Accessory pathways with anterograde decremental conduction properties usually are characterized by presence of antegrade preexcitation during atrial pacing. We report a 38-year-old man with frequent episodes of palpitation. No evidence of ventricular preexcitation was seen during sinus rhythm or atrial pacing. All electrophysiologic maneuvers were compatible with an antidromic tachycardia using atriofascicular pathway as the antegrade limb and the atrioventricular nodal pathway as retrograde limb. Radiofrequency ablation at recording site of accessory pathway potential resulted in cure of tachycardia with no recurrence during 3-month follow-up. This report indicated that atriofascicular pathway-mediated tachycardia should be considered in differential diagnosis of all cases of wide complex tachycardia with left bundle branch morphology and left axis. Â© 2006, The Authors

Alizadeh, A.

Emkanjoo, Z.

Fazelifar, A.F.

Haghjoo, M.

Jorat, M.V.

Nikoo, M.H.

Sadr-Ameli, M.A.

English

eprints Iran University of Medical Sciences

CASE REPORTLatent Atriofascicular Pathway Participatingin a Wide Complex Tachycardia: Differentiationfrom Ventricular TachycardiaMOHAMMAD V. JORAT, M.D., MAJID HAGHJOO, M.D., ABOLFATH ALIZADEH, M.D.,AMIR FARJAM FAZELIFAR, M.D., MOHAMMAD H. NIKOO, M.D.,ZAHRA EMKANJOO, M.D., and MOHAMMAD A. SADR-AMELI, M.D.From the Department of Pacemaker and Electrophysiology, Rajaie Cardiovascular Medical and Research Center,School of Medicine, Iran University of Medical Sciences, Tehran, IranAccessory pathways with anterograde decremental conduction properties usually are characterizedby presence of antegrade preexcitation during atrial pacing. We report a 38-year-old man with frequentepisodes of palpitation. No evidence of ventricular preexcitation was seen during sinus rhythm or atrialpacing. All electrophysiologic maneuvers were compatible with an antidromic tachycardia using atri-ofascicular pathway as the antegrade limb and the atrioventricular nodal pathway as retrograde limb.Radiofrequency ablation at recording site of accessory pathway potential resulted in cure of tachycardiawith no recurrence during 3-month follow-up. This report indicated that atriofascicular pathway-mediatedtachycardia should be considered in differential diagnosis of all cases of wide complex tachycardia withleft bundle branch morphology and left axis. (PACE 2006; 29:1434–1437)latent atriofascicular pathway, wide complex tachycardia, electrophysiologyIntroductionIn a series of papers published between 1932and 1947, Mahaim and his coworkers originallydescribed anatomical connections of the atrioven-tricular (AV) node to the bundle branches or ven-tricular myocardium, bypassing the His bundle,in pathological specimens.1–3 The true nature ofthese pathways was first characterized by Kleinet al.4 and Tchou et al.5 at almost the same time.These fibers were later thought to be cause of anunusual form of preexcitation syndrome whichwas characterized by a left bundle branch blockmorphology (LBBB) tachycardia with long AV andshort ventriculoatrial (VA) intervals.6 Currently, itis demonstrated that these pathways located onthe right atrium (crossing the tricuspid annuluson the free wall rather than the septum). Thereare several variants for these fibers; fibers that me-diate tachycardia with true nodofascicular con-nection,7 left-sided decremental atrioventricularconnection8 and concealed nodoventricular fiber9that conducting only in retrograde direction. Thereis only one report of latent atriofascicular path-way (evident only during antidromic reciprocat-Address for reprints: Majid Haghjoo M.D., Department ofPacemaker and Electrophysiology, Rajaie Cardiovascular Med-ical and Research Center, Mellat Park, Vali-e-Asr Avenue,Tehran 1996911151 Iran. Fax: +9821-2204-8174; e-mail:majid.haghjoo@gmail.comReceived July 1, 2006; revised August 14, 2006; accepted Au-gust 29, 2006.ing tachycardia with no anterograde conductionduring sinus rhythm or atrial pacing) in the liter-ature.10 Here we present another interesting caseof latent atriofascicular pathway who followed formany years as a case of ventricular tachycardia.Case ReportA 38-year-old man with no evidence of struc-tural heart