Br Heart J 1984; 51: 84-90

Pharmacological observations in patients withnodoventricular pathwaysBORIS STRASBERG,* ALDO COELHO, EDWIN PALILEO, ROBERT BAUERNFEIND,STEVEN SWIRYN, DANIEL SCAGLIOTTI, KENNETH M ROSENtFrom the Section ofCardiology, Depatmen ofMedicine, Abraham Lincoln School ofMedicine, University ofIllinoisColege of M&dicine, Chicago, IUinois, USA

suMMARY Three patients with accessory nodoventricular pathways and re-entry tachycardia arereported. In all three patients the accessory nodoventricular pathway formed the anterograde limbof the re-entry circuit while the His-Purkinje-atrioventricular node axis formed the retrograde limbof the tachycardia in two of the patients and a concealed accessory pathway formed the retrogradelimb in the remaining patient. All three patients also manifested dual anterograde atrioventricularnodal pathways with conduction through the accessory nodoventricular pathways being associatedwith the atrioventricular nodal fast pathway. Type I antiarrhythmic drugs, especially disopyramideand quinidine, were effective for the treatment of the re-entry tachycardia because of their depres-sive action on the nodoventricular pathway. Beta blockers were also effective because of their actionon the atrioventricular nodal portion of the re-entry circuit in one patient and most probably due toatypical (atrioventricular nodal like) properties of a retrogradely conducting accessory pathway in asecond patient.

One of the rare types of re-entrant paroxysmaltachycardia reflects the occurrence of re-entrance vianodoventricular fibres. In these unusual tachycardiasanterograde conduction is usually via a right sidedinserting nodoventricular pathway, producing atachycardia resembling ventricular tachycardia with aleft bundle branch block pattern.

Nodoventricular pathways might respond with anincrease in refractoriness to drugs which depress theatrioventricular node or quinidine like agents, orboth. There are few systemic data concerning thepharmacology of nodoventricular fibres and circusmovement tachycardias using these fibres.We report the drug responses, the electrophysiol-

ogy of nodoventricular fibres as related to anterogradedual atrioventricular nodal pathways, and observa-tions on the nature of retrograde conduction duringnodoventricular circus movement tachycardia in threepatients with re-entrant paroxysmal tachycardia.

*Present address: Coronary Cae Unit, Beilinson Medical Center, Petah Tiqva49100, Israel.tDeceased.Accepted for publication 7 July 1983

Case I

A 20 year old man with a five year history of parox-ysmal tachycardia and no evidence of organic heartdisease was studied. Electrocardiograms during sinusrhythm were normal (Fig. 1). During episodes oftachycardia the electrocardiogram showed wide QRScomplexes (0.12 s) with left bundle branch blockmorphology, an axis of -20", and a heart rate of 230beats/min.

ELECTROPHYSIOLOGICAL STUDIESElectrophysiological studies showed normal conduc-tion intervals during sinus rhythm (AH: 70 msec,HV: 47 msec, QRS: 90 msec). With incremental atrialpacing from heart rates of 100 to 160 beats/min theAH interval gradually increased from 75 to 105 msecand concomitantly the HV interval graduallydecreased from 30 to 10 msec with the appearance ofpartial pre-excitation. At atrial paced rates of 170 to200 beats/min the His bundle electrogram mergedinto the QRS complex, which had a left bundlebranch block appearance similar to his spontaneoustachycardia (Fig. 2). The time from stimulus to theonset of the QRS complex increased from 130 to 165msec despite the shortening HV interval and appear-

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Pharmacological observatioms in patients with nodoventricular pathways

Sinus rhythm TachycardiaII III Vi V6 I II III

case l

viI II III V1 V6iuA.i.W

I. FW.Mi . fig |....i! IZCase 2

Fig. 1 Electrocardiograms of thethree reported patius during sinusrhythm and dunng tachycardia.

ICae II III Vi V6 I II iX3V6

Case 3

ance of complete pre-excitation. The anterogradeblock rate for the anomalous pathway was 210 beats/min, with conduction continuing through the normalatrioventricular nodal pathway with a right bundlebranch block aberration.

