REVIEW
Classification and differential diagnosis of atrioventricular nodal re-entrant tachycardia
Department of Cardiology Athens Euroclinic, 9 Athanassiadou Street, Athens 11521 Greece; Cardiothoracic Centre, St Thomas' Hospital London UK; Department of Cardiological Sciences, St George's Hospital Medical School London UK
Manuscript submitted 3 March 2005. Accepted after revision 21 August 2005.
Corresponding author. Tel: +44 210 6416600; fax: +44 210 6416661/6819779. E-mail address: dkatrits{at}otenet.gr
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Abstract |
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Recent evidence on atrioventricular nodal re-entrant tachycardia has identified 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 classification of the various forms of the arrhythmia.
Key Words: Atrioventricular nodal re-entrant tachycardia
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Introduction |
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TopAbstractIntroductionDiagnostic problemsAVNRT typesDifferential diagnosisConclusionsReferences |
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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 confined 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,5–10 the exact circuit responsible for the re-entrant tachycardia is unknown. Furthermore, there is no unanimously accepted scheme for the diagnosis and classification 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 classification of the various forms of the arrhythmia. |
Diagnostic problems |
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TopAbstractIntroductionDiagnostic problemsAVNRT typesDifferential diagnosisConclusionsReferences |
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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.13–15 Conversely, antegrade dual pathways can be demonstrated in subjects without tachycardia.16–20
In patients with the fast–slow 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 fast–slow 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 classified as slow–fast or typical AVNRT, and fast–slow 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 coronary sinus ostium.6 Indeed, in the majority of slow–fast cases of AVNRT, the site of the earliest atrial activation is close to the apex of Koch's triangle, near the AV node-His bundle junction, i.e. anterior to the AV node.24,25 In the fast–slow form, the site of the earliest atrial activation is usually recorded posterior to the AV node near the orifice 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 classification attempts more complicated. Previous studies have reported on a posterior (or type B) variety of presumed slow–fast 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 fast–slow31,32 as well as the slow–slow31,32 forms has also been reported. It is now becoming evident that fast–slow 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 fast–slow or slow–slow 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 fluoroscopy times and unnecessary radiofrequency lesions.
VA conduction time
Traditionally, a VA interval measured from the onset of ventricular activation on surface ECG to the earliest deflection 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 (100–200 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 slow–fast AVNRT provided, of course, that atrial tachycardia has been excluded.35,36
Lower common pathway
The lower common pathway is defined 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 slow–fast AVNRT, as opposed to fast–slow or slow–slow AVNRT, and have actually used the demonstration of a lower common pathway in order to categorize AVNRT as atypical (either fast–slow or slow–slow).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.
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AVNRT types |
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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 definitive diagnosis as well as the identification 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
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Considering the published evidence so far, the following diagnostic criteria and classification of AVNRT types can be proposed (Table 1).
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Typical AVNRT
Slow–fast
In the slow–fast 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 deflection 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 slow–fast 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
Fast–slow
In the fast–slow form of AVNRT (5–10% of all AVNRT cases), retrograde atrial electrograms begin well after ventricular activation with an AH/HA ratio <1, indicating that retrograde conduction is slower than antegrade conduction.22 The VA interval measured from the onset of ventricular activation on surface ECG to the earliest deflection 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 fast–slow cases, the site of the earliest atrial activation is posterior to the AV node near the orifice of the coronary sinus.47,48 However, anterior and mid-forms of fast–slow AVNRT have also been described.32
Slow–slow
In the slow–slow 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 slow–fast 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 slow–fast AV junctional re-entry tachycardia (AVJRT) may actually represent the slow–slow form.2,28
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Differential diagnosis |
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TopAbstractIntroductionDiagnostic problemsAVNRT typesDifferential diagnosisConclusionsReferences |
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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.50–52 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 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 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 
AH>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 Finally, the difference of the post-pacing interval and the tachycardia cycle length (PPI–TCL interval) as described by Michaud et al.,46 may also be of help.
AVNRT vs. AVRT due to septal accessory pathways
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 fast–slow or slow–slow 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 identification of retrograde P waves, ECG criteria can be applied for diagnosis. The presence of a pseudo-r' 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
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 significant 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
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 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 specific but not a highly sensitive criterion for differential diagnosis.
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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 RP' tachycardias. A
AH>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 defined the pre-excitation 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 with AVRT studied at St George's Hospital in London, the ratio between the minimum VA interval during tachycardia and ventricular pacing was 0.32–0.27 in AVNRT, 0.91–1.08 in AVRT using a posteroseptal pathway, and 0.94–1.29 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
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 (HA). In 84 patients, a retrograde His was present in 93% of them and the HA was >0 ms in AVNRT and <–27 ms in orthodromic AVRT incorporating a septal accessory pathway. Thus an intermediate value of HA=–10 ms had 100% sensitivity, specificity, 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.
