe considered in the context of the inferior nodal extensions

    model of the AVNRT circuit. The inferior nodal extensionsare basically part of the AV node and facilitate atrialinputs that also contain transitional cells connecting atrialmyocardium with the nodal extensions. They have been pro-posed as the anatomic substrate of the slow pathway.9,42,43

    Recently, we have shown that extrastimuli delivered at theleft inferoparaseptal area, close to the His bundle, mayreset the AVNRT probably by engaging the left inferiornodal extension (Figure 2).43 Thus, various AVNRT typescould be explained on the basis of variable anatomicalcharacteristics and orientation of these extensions.Observations on simultaneous recording of His bundle acti-vation from both sites of the septum during slow pathwayablation43 as well as reports of successful slow pathway

    ablation from the left septum are also in support of thishypothesis.44,45

    Considering the published evidence so far, the followingdiagnostic criteria and classification of AVNRT types can beproposed (Table 1).

    Typical AVNRT

    Slowfast

    In theslowfast formof AVNRT, the onset of atrial activationappears early, at the onset or just after the QRS complexthus maintaining an atrial-His/His-atrial ratio AH/HA . 1.In particular, an AH/HA ratio .3,25 and a VA intervalmeasured from the onset of ventricular activation on

    surface ECG to the earliest deflection of the atrial activationin the His bundle electrogram ,60 ms, or a VA intervalmeasured at the high right atrium ,95 ms34 are diagnosticof the slowfast AVNRT type. Although, typically, the ear-liest retrograde atrial activation is being recorded at theHis bundle electrogram, cases of posterior retrograde fastpathways, i.e. with the earliest retrograde atrial activationat the CS os28 have been described.

    Atypical AVNRT

    Fastslow

    In thefastslow formof AVNRT (510% of all AVNRT cases),retrograde atrial electrograms begin well after ventricular

    activation with an AH/HA ratio ,1, indicating that

    30 D.G. Katritsis and A.J. Camm

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    retrograde conduction is slower than antegrade conduc-tion.22 The VA interval measured from the onset of ventricu-lar activation on surface ECG to the earliest deflection ofthe atrial activation in the His bundle electrogram is.60 ms, and in the high right atrium .100 ms.46 In themajority of fastslow cases, the site of the earliest atrialactivation is posterior to the AV node near the orifice ofthe coronary sinus.47,48 However, anterior and mid-formsof fastslow AVNRT have also been described.32

    Slowslow

    In the slowslow form, the AH/HA ratio is .1 but the VAinterval is .60 ms, suggesting that two slow pathways areutilized for both anterograde and retrograde activations.31,49

    Usually, but not always, the earliest atrial activation is at theposterior 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 Inposterior tachycardia, the VA times (as measured from theonset of ventricular activity to the onset of atrial activityby whichever electrode recorded the earliest interval) maybe prolonged, ranging from 76 to 168 ms.26 The atrial-His/His-atrial ratio, however, remains more than 1. It seemsthat the reported cases of posterior slowfast AV junctionalre-entry tachycardia (AVJRT) may actually represent the

    slow

    slow form.2,28

    Differential diagnosis

    In the presence of a narrow-QRS tachycardia, AVNRT shouldbe differentiated from atrial tachycardia or orthodromicatrioventricular re-entrant tachycardia (AVRT) due to anaccessory pathway. When a wide-QRS tachycardia is encoun-tered, antidromic AVRTshould be differentiated from AVNRTwith a bystanding accessory pathway and the possibilities ofAVNRT or atrial tachycardia with aberrant conduction due tobundle branch block should also be considered.

    AVNRT vs. atrial tachycardia

    Demonstration of change in AA interval when a ventricularextrastimulus is delivered during tachycardia, tachycardiatermination by a ventricular extrastimulus that did notconduct to the atrium, constant His-atrial interval of thereturn cycle after introduction of a premature atrialimpulse with a wide range of coupling intervals duringtachycardia, and demonstration of ventricle to atrium toHis sequence during retrograde initiation of tachycardiaindicate aetiology other than atrial tachycardia.5052 Inparticular, the atrial response upon cessation of ventricularpacing associated with 1:1 VA conduction during tachycardiacan distinguish between atrial tachycardia and AVNRT orAVRT. Atrial tachycardia is associated with an A-A-V response

    whereas AVNRT or AVRT produce an A-V response.52

    This rule

    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 AVNRTcircuits 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.