Atrial extrastimulus testing performed at three dif-ferent cycle lengths showed dual atrioventricularnodal pathways. Accessory pathway beats were shownat the three atrial cycle lengths tested, the effectiverefractory periods being 410, 335, and 335 msec. The

Control

LILIIL III

Vi

HRA

PCs A

HBE.IRVE t-,

accessory pathway beats occurred when the atrioven-tricular nodal fast pathway was used, and they had aneffective refractory period longer than the effectiverefractory period of the atrioventricular nodal fastpathway.

Incremental ventricular pacing showed a normalretrograde sequence with a retrograde atrioventricularnodal block rate of 200 beats/min. From paced ratesof 150 beats/min and faster a retrograde His deflectionwas clearly seen. Ventricular extrastimulus testing

iininuuriqinmn1

Propranotol + LIouabciin

Fig. 2 Case 1. Atrialpacingfrom the high rightatrium (HRA) showing pre-excitation beats withleft bundle branch block pattem during controlstudy and after admininstration ofpropranolol andouabain. Type I antiarrhythmics (procainamide,quinidine, disopyramide) resulted in loss ofprexcitation. PCS, proximal coronary sinus;HBE, His bundle electrogram; RVE, rightventricular electrogram; S, stimulus artefact.

Procainamide ALI

Quinidine LI

Dysopyramide LI _ _

V1 V6

r-=7n. -=

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Strasberg, Coelho, Palileo, Bauernfeind, Swiryn, Scaglioti, RosenControl

Propranolol + ouaboin

I f iIIi I I I I

Procainamide

QuiNdine

s ;V__m. .A

=Disopyromide

LII

LIIIVi AAA A A

HRA

Fig. 3 Study ofnodoventiuar re-entry, tachvsingle ventricular extrastimulus technique. Sustawas induced before and after administration ofIouabain. Non-sustained tachycardia or single vwere induced after type I antarrhythmics. AbbrFig. 2.

showed a single continuous retrogradnormal retrograde sequence. A retrogratial was always seen, and at close coulincreases in VA paralleled increases inzone for antidromic re-entrant echo beat

Nodoventricular re-entrant tachycardia (Fig. 3) wasreadily induced with ventricular pacing or extra-stimulus. Spontaneous episodes were started by rightventricular premature contractions. The tachycardiawas characterised by a left bundle branch block pat-tern (identical to the spontaneous arrhythmia and tothe left bundle branch block pattern paced atrialbeats). The cycle length of the tachycardia was 300msec (heart rate of 200 beats/min). His potentialswere clearly seen after the ventricular electrogram,most probably because of exclusive retrograde con-duction through the left bundle branch His bundle(retrograde right bundle branch block). Endocardialventricular activation mapping during tachycardiashowed the proximal right ventricular outflow tract asthe earliest site of ventricular activation. Retrogradeatrial sequence mapping was normal with a ven-triculoatrial conduction time of 125 msec.

PHARMACOLOGICAL STUDIESAfter two control studies (on two separate days),which showed inducible sustained nodoventricular

...,~._tachycardia (see above), serial drug testing was per--- v-< formed over several days (Fig. 2 and 3). Intravenous

propranolol (0-1 mg/kg) had no effect on the antero-grade anomalous pathway block rate and decreasedthe retrograde atrioventricular nodal block rate by 10beats/min. Addition of ouabain (0.01 mg/kg) resultedin no change in the anterograde anomalous pathwayblock rate and a further 10 beats/min decrease in theretrograde atrioventricular nodal block rate. Re-entrant tachycardia was sustained with both drugswith an increase in the tachycardia cycle length of 20msec.