disease referred to our center for eval-uation of long-standing palpitation. The struc-tural heart disease was excluded by physicalexamination and transthoracic echocardiography.Transthoracic echocardiography showed normalcardiac chambers (including right ventricle), nor-mal valvular function, and ejection fraction with-out any wall motion abnormalities. During anepisode of palpitation, the standard 12-lead elec-trocardiogram (ECG) showed documented widecomplex tachycardia with a heart rate of 210 beatsper minute (bpm). The tachycardia was refractoryto two antiarrhythmics (verapamil, sotalol). Thewide complex tachycardia had LBBB morphologyand left axis (Fig. 1). The baseline ECG showed noabnormality.After obtaining written informed consent,electrophysiologic study was done in the postab-sorptive and nonsedated state. All antiarrhyth-mic drugs were interrupted for at least fivehalf-lives before procedure. At electrophysiologystudy, rapid pacing from high right atrium (HRA)(Fig. 2A), different parts of right atrium (RA)and coronary sinus ostium failed to demonstrateC©2006, The Authors. Journal compilation C©2006, Blackwell Publishing, Inc.1434 December 2006 PACE, Vol. 29LATENT ATRIOFASCICULAR PATHWAYFigure 1. Twelve-lead ECG obtained during palpitation showing wide complex tachycardia withLBBB morphology and left axis.preexcitation with and without isoproterenol.Dual AV nodal physiology was evident by atrial-His (AH) jump without reentry. During pacingfrom right ventricular apex (RVA), retrograde con-duction occurred via AV node. Atrial stimula-tion failed to induced arrhythmia but ventricu-lar extrastimulation (S1 = 400, S2 = 270 ms)resulted in the induction of a wide QRS tachy-cardia (Fig. 2B) with the following characteristics:cycle length = 280 ms; LBBB morphology and leftaxis; His-ventricular (HV) shortening (from 50 msto −16 ms). During tachycardia, sequence of Hisbundle activation was reversed consistent with ret-rograde activation of this bundle (Fig. 2B). Tachy-cardia could be entrained from lateral RA and ter-minated by both RA and RVA pacing. Delivery ofatrial extrastimuli from lateral RA advanced subse-quent ventricular activation without affecting thetiming of the atrial signal in His bundle recording(Fig. 2C). During atrial fibrillation (AF) rhythm thatoccurred during atrial pacing, some conductedbeats characterized by LBBB and left axis morphol-ogy identical to that observed in tachycardia, HVshortening, and reversal of His bundle activation(Fig. 2D).By impression of latent atriofascicular path-way, tricuspid annulus was mapped duringtachycardia. During mapping of lateral tricuspidannulus (9 o’clock), catheter bump resulted intachycardia termination at the site of discrete po-tentials. Radiofrequency (RF) energy application atthis site resulted in accelerated preexcited rhythmand then loss of preexcitation and noninducibil-ity of tachyarrhythmia. During 3-month follow-up, he was free of symptoms with no antiarrhyth-mic drugs and no recurrence of tachycardia wasseen.DiscussionIn this report, we describe a case of wide com-plex tachycardia compatible with antidromic re-ciprocating tachycardia using a right-sided atrio-fascicular pathway as the antegrade limb and theAV node as the retrograde limb. The distal in-sertion was considered fascicular (atriofascicularfiber) because the earliest ventricular activationwas recorded in the right ventricular (RV) api-cal region rather than tricuspid valve ring andVentricular-His (VH) interval is relatively short(16 ms). The unusual feature in this case was theabsence of anterograde conduction during sinusrhythm and pacing from several right atrial andcoronary sinus sites. The anterograde conductionthrough atriofascicular pathway was evident onlyduring antidromic reciprocating tachycardia andintermittently during atrial fibrillation.The amount of preexcitation is determined bythe competition between conduction through AVnode and accessory pathway. Therefore lack of pre-excitation during atrial pacing or sinus rhythmcan be explained by combination of the acceler-ated AV nodal conduction and/or prolonged con-duction through the accessory pathway. Anotherexplanation for it can be concealed retrogradepenetration