    Classification and differential diagnosis of AVNRT 31

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

    The His deflection should also be considered in this respect,since a late V electrogram might give an apparent AAVresponse that is actually AH/AV response in the presenceAVNRT or AVRT, as opposed to an AA/HV one in the presenceof atrial tachycardia.53,54 The difference in the AH intervalbetween atrial pacing and the tachycardia may also allowdifferentiation of atypical AVNRT from other types of longRP tachycardias. A DAH . 40 ms indicates AVNRT, whereasin patients with AVRT due to septal pathways or atrial tachy-

    cardia these differences are ,20 and 10 ms, respectively.50

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

    tachycardia cycle length (PPI

    TCL interval) as described byMichaud et al.,46 may also be of help.

    AVNRT vs. AVRT due to septal accessory pathways

    The eccentric retrograde atrial activation during ventricularstimulation or tachycardia and the demonstration of con-tinuous AV or VA conduction curves usually characterizingnon-septal concealed accessory pathways differentiate thisform of atrioventricular re-entry from AVNRT. However,AVNRT is now known to occur with eccentric atrial activationand, in addition, decremental septal pathways may mimicAVNRT especially of the fastslow or slowslow forms.Septal pathways may have the property of decremental con-duction and normal atrial retrograde activation duringtachycardia.55

    ECG criteria

    In case of relatively delayed retrograde conduction thatallows the identification of retrograde P waves, ECG criteriacan be applied for diagnosis. The presence of a pseudo-r0

    wave in lead V1 or a pseudo-S wave in leads II, III, and aVFhas been reported to indicate anterior AVNRT with an accu-racy of 100%. A difference of.20 ms in RP intervals in leadsV1 and III was indicative of posterior AVNRTrather than AVRT

    due to a posteroseptal pathway.56

    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.

    Table 1 Classification of AVNRT types

    AH/HA VA (His) (ms) Usual ERAAa

    Typical AVNRTSlowfast .1 ,60 His

    Atypical AVNRTFastslow ,1 .60 CS os/LRASSlowslow .1 .60 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 deflection of the atrial activation in the His bundle electro-

    gram; ERAA, earliest retrograde atrial activation; CS os, ostium of the

    coronary sinus.aVariable earliest retrograde atrial activation has been described for all

    types.

    32 D.G. Katritsis and A.J. Camm

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    Development of AV block or bundle branch block

    The documentation of pre-excited beats as well as AV dis-sociation and the induction of bundle branch block duringtachycardia may assist the differential diagnosis. The dem-onstration of AV block or AV dissociation during tachycardiais characteristic of AVNRT excluding the presence of anaccessory pathway.57,58 Similarly, the development ofbundle branch block either spontaneously or after introduc-

    tion of ventricular extrastimuli during AVNRT does notchange the AA or HH intervals. A significant change in theVA interval with the development of bundle branch blockis diagnostic of orthodromic AVRT and localizes thepathway to the same side as the block.59

    His-synchronous ventricular extrastimulation

    In the presence of septal decremental pathways, ventricularextrastimuli introduced whereas the His bundle is refractoryduring tachycardia (i.e. delivered coincident with the Hispotential or up to 50 ms before this) may advance or delaysubsequent atrial activation (extranodal capture).60 InAVNRT, atrial activity is not perturbed with His-synchronousventricular extrastimulation (Figure 3). Failure to reset theatria suggests, but does not prove, that an accessorypathway is not present or that it is relatively far from thesite of premature stimulation.61 Theoretically, it is possi-ble that resetting of the atrium might be a result of anincrease in conduction time over such a pathway of a mag-nitude equal to the interval by which the extrastimulus

    preceded atrial activation, but such a coincidence is rare.In addition, at the time of His bundle activation the acces-sory pathway may be refractory and resetting by ventricularextrastimuli may not be seen. Thus, resetting or terminationof the tachycardia with His-refractory ventricular extra-stimuli is specific but not a highly sensitive criterion fordifferential diagnosis.