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 SA–VA intervals >85 ms and PPI–TCL 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 pre-excited 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 pre-excited QRS complex, the next retrograde His bundle deflection where apparent, and the subsequent atrial deflection, as may happen in the presence of a macro-re-entrant 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 finding is a narrow QRS tachycardia with AV dissociation. Occasionally, the tachycardia might be irregular thus resembling atrial fibrillation. 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
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Conclusions |
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TopAbstractIntroductionDiagnostic problemsAVNRT typesDifferential diagnosisConclusionsReferences |
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- Recent evidence has identified several types of AVNRT which is the most common paroxysmal supraventricular arrhythmia in the human.
- AVNRT types are classified as typical (slow–fast) and atypical (fast–slow and slow–slow), 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 atrial activation. However, variable sites of retrograde atrial activation have been described for all types of this arrhythmia.
- 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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References |
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[1] Josephson ME and Wellens HJ. Electrophysiologic evaluation of supraventricular tachycardia. Cardiol Clin 1997; 15: 567–586.[Medline]
[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: implications for the reentrant circuits. In Zipes DP and Jalife J (Eds.). Cardiac Electrophysiology: From Cell to Bedside 2004; 3rd ed. Philadelphia, PA W.B. Saunders Company pp. 537–557.
[3] Becker AE and Anderson RH. Morphology of the human atrioventricular junctional area. In Wellens HJJ, Lie KI, Janse MJ (Eds.). The Conduction System of the Heart: Structure, Function and Clinical Implications 1976; Leiden HE Stenfert Kroese BV pp. 263–286.
[4] Camm AJ and Katritsis D. The diagnosis of tachyarrhythmias. In Julian DG, Camm AJ, Fox KM, Hall RJC, Poole-Wilson PA (Eds.). Heart Disease 1996; 2nd ed. Philadelphia, PA, USA Saunders pp. 6606–6621.
[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: 884–895.[Abstract]
[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: 919–925.
[7] Spach MS and Josephson ME. Initiating reentry: the role of nonuniform anisotropy in small circuits. J Cardiovasc Electrophysiol 1994; 5: 182–209.[Web of Science][Medline]
[8] Patterson E and Scherlag BJ. Anatomic and functional fast atrioventricular conduction pathway. J Cardiovasc Electrophysiol 2002; 13: 945–949.[CrossRef][Medline]
[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: 582–586.[CrossRef][Web of Science][Medline]
[10] Kwaku KF and Josephson ME. Typical AVNRT: an update on mechanisms and therapy. Cardiac Electrophysiol Rev 2002; 6: 414–421.[CrossRef][Medline]
[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: 549–555.
[12] Josephson ME and Kastor JA. Supraventricular tachycardia: mechanisms and management. Ann Intern Med 1977; 87: 346–358.
[13] Tai CT, Chen SA, Chiang CE, et al. Complex electrophysiological characteristics in atrioventricular nodal re-entrant tachycardia with continuous atrioventricular node function curves. Circulation 1997; 95: 2541–2547.
[14] Kuo CT, Lin KH, Cheng NJ, et al. Characterization of atrioventricular nodal reentry with continuous atrioventricular node conduction curve by double atrial extrastimulation. Circulation 1999; 99: 659–665.
[15] Sheahan RG, Klein GJ, Yee R, Le Feuvre CA, Krahn AD. Atrioventricular node reentry with ‘smooth’ AV node function curves: a different arrhythmia substrate? Circulation 1996; 93: 969–972.
[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 J 1975; 37: 1069–1076.
[17] Levites R and Haft JI. Evidence suggesting dual AV nodal pathways in patients without supraventricular tachycardias. Chest 1975; 67: 36–42.
[18] Thapar MK and Gillette PC. Dual atrioventricular nodal pathways: a common electrophysiologic response in children. Circulation 1979; 60: 1369–1374.
[19] Casta A, Wolff GS, Mehta AV, et al. Dual atrioventricular nodal pathways: a benign finding in arrhythmia-free children with heart disease. Am J Cardiol 1980; 46: 1013–1018.[CrossRef][Medline]
[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 J 1984; 107: 685–697.[CrossRef][Medline]
[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: 50–59.
[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: 404–415.[CrossRef][Medline]
[23] Coumel P, Attuel P, Leclercq JF. Permanent form of junctional reciprocating tachycardia: mechanism, clinical and therapeutic implications. In Narula OS (Ed.). Cardiac Arrhythmias: Electrophysiology, Diagnosis and Management 1979; Baltimore Williams and Wilkins 347–363.