of accessory pathway by conductedimpulse through AV node.10 In our case, short AHinterval during sinus rhythm and atrial pacing andlong atrium to accessory pathway potential duringantidromic reciprocating tachycardia are in favorof former mechanism.In our patient, other evidence for conduc-tion through atriofascicular pathway was runs ofovert preexcitation followed by runs of absentpreexcitation during atrial fibrillation (Fig 2D). Itappears that concealed conduction is the mostPACE, Vol. 29 December 2006 1435JORAT, ET AL.Figure 2. (A) Part of incremental right atrial pacing at faster rates approaching tachycardia cyclelength (290 and 280 ms) where AV node conduction would be slower. Note that there is no evidenceof anterograde conduction through atriofascicular pathway. (B) Onset of clinical tachycardia byprogrammed ventricular stimulation. Tachycardia characterized by left bundle branch morphol-ogy, VH interval of 16 ms and reversal of His bundle activation. The arrows indicate retrogradeHis bundle activation from distal to proximal during atriofascicular pathway conduction. (C) An-tidromic reciprocating tachycardia is reset (20 ms) with a late atrial extrastimulus (S2) deliveredfrom the lateral right atrium without anterograde penetration into the normal AV node and with-out a change in the QRS morphology, ventricular activation sequence and timing indicating theextranodal origin of atriofascicular pathway and excluding ventricular tachycardia. (D) Duringatrial fibrillation, runs of overt preexcitation followed by runs of absent preexcitation. Some con-ducted beats (three beats in the middle of tracing) characterized by left bundle branch morphologyidentical to that observed in tachycardia, HV shortening, and reversal of His bundle activation.In first two beats and last three beats, arrows indicate anterograde His bundle activation fromproximal to distal during AV nodal conduction. The arrows in the middle of tracing indicate ret-rograde His bundle activation from distal to proximal during atriofascicular pathway conduction.HRA = recording from distal poles of HRA catheter; RVA = recording from distal poles of RVAcatheter; His-p = recording from proximal poles of His catheter; His-d = recording from distalpoles of His catheter; CS = recordings from proximal and distal poles of multipolar coronarysinus catheter; A = atrial activation; I, III, V1, and V6 = surface ECG leads.possible explanation for this phenomenon. Thisobservation is another evidence for importance ofaccelerated AV nodal conduction in preventing ex-pression of antegrade conduction through atriofas-cicular pathway.Another interesting feature in our patient wasthe presence of single wide complex beat havingthe identical morphology to that of preexcited beatwith no preceding P-wave (Fig. 3). We consid-ered two possibilities for this feature: (1) two-for-one phenomenon; (2) premature ventricular beat.The QRS morphology identical to that observedduring antidromic reciprocating tachycardia, rel-atively short His-atrial (HA) interval in His elec-trogram and its disappearance after ablation areall in favor of the first possibility. The two-for-onephenomenon was the only evidence for presenceof anterograde conduction through atriofascicu-lar pathway during sinus rhythm. In this situa-tion, one sinus beat was conducted down bothfast AV nodal pathway and slow AV nodal andatriofascicular pathways, in which case atriofasci-cular pathway acted as innocent bystander. Thiscooperation between dual AV nodal physiology1436 December 2006 PACE, Vol. 29LATENT ATRIOFASCICULAR PATHWAYFigure 3. 