    AH conduction

    The difference in the AH interval between atrial pacing andthe tachycardia may allow differentiation of atypical AVNRTfrom other types of long RP0 tachycardias. A DAH . 40 mshas been reported to indicate AVNRT, whereas in patientswith AVRT due to septal pathways or atrial tachycardiathese differences were ,20 and 10 ms, respectively.50

    VA conduction indices

    Using ventricular-induced atrial pre-excitation, Mileset al.62 devised a pre-excitation index for the differen-tiation of AVNRT and AVRT using an accessory pathway.Progressively premature right ventricular extrastimuliwere introduced during tachycardia and the differencebetween the TCL and the longest stimulation interval atwhich atrial pre-excitation occurred defined the pre-excitation index. A pre-excitation index of 100 ms orgreater characterized AVJRT, whereas an index less than45 ms characterized AVRT using a septal pathway. Inanother 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.

    Classification and differential diagnosis of AVNRT 33

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    with AVRT studied at St Georges Hospital in London, theratio between the minimum VA interval during tachycardiaand ventricular pacing was 0.320.27 in AVNRT, 0.911.08in AVRT using a posteroseptal pathway, and 0.941.29 inAVRT using an anteroseptal pathway.35 A difference in theVA interval during tachycardia and right apical ventricularpacing .90 ms has also been reported to differentiatepatients with AVNRT from those with AVRT.63 The difference

    between the VA interval obtained during apical pacing andthat obtained during posterobasal pacing (VA index) canalso discriminate between patients with posteroseptalpathways (.10 ms) and patients with nodal retrogradeconduction (,5 ms).64

    Retrograde conduction (HA)

    Miller et al.65 found the His to atrial (HA) intervals to offermore precise discrimination. Their criterion is the differencebetween His to atrial intervals during pacing and duringtachycardia (DHA). In 84 patients, a retrograde His waspresent in 93% of them and the DHA was .0 ms in AVNRTand ,227 ms in orthodromic AVRT incorporating a septal

    accessory pathway. Thus an intermediate value ofDHA 210 ms had 100% sensitivity, specificity, and predic-tive accuracy in differentiating the two forms of tachy-cardia. Para-Hisian pacing and the change in timing andsequence of retrograde atrial activation between His andproximal right bundle branch capture and non-capturehave also been used for differentiation between AV nodaland septal pathway retrograde conductions.66 The responseis considered extranodal when the retrograde atrialactivation during His bundle capture is the same as duringventricular capture without His bundle capture. These tech-niques, however, require recording of both antegrade andretrograde His bundle activations.

    Tachycardia resetting criteria

    Right apical stimulation is relatively close to the insertion ofa septal accessory pathway as opposed to the AV junction.Thus, ventricular fusion during resetting or entrainment oftachycardia has been reported to occur in patients withAVRT due to septal pathways but not with AVNRT.67

    Michaud et al.46 have proposed two additional criteria fordifferential diagnosis. The VA interval and total cyclelength (TCL) were measured during tachycardia, andentrainment of the tachycardia was accomplished withright apical ventricular pacing. The intervals between thelast ventricular pacing stimulus and the last entrainedatrial depolarization during tachycardia (SA) as well as the

    PPI were considered. All patients with AVNRT had SA

    VAintervals .85 ms and PPITCL intervals .114 ms.46

    It should be noted that in clinical practice, pacing or othermanoeuvres cannot be applied to all cases and multiple cri-teria have to be used for the differential diagnosis of narrowcomplex tachycardias with atypical characteristics.36

    AVNRT with bystanding accessory pathway vs.antidromic AVRT

    Antidromic AVRT, i.e. tachycardia using the accessorypathway for antegrade conduction and the AV node forretrograde conduction, may be induced in 6% of patientswith 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 junctionalre-entry may be the underlying mechanism of the pre-excited tachycardia and the possibility of AVJRT conductingover a bystanding accessory pathway should be consideredin the presence of transition from narrow to widecomplex tachycardia of a similar cycle length and withoutdisturbing the HH intervals.69 In this case, atrial extra-stimuli fail to induce advancement of the following pre-

    excited QRS complex, the next retrograde His bundledeflection where apparent, and the subsequent atrialdeflection, as may happen in the presence of a macro-re-entrant loop.70

    AVNRT vs. non-paroxysmal AV junctionaltachycardia and focal junctional tachycardia

    Non-paroxysmal junctional tachycardia was frequently diag-nosed in the past as a junctional rhythm of gradual onset andtermination with a rate between 70 and 130 b.p.m., and wasconsidered a typical example of digitalis-induced arrhyth-mias.71 It may also occur in patients with underlying heartdisease such as myocardial infarction, or after open heartsurgery, and, very rarely, even in apparently normalpersons.72,73 Although these tachycardias can be inducedby atrial ectopics or atrial pacing, they are not re-entrant;most cases, especially the digitalis-induced, are caused bydelayed after-depolarizations and triggered activity in theAV node.74