[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 J 1976; 38: 355–362.
[25] Akhtar M, Damato AN, Ruskin JN, et al. Antegrade and retrograde conduction characteristics in three patterns of paroxysmal atrioventricular junctional reentrant tachycardia. Am Heart J 1978; 95: 22–42.[CrossRef][Web of Science][Medline]
[26] McGuire MA, Lau K-C, Johnson DC, Richards DA, Uther JB, Ross DL. Patients with two types of atrioventricular junctional (AV nodal) reentrant tachycardia: evidence that a common pathway of nodal tissue is not present above the reentrant circuit. Circulation 1991; 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: 1383–1392.[Abstract]
[28] Engelstein ED, Stein KM, Markowitz SM, Lerman BB. Posterior fast atrioventricular node pathways: implications for radiofrequency catheter ablation of atrioventricular node reentrant tachycardia. J Am Coll Cardiol 1996; 27: 1098–1105.[Abstract]
[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 radiofrequency ablation of atrioventricular node reentrant tachycardia. Pacing Clin Electrophysiol 2001; 24: 1725–1731.[CrossRef][Medline]
[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 Koch's triangle. Circulation 1996; 93: 960–968.
[31] Hwang C, Martin DJ, Goodman JS, et al. Atypical atrioventricular node reciprocating tachycardia masquerading as tachycardia using a left-sided accessory pathway. J Am Coll Cardiol 1997; 30: 218–225.[Abstract]
[32] Nawata H, Yamamoto N, Hirao K, et al. Heterogeneity of anterograde fast-pathway and retrograde slow-pathway conduction patterns in patients with the fast–slow form of atrioventricular nodal re-entrant tachycardia: electrophysiologic and electrocardiographic considerations. J Am Coll Cardiol 1998; 32: 1731–1740.
[33] Vijayaraman P, Kok LC, Rhee B, Ellenbogen KA. Unusual variant of atrioventricular nodal re-entrant tachycardia. Heart Rhythm 2004; 2: 100–102.[CrossRef]
[34] Benditt DG, Pritchett ELC, Smith WM, Gallagher JJ. Ventriculoatrial intervals: diagnostic use in paroxysmal supraventricular tachycardias. Ann Intern Med 1979; 191: 161–166.
[35] Crozier I, Wafa S, Ward D, Camm J. Diagnostic value of comparison of ventriculoatrial interval during junctional tachycardia and right ventricular apical pacing. Pacing Clin Electrophysiol 1989; 12: 942–953.[CrossRef][Medline]
[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: 574–582.
[37] Miller JM, Rosenthal ME, Vassalo JA, Josephson ME. Atrioventricular nodal reentrant tachycardia: studies on upper and lower ‘common pathways’. Circulation 1987; 75: 930–940.
[38] Heidbüchel 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: 209–216.[CrossRef][Medline]
[39] Heidbüchel H and Jackman WM. Characterization of subforms of AV nodal reentrant tachycardia. Europace 2004; 6: 316–329.
[40] Tai CT, Chen SA, Chiang CE, et al. Electrophysiologic characteristics and radiofrequency catheter ablation in patients with multiple atrioventricular nodal reentry tachycardias. Am J Cardiol 1996; 77: 52.[CrossRef][Medline]
[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.[Medline]
[42] Inoue S and Becker AE. Posterior extensions of the human compact atrioventricular node: a neglected anatomic feature of potential clinical significance. Circulation 1998; 97: 188–193.
[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] Jaïs P, Haïssaguerre M, Shah DC, Coste P, Takahashi A, Barold SS, Clémenty J. Successful radiofrequency ablation of a slow atrioventricular nodal pathway on the left posterior atrial septum. Pacing Clin Electrophysiol 1999; 22: 525–527.[Medline]
[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: 1343–1349.[CrossRef][Medline]
[46] Michaud GF, Tada H, Chough S, et al. Differentiation of atypical atrioventricular node re-entrant tachycardia from orthodromic reciprocating tachycardia using a septal accessory pathway by the response to ventricular pacing. J Am Coll Cardiol 2001; 38: 1163–1167.
[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: 1675–1688.
[48] Jazayeri MR, Hempe SL, Sra JS, et al. Selective transcatheter ablation of the fast and slow pathways using radiofrequency energy in patients with atrioventricular nodal reentrant tachycardia. Circulation 1992; 85: 1318–1328.
[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: 2270–2282.[CrossRef][Medline]
[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: 700–710.[Web of Science][Medline]
[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: 1302–1308.[Medline]
[52] Knight BP, Zivin A, Souza J, et al. A technique for the rapid diagnosis of atrial tachycardia in the electrophysiology laboratory. J Am Coll Cardiol 1999; 33: 775–781.