2-for-1 phenomenon observed during sinus rhythm, in which an spontaneous si-nus impulse produces two QRS complexes, first beat narrow complex and second widecomplex, presumably resulting from conduction down both fast AV nodal pathway (nar-row beat) and simultaneous slow AV nodal and atriofascicular pathways (preexcitedbeat). This was the only evidence for anterograde conduction seen during sinus rhythm.A = atrial activation; H = His bundle activation; V = ventricular activation; HRA = record-ing from distal poles of HRA catheter; RVA = recording from distal poles of RVA catheter; His-d= recording from distal poles of His catheter; I, III, V1, and V6 = surface ECG leads.and atriofascicular pathway only resulted in asingle echo beat without induction of AV nodalreentry. No such triple conduction occurred aftersuccessful catheter ablation of the atriofascicularpathway.There is only one prior report of “latent atrio-fascicular pathway.”10 However, there are a pre-vious report of latent accessory pathways withdecremental properties in other locations, one inthe right posteroseptal area and the other in theleft posterior region.11 In the first cases of latentatriofascicular pathway, Davidson et al.10 reportedmany observations like those in our case: long-standing history of wide complex tachycardia; lackof preexcitation in baseline 12-lead ECG; arrhyth-mia induction only by the programmed ventricu-lar stimulation; intermittent ventricular preexcita-tion during atrial fibrillation; and long-term cure ofarrhythmia by delivery of RF energy at recordingsite of accessory pathway potential. As we men-tioned earlier, the initial diagnosis had been ven-tricular tachycardia in the case described here, andDavidson et al. were faced with the same dilemma.We excluded this diagnosis by ability of the lateatrial extrastimuli delivered during tachycardia toadvance ventricular activation without enteringAV node, indicating engagement of atriofascicularpathway in the tachycardia circuit.This case report reinforces importance ofthe diagnostic maneuvers (continuous and singleatrial extrastimulation) in every case of the widecomplex tachycardia with LBBB morphology andleft axis despite absence of antegrade preexcitationduring atrial pacing.References1. Mahaim I. Le bloc bilateral manque´, nouvelle forme anatomique debloc du coer, a` substituer au bloc dit “d’ arborisations.” Ann de Me´d1932; 32:347.2. Mahaim I, Benatt A. Nouvelles recherches sur les connexionssupe´rieures de la branch gauche faisceau de His-Tawara avec clo-sion interventriculaire. Cardiologica 1938; 1:61–76.3. Mahaim I. Kent’s fibers and the A-V paraspecific conduction throughthe upper connections of the bundle of His-Tawara. Am Heart J 1947;33:651–653.4. Klein GJ, Guiraudon GM, Kerr CR, Sharma AD, Yee R, Szabo T, WahJA. “Nodoventricular” accessory pathway: Evidence for a distinctaccessory atrioventricular pathway with atrioventricular node-likeproperties. J Am Coll Cardiol 1988; 11:1035–1040.5. Tchou P, Lehmann MH, Jazayeri M, Akhtar M. Atriofascicular con-nection or a nodoventricular Mahaim fiber? Electrophysiologic elu-cidation of the pathway and associated reentrant circuit. Circulation1988; 77:837–848.6. Lev M, Fox SM, Bharati S, Greenfield JC Jr, Rosen Km, Pick A. Ma-haim and James fibers as a basis for a unique variety of ventricularpre-excitation. Am J Cardiol 1975; 36:880–887.7. Haissaguerre M, Campos J, Marcus FI, Papouin G, Clementy J.Involvement of a nodofascicular connection in supraventriculartachycardia with VA dissociation. J Cardiovasc Electrophysiol 1994;5:854–862.8. Tada H, Nogami A, Naito S, Oshima S, Taniguchi K, KutsumiY. Left posteroseptal Mahaim fiber associated with marked lon-gitudinal dissociation. Pacing Clin Electrophysiol 1999; 22:1696–1699.9. Hluchy J, Schlegelmilch P, Schickel S, Jorger U, Jurkovicova O,Sabin GV. Radiofrequency ablation of a concealed nodoventricularMahaim fiber guided by a discrete potential. J Cardiovasc Electro-physiol 1999; 10:603–610.10. Davidson NC, Morton JB, Sanders P, Kalman J. Latent Mahaimfiber as a cause of antidromic reciprocating tachycardia: Recognitionand successful radiofrequency ablation. J Cardiovasc Electrophysiol2002; 13:74–78.11. Goldberger JJ, Pederson DN, Damle RS, Kim YH, Kadish AH. An-tidromic tachycardia utilizing decremental, latent accessory atri-oventricular fibers: Differentiation from adenosine-sensitive ventric-ular tachycardia. J Am Coll Cardiol 1994; 24:732–738.PACE, Vol. 29 December 2006 1437

Latent atriofascicular pathway participating in a wide complex tachycardia: Differentiation from ventricular tachycardia

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Latent atriofascicular pathway participating in a wide complex tachycardia: Differentiation from ventricular tachycardia

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