    Focal junctional tachycardia, also called automaticjunctional tachycardia, junctional ectopic tachycardias,and His bundle tachycardia, may occur as a congenitalarrhythmia or early after infant open heart surgery.75,76

    Diagnosis is made on the ECG which shows a narrow QRStachycardia with slower and dissociated P waves. At electro-physiological study, there are normal HV intervals and

    normal AV conduction curves.77,78

    In adult patients, thistachycardia is associated with a structurally normal heartand the prognosis is usually benign.79 The usual electrocar-diographic finding is a narrow QRS tachycardia with AV dis-sociation. Occasionally, the tachycardia might be irregularthus resembling atrial fibrillation. In the electrophysio-logical laboratory, the arrhythmia is not inducible byprogrammed electrical stimulation but is sensitive to iso-prenaline administration, and in some cases, rapid atrialor ventricular pacing may result in tachycardia induction.During tachycardia, there is a normal or increased HVinterval with atrioventricular dissociation that is interruptedby frequent episodes of VA conduction with the earliestatrial activation in the posteroseptal, anteroseptal, or mid-

    septal regions. At times, the mode of tachycardia inductionresembles a double AV nodal response that is characteristicof AVNRT.75

    Conclusions

    (i) Recent evidence has identified several types of AVNRTwhich is the most common paroxysmal supraventricu-lar arrhythmia in the human.

    (ii) AVNRT types are classified as typical (slowfast) andatypical (fastslow and slowslow), according to theratio of atrial-His/His-atrial intervals, the VA intervalmeasured on the His bundle and high right atrial elec-

    trograms, and the site of the earliest retrograde

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    atrial activation. However, variable sites of retrogradeatrial activation have been described for all types ofthis arrhythmia.

    (iii) Several electrocardiographic and electrophysiologicalcriteria have been used for differential diagnosis ofAVNRT vs. atrial tachycardia, AVNRT vs. AVRT due toa septal accessory pathway, AVNRT with bystandingaccessory pathway vs. antidromic AVRT, and AVNRT

    vs. non-paroxysmal junctional tachycardia and focaljunctional tachycardia. In clinical practice, not allproposed manoeuvres can be universally applied andmultiple criteria have to be used for the differentialdiagnosis of narrow complex tachycardias withatypical characteristics.

    References

    1. Josephson ME, Wellens HJ. Electrophysiologic evaluation of supraventri-

    cular tachycardia. Cardiol Clin 1997;15:567586.

    2. Lockwood D, Otomo K, Wang Z, Forresti S, Nakagawa H, Beckman K,

    Scherlag B, Patterson E, Lazarra R, Jackman WM. Electrophysiologic

    characteristics of atrioventricular nodal reentrant tachycardia: impli-

    cations for the reentrant circuits. In: Zipes DP and Jalife, J, eds.Cardiac Electrophysiology: From Cell to Bedside. 3rd ed. Philadelphia,

    PA: W.B. Saunders Company; 2004. p537557.

    3. Becker AE, Anderson RH. Morphology of the human atrioventricular junc-

    tional area. In: Wellens HJJ, Lie KI, Janse MJ, eds. The Conduction

    System of the Heart: Structure, Function and Clinical Implications.

    Leiden: HE Stenfert Kroese BV; 1976. p263286.

    4. Camm AJ, Katritsis D. The diagnosis of tachyarrhythmias. In Julian DG,

    Camm AJ, Fox KM, Hall RJC, Poole-Wilson PA, eds. Heart Disease. 2nd

    ed. Philadelphia, PA, USA: Saunders; 1996. p66066621.

    5. Wu D, Yeh S-J, Wang C-C, Wen M-S, Chang H-J, Lin F-C. Nature of dual

    atrioventricular node pathways and the tachycardia circuit as defined

    by radiofrequency ablation technique. J Am Coll Cardiol 1992;

    20:884895.

    6. Keim S, Werner P, Jazayeri M, Akhtar M, Tchou P. Localization of the fast

    and slow pathways in atrioventricular nodal reentrant tachycardia by

    intraoperative ice mapping. Circulation 1992;86:919925.

    7. Spach MS, Josephson ME. Initiating reentry: the role of nonuniform aniso-tropy in small circuits. J Cardiovasc Electrophysiol 1994;5:182209.