[53] Gula LJ, Skanes A, Krahn AD, Klein GJ. Novel approach to diagnosis of a wide-complex tachycardia. J Cardiovasc Electrophysiol 2004; 15: 466–469.[CrossRef][Medline]
[54] Vijayaraman P, Kok LC, Rhee B, Ellenbogen KA. Wide complex tachycardia: what is the mechanism? Heart Rhythm 2004; 2: 107–109.
[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: 1099–1109.[CrossRef][Web of Science][Medline]
[56] Tai CT, Chen SA, Chiang CE, et al. A new electrocardiographic algorithm using retrograde P waves for differentiating atrioventricular node reentrant tachycardia from atrioventricular reciprocating tachycardia mediated by concealed accessory pathway. J Am Coll Cardiol 1997; 29: 394–402.[Abstract]
[57] Vassalo JA, Cassidy DM, Josephson ME. Atrioventricular nodal supraventricular tachycardia. Am J Cardiol 1985; 56: 193–195.[CrossRef][Web of Science][Medline]
[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 Cardiol 1990; 15: 385–392.[Abstract]
[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: 196–201.
[60] Ross DL and Uther JB. Diagnosis of concealed accessory pathways in supraventricular tachycardia. Pacing Clin Electrophysiol 1983; 7: 1069–1085.
[61] Benditt DG, Benson DW Jr, Dunnigan A, et al. Role of extrastimulus site and tachycardia cycle length in inducibility of atrial preexcitation by premature ventricular stimulation during reciprocating tachycardia. Am J Cardiol 1987; 60: 811–819.[CrossRef][Medline]
[62] Miles WM, Yee R, Klein GJ, Zipes DP, Prystowsky EN. The preexcitation index: an aid in determining the mechanism of supraventricular tachycardia 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: 500–511.[CrossRef][Medline]
[64] Martinez-Alday JD, Almendral J, Arenal A, et al. Identification of concealed posteroseptal Kent pathways by comparison of ventriculoatrial intervals from apical and posterobasal right ventricular sites. Circulation 1994; 89: 1060–1067.
[65] Miller JM, Rosenthal ME, Gottlieb CD, Vassalo JA, Josephson ME. Usefulness of the HA interval to accurately distinguish atrioventricular nodal reentry from orthodromic septal bypass tract tachycardias. Am J Cardiol 1991; 68: 1037–1044.[CrossRef][Web of Science][Medline]
[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: 1027–1035.
[67] Ormaetxe JM, Almendral J, Arenal A, et al. Ventricular fusion during resetting and entrainment of orthodromic supraventricular tachycardia involving septal accessory pathways: implications for the differential diagnosis with atrioventricular nodal reentry. Circulation 1993; 88: 2623–2631.
[68] Packer DL, Gallagher JJ, Prystowsky EN. Physiological substrate for antidromic reciprocating tachycardia: prerequisite characteristics of the accessory pathway and atrioventricular conduction system. Circulation 1992; 85: 574–588.
[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: 537–543.[Medline]
[70] Atie J, Brugada P, Brugada J, et al. Clinical and electrophysiologic characteristics of patients with antidromic circus movement tachycardia in the Wolff–Parkinson–White syndrome. Am J Cardiol 1990; 66: 1082–1091.[Medline]
[71] Pick A and Dominguez P. Nonparoxysmal A-V nodal tachycardia. Circulation 1967; 16: 1022–1031.
[72] Rosen KM. Junctional tachycardia: mechanisms, diagnosis, differential diagnosis and management. Circulation 1973; 67: 654–664.
[73] Palileo EV, Bauernfeind RA, Swiryn SP, Wyndham CR, Rosen KM. Chronic nonparoxysmal junctional tachycardia. Chest 1981; 80: 106–108.
[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: 1272–1284.[CrossRef][Web of Science][Medline]
[75] Hamdan MH, Badhwar N, Scheinman MM. Role of invasive electrophysiologic testing in the evaluation and management of adult patients with focal junctional tachycardia. Card Electrophysiol Rev 2002; 6: 431–435.[Medline]
[76] Gillette PC. Diagnosis and management of postoperative junctional ectopic tachycardia. Am Heart J 1989; 118: 192–194.[CrossRef][Web of Science][Medline]
[77] Villain E, Vetter VL, Garcia JM, Herre J, Cifarelli A, Garson A Jr. Evolving concepts in the management of congenital junctional ectopic tachycardia: a multicenter study. Circulation 1990; 81: 1544–1549.
[78] Wren C. Incessant tachycardias. Eur Heart J 1998; 19:Suppl. E, E32–E36.
[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: 565–572.[CrossRef][Web of Science][Medline]
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