    8. Patterson E, Scherlag BJ. Anatomic and functional fast atrioventricular

    conduction pathway. J Cardiovasc Electrophysiol 2002;13:945949.

    9. Katritsis DG, Becker AE, Ellenbogen KA, Giazitzoglou E, Korovesis S,

    Camm AJ. The right and left inferior extensions of the atrioventricular

    node may represent the anatomic substrate of the slow pathway in the

    human.Heart Rhythm 2004;1:582586.

    10. Kwaku KF, Josephson ME. Typical AVNRT: an update on mechanisms and

    therapy. Cardiac Electrophysiol Rev2002;6:414421.

    11. Denes P, Wu D, Dhingra RC, Chuquimia R, Rosen KM. Demonstration of

    dual AV nodal pathways in patients with paroxysmal supraventricular

    tachycardia.Circulation 1973;48:549555.

    12. Josephson ME, Kastor JA. Supraventricular tachycardia: mechanisms and

    management.Ann Intern Med1977;87:346358.

    13. Tai CT, Chen SA, Chiang CE et al.Complex electrophysiological character-

    istics in atrioventricular nodal re-entrant tachycardia with continuousatrioventricular node function curves. Circulation 1997;95:2541

    2547.

    14. Kuo CT, Lin KH, Cheng NJet al.Characterization of atrioventricular nodal

    reentry with continuous atrioventricular node conduction curve by

    double atrial extrastimulation. Circulation 1999;99:659665.

    15. Sheahan RG, Klein GJ, Yee R, Le Feuvre CA, Krahn AD. Atrioventricular

    node reentry with smooth AV node function curves: a different arrhyth-

    mia substrate? Circulation 1996;93:969972.

    16. Denes P, Wu D, Dhingra R, Amat-y-Leon F, Wyndham C, Rosen KM. Dual

    atrioventricular nodal pathways: a common electrophysiological

    response. Br Heart J1975;37:10691076.

    17. Levites R, Haft JI. Evidence suggesting dual AV nodal pathways in patients

    without supraventricular tachycardias. Chest1975;67:3642.

    18. Thapar MK, Gillette PC. Dual atrioventricular nodal pathways: a common

    electrophysiologic response in children. Circulation 1979;60:13691374.

    19. Casta A, Wolff GS, Mehta AVet al.Dual atrioventricular nodal pathways: a

    benign finding in arrhythmia-free children with heart disease. Am J

    Cardiol 1980;46:1013

    1018.

    20. Brugada P, Heddle B, Green M, Wellens HJ. Initiation of atrioventricular

    nodal reentrant tachycardia in patients with discontinuous anterograde

    atrioventricular nodal conduction curves with and without documented

    supraventricular tachycardia: observations on the role of discontinuous

    retrograde conduction curve. Am Heart J1984;107: 685697.

    21. Wu D, Denes P, Amat-y-Leon F, Wyndham CR, Dhingra R, Rosen KM. An

    unusual variety of atrioventricular nodal re-entry due to retrograde

    dual atrioventricular nodal pathways. Circulation 1977;56:5059.

    22. Sung RJ, Styperek JL, Myerburg RJ, Castellanos A. Initiation of two

    distinct forms of atrioventricular nodal reentrant tachycardia during

    programmed ventricular stimulation in man. Am J Cardiol 1978;

    42:404415.

    23. Coumel P, Attuel P, Leclercq JF. Permanent form of junctional reciprocat-

    ing tachycardia: mechanism, clinical and therapeutic implications. In

    Narula OS, ed. Cardiac Arrhythmias: Electrophysiology, Diagnosis and

    Management. Baltimore: Williams and Wilkins; 1979. p347363.

    24. Amat-y-Leon F, Dhingra R, Wu D, Denes P, Wyndham C, Rosen KM.

    Catheter mapping of retrograde atrial activation: observations during

    ventricular pacing and AV nodal re-entrant paroxysmal tachycardia.

    Br Heart J1976;38:355362.

    25. Akhtar M, Damato AN, Ruskin JN et al. Antegrade and retrograde con-

    duction characteristics in three patterns of paroxysmal atrioventricular

    junctional reentrant tachycardia. Am Heart J1978;95:2242.

    26. McGuire MA, Lau K-C, Johnson DC, Richards DA, Uther JB, Ross DL.

    Patients with two types of atrioventricular junctional (AV nodal) reen-

    trant tachycardia: evidence that a common pathway of nodal tissue is

    not present above the reentrant circuit. Circulation1991;83:1232

    1246.27. Ross DL, Johnson DC, Dennis AR, Cooper MJ, Richards DA, Uther JB.

    Curative surgery for atrioventricular junctional (AV nodal) reentrant

    tachycardia.J Am Coll Cardiol 1985;6:13831392.

    28. Engelstein ED, Stein KM, Markowitz SM, Lerman BB. Posterior fast atrio-

    ventricular node pathways: implications for radiofrequency catheter

    ablation of atrioventricular node reentrant tachycardia. J Am Coll

    Cardiol 1996;27:10981105.

    29. Delise P, Bonso A, Coro L et al. Pacemapping of the triangle of Koch: a

    simple method to reduce the risk of atrioventricular block during radio-

    frequency ablation of atrioventricular node reentrant tachycardia.

    Pacing Clin Electrophysiol 2001;24:17251731.

    30. Anselme F, Hook B, Monahan K et al. Heterogeneity of retrograde fast-

    pathway conduction pattern in patients with atrioventricular nodal

    reentry tachycardia: observations by simultaneous multisite catheter

    mapping of Kochs triangle. Circulation 1996;93:960968.

    31. Hwang C, Martin DJ, Goodman JS et al. Atypical atrioventricular nodereciprocating tachycardia masquerading as tachycardia using a left-

    sided accessory pathway. J Am Coll Cardiol 1997;30:218225.

    32. Nawata H, Yamamoto N, Hirao Ket al.Heterogeneity of anterograde fast-

    pathway and retrograde slow-pathway conduction patterns in patients

    with the fastslow form of atrioventricular nodal re-entrant tachycardia:

    electrophysiologic and electrocardiographic considerations. J Am Coll

    Cardiol 1998;32:17311740.

    33. Vijayaraman P, Kok LC, Rhee B, Ellenbogen KA. Unusual variant of atrio-

    ventricular nodal re-entrant tachycardia.Heart Rhythm2004;2:100102.

    34. Benditt DG, Pritchett ELC, Smith WM, Gallagher JJ. Ventriculoatrial

    intervals: diagnostic use in paroxysmal supraventricular tachycardias.

    Ann Intern Med1979;191:161166.

    35. Crozier I, Wafa S, Ward D, Camm J. Diagnostic value of comparison of

    ventriculoatrial interval during junctional tachycardia and right ventri-

    cular apical pacing. Pacing Clin Electrophysiol 1989;12:942953.

    36. Knight BP, Ebinger M, Oral H et al. Diagnostic value of tachycardia

    features and pacing maneuvers during paroxysmal supraventricular

    tachycardia.J Am Coll Cardiol 2000;36:574582.

    37. Miller JM, Rosenthal ME, Vassalo JA, Josephson ME. Atrioventricular nodal

    reentrant tachycardia: studies on upper and lower common pathways.

    Circulation 1987;75:930940.

    38. Heidbuchel H, Ector H, Van de Werf F. Prospective evaluation of the

    length of the lower common pathway in the differential diagnosis of

    various forms of AV nodal reentrant tachycardia. Pacing Clin

    Electrophysiol 1998;21:209216.

    39. Heidbuchel H, Jackman WM. Characterization of subforms of AV nodal

    reentrant tachycardia. Europace2004;6:316329.

    40. Tai CT, Chen SA, Chiang CE et al. Electrophysiologic characteristics and

    radiofrequency catheter ablation in patients with multiple atrioventri-

    cular nodal reentry tachycardias. Am J Cardiol 1996;77:52

    41. Katritsis D, Slade A, Camm AJ, Rowland E. Atrioventricular junctional

    reentrant tachycardia utilising multiple retrograde fibres during ablation

    of the slow pathway. Clin Cardiol 1993;16:889

    891.

    Classification and differential diagnosis of AVNRT 35

  • 7/23/2019 29.full

    8/8

    42. Inoue S, Becker AE. Posterior extensions of the human compact atrio-

    ventricular node: a neglected anatomic feature of potential clinical

    significance.Circulation 1998;97:188193.

    43. Katritsis D, Becker A, Ellenbogen K, Giazitzoglou E, Korovesis S,

    Karabinos I, Camm AJ. Slow-pathway ablation in atrioventricular nodal

    reentrant tachycardia modifies the electrophysiologic characteristics

    of the right inferior atrial input to thehuman atrioventricular node.

    (Abstract). Heart Rhythm 2005;2(Suppl. 1):S117.

    44. Jas P, Hassaguerre M, Shah DC, Coste P, Takahashi A, Barold SS,

    Clementy J. Successful radiofrequency ablation of a slow atrioventricular

    nodal pathway on the left posterior atrial septum. Pacing Clin

    Electrophysiol 1999;22:525527.

    45. Sorbera C, Cohen M, Woolf P, Kalapatapu SR. Atrioventricular nodal

    reentry tachycardia: slow pathway ablation using the transseptal

    approach. Pacing Clin Electrophysiol 2000;23:13431349.

    46. Michaud GF, Tada H, Chough S et al. Differentiation of atypical atrio-

    ventricular node re-entrant tachycardia from orthodromic reciprocating

    tachycardia using a septal accessory pathway by the response to ventri-

    cular pacing. J Am Coll Cardiol 2001;38:11631167.

    47. Kay GN, Epstein AE, Dailey SM, Plumb VJ. Selective radiofrequency

    ablation of the slow pathway for the treatment of atrioventricular

    nodal reentrant tachycardia: evidence for involvement of perinodal

    myocardium within the reentrant circuit. Circulation 1992;85:

    16751688.

    48. Jazayeri MR, Hempe SL, Sra JSet al. Selective transcatheter ablation of

    the fast and slow pathways using radiofrequency energy in patients with

    atrioventricular nodal reentrant tachycardia. Circulation 1992;85:13181328.

    49. Goldberger J, Brooks R, Kadish A. Physiology of atypical atrioventricular

    junctional reentrant tachycardia occurring following radiofrequency

    catheter modification of the atrioventricular node. Pacing Clin

    Electrophysiol 1992;15:22702282.

    50. Man KC, Niebauer M, Daoud E et al. Comparison of atrial-His intervals

    during tachycardia and atrial pacing in patients with long RP tachycardia.

    J Cardiovasc Electrophysiol 1995;6:700710.

    51. Taniguchi Y, Yeh SJ, Wen MS, Wang CC, Wu D. Atypical atrioventricular

    nodal reentry tachycardia with atrioventricular block mimicking atrial

    tachycardia: electrophysiologic properties and radiofrequency ablation

    therapy. J Cardiovasc Electrophysiol 1997;8:13021308.

    52. Knight BP, Zivin A, Souza J et al. A technique for the rapid diagnosis of

    atrial tachycardia in the electrophysiology laboratory. J A m Coll

    Cardiol 1999;33:775781.

    53. Gula LJ, Skanes A, Krahn AD, Klein GJ. Novel approach to diagnosis

    of a wide-complex tachycardia. J Cardiovasc Electrophysiol 2004;15:466469.

    54. Vijayaraman P, Kok LC, Rhee B, Ellenbogen KA. Wide complex tachycar-

    dia: what is the mechanism? Heart Rhythm 2004;2:107109.

    55. Farre J, Ross DL, Wiener I, Bar FW, Vanagt EJ, Wellens HJJ. Reciprocal

    tachycardias using accessory pathways with long conduction times. Am

    J Cardiol 1979;44:10991109.

    56. Tai CT, Chen SA, Chiang CE et al. A new electrocardiographic algorithm

    using retrograde P waves for differentiating atrioventricular node reen-

    trant tachycardia from atrioventricular reciprocating tachycardia

    mediated by concealed accessory pathway. J Am Coll Cardiol

    1997;29:394402.

    57. Vassalo JA, Cassidy DM, Josephson ME. Atrioventricular nodal supraven-

    tricular tachycardia. Am J Cardiol 1985;56:193195.

    58. Yeh S-J, Yamamoto T, Lin F-C, Wu D. Atrioventricular block in the atypical

    form of junctional reciprocating tachycardia: evidence supporting the

    atrioventricular node as the site of reentry. J Am Coll Cardiol1990;15:385392.

    59. Kerr CR, Gallagher JJ, German LD. Changes in ventriculoatrial intervals

    with bundle branch block aberration during reciprocating tachycardia

    in patients with accessory atrioventricular pathways. Circulation

    1982;66:196201.

    60. Ross DL, Uther JB. Diagnosis of concealed accessory pathways in supra-

    ventricular tachycardia. Pacing Clin Electrophysiol 1983;7:10691085.

    61. Benditt DG, Benson DW Jr, Dunnigan A et al. Role of extrastimulus site

    and tachycardia cycle length in inducibility of atrial preexcitation by pre-

    mature ventricular stimulation during reciprocating tachycardia. Am J

    Cardiol 1987;60:811819.

    62. Miles WM, Yee R, Klein GJ, Zipes DP, Prystowsky EN. The preexcitation

    index: an aid in determining the mechanism of supraventricular tachycar-

    dia and localizing accessory pathways. Circulation 1986;74:493

    500.

    63. Tai CT, Chen SA, Chiang CE, Chang MS. Characteristics and radiofrequency

    catheter ablation of septal accessory atrioventricular pathways. Pacing

    Clin Electrophysiol 1999;22:500511.

    64. Martinez-Alday JD, Almendral J, Arenal A et al. Identification of con-

    cealed posteroseptal Kent pathways by comparison of ventriculoatrial

    intervals from apical and posterobasal right ventricular sites.

    Circulation 1994;89:10601067.

    65. Miller JM, Rosenthal ME, Gottlieb CD, Vassalo JA, Josephson ME.

    Usefulness of the DHA interval to accurately distinguish atrioventricular

    nodal reentry from orthodromic septal bypass tract tachycardias.Am J

    Cardiol 1991;68:10371044.

    66. Hirao K, Otomo K, Wang X et al. Para-Hisian pacing: a new method for

    differentiating retrograde conduction over an accessory AV pathway

    from conduction over the AV node. Circulation 1996;94:10271035.

    67. Ormaetxe JM, Almendral J, Arenal A et al. Ventricular fusion during

    resetting and entrainment of orthodromic supraventricular tachycardiainvolving septal accessory pathways: implications for the differential

    diagnosis with atrioventricular nodal reentry. Circulation 1993;

    88:26232631.

    68. Packer DL, Gallagher JJ, Prystowsky EN. Physiological substrate for anti-

    dromic reciprocating tachycardia: prerequisite characteristics of the

    accessory pathway and atrioventricular conduction system. Circulation

    1992;85:574588.

    69. Smith WM, Broughton A, Reiter MJ, Benson DW, Grant AO, Gallagher JJ.

    Bystander accessory pathway during AV node reentrant tachycardia.

    Pacing Clin Electrophysiol 1983;6:537543.

    70. Atie J, Brugada P, Brugada Jet al.Clinical and electrophysiologic charac-

    teristics of patients with antidromic circus movement tachycardia in

    the WolffParkinsonWhite syndrome.Am J Cardiol 1990;66:10821091.

    71. Pick A, Dominguez P. Nonparoxysmal A-V nodal tachycardia. Circulation

    1967;16:10221031.

    72. Rosen KM. Junctional tachycardia: mechanisms, diagnosis, differentialdiagnosis and management. Circulation 1973;67:654664.

    73. Palileo EV, Bauernfeind RA, Swiryn SP, Wyndham CR, Rosen K M. Chronic

    nonparoxysmal junctional tachycardia. Chest1981;80:106108.

    74. Rosen MR, Fisch C, Hoffman BF, Danilo P, Lovelace DE, Knoebel JB. Can

    accelerated atrioventricular junctional escape rhythms be explained by

    delayed afterdepolarizations? Am J Cardiol 1980;45:12721284.

    75. Hamdan MH, Badhwar N, Scheinman MM. Role of invasive electrophysio-

    logic testing in the evaluation and management of adult patients with

    focal junctional tachycardia. Card Electrophysiol Rev2002;6:431435.

    76. Gillette PC. Diagnosis and management of postoperative junctional

    ectopic tachycardia. Am Heart J1989;118:192194.

    77. Villain E, Vetter VL, Garcia JM, Herre J, Cifarelli A, Garson A Jr. Evolving

    concepts in the management of congenital junctional ectopic tachycar-

    dia: a multicenter study. Circulation 1990;81:15441549.

    78. Wren C. Incessant tachycardias.Eur Heart J1998;19(Suppl. E):E32E36.

    79. Scheinman MM, Gonzalez RP, Cooper MW, Lesh MD, Lee RJ, Epstein LM.Clinical and electrophysiologic features and role of catheter ablation

    techniques in adult patients with automatic atrioventricular junctional

    tachycardia.Am J Cardiol 1994;74:565572.

    36 D.G. Katritsis and A.J. Camm