After administration of procainamide 1-5 gintravenously the anomalous pathways were not seenduring anterograde stimulation (increased refractori-ness) and the retrograde block rate (atrioventricularnodal) decreased from 210 to 180 beats/min. Non-sustained re-entry tachycardia (maximum of threebeats) was induced. A spontaneous sustained episodeof tachycardia with a slight increase in cycle lengthwas observed only at the end of the study while theprocainamide concentration was decreasing (concen-

icardia using the tration of 6.1 mg0/o). Quinidine 1-6 g/day decreasedied tachycardia the anterograde aniomalous pathways block rate topropranolol and below 160 beats/min and the retrograde atrioventricu-reniations as in lar nodal block rate to 170 beats/min. No tachycardiacould be induced. Disopyramide 1-2 g/day had an

identical effect to quinidine on the anomalous path-way anterograde block rate but decreased the retro-

le curve with grade atrioventricular nodal block rate to 140 beats/ide His poten- min. No tachycardia could be induced. Testing withpling intervals the three type I antiarrhythmic drugs showed thatVH. An echo induced non-sustained tachycardia or ventricularts was defined. echoes always terminated with block in the anomalous

LILIILIIIvi

UDA

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LDA

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87Pharmacological observations in patients with nodoventricular pathways

pathway (anterograde weak link). The patient hasremained asymptomatic with quinidine for 10 months(previously having averaged one episode of tachycar-dia a month).

Case 2

A 44 year old woman with a five year history of recur-rent palpitations and no evidence of organic heart dis-ease was studied. Treatment at different times withdigoxin, propranolol, or both, had had no affect onthe incidence or duration of the palpitations. Treat-ment with quinidine and procainamide was startedbut had to be stopped promptly because of sideeffects. The resting electrocardiogram was normal(Fig. 1). A rhythm strip during an attack showedparoxysmal tachycardia (QRS complex of 0-08 s) at arate of 250 beats/min and a paroxysm ofnon-sustainedtachycardia (six beats) with wide QRS complexes.Twelve lead electrocardiograms of the tachycardiaobtained during electrophysiological study showed awide QRS complex tachycardia with left bundlebranch block morphology and an axis of 600 (Fig. 1).

ELECTROPHYSIOLOGICAL STUDIESElectrophysiological studies showed normal conduc-tion intervals (AH: 66 msec, HV: 43 msec, QRS: 87msec). Incremental atrial pacing from rates of 100 to130 beats/min showed gradual increases in AH inter-vals from 70 to 100 msec. At paced rates of 130 to 190beats/min, with the beginning of pacing and prolonga-tion of the AH intervals, the HV interval shortenedup to the point of merging inside the QRS complex.With the shortening of the HV interval the conductedbeats had an incomplete left bundle branch block pat-tern and developed a complete left bundle branchblock pattern when the His potential had completelymerged inside the QRS complex. The time betweenthe stimulus and the onset of the QRS complexincreased from 170 to 190 msec despite the shorteningof the HV interval and the appearance of completepre-excitation. One to one conduction through theanomalous pathway was present up to paced atrialrates of 190 beats/min. At 200 beats/min Wenckebachperiodicity with a narrow QRS complex was observed(anomalous pathway and atrioventricular nodal blockrates). Atrial extrastimulus testing performed at dri-ven cycle lengths of 500 and 400 msec showed dualatrioventricular nodal pathways with single atrioven-tricular nodal re-entrant atrial echoes (usual variety)and anomalous pathway conducted beats when a criti-cal atrioventricular nodal conduction delay wasachieved. The anomalous pathway effective refractoryperiod was 300 to 250 msec (atrial limited) respec-tively. The anomalous pathway seemed to be func-tionally related to the atrioventricular nodal fast

pathway since fusion beats (between conductionthrough the His Purkinje system and anomalouspathway) were observed at the early portion of thecurve while conduction occurred through the fastpathway. The atrioventricular nodal slow pathway(with single atrioventricular nodal re-entry atrialechoes) was observed only when conduction over theanomalous pathway failed.

Incremental ventricular pacing showed a normalretrograde sequence and a retrograde block rate of 200beats/min. Ventricular extrastimulus testing showed asingle retrograde conduction curve (with normalsequence). The H potential together with the retro-grade A wave moved out of the ventricular electrogramwhen the ventricular extrastimulus was closely cou-pled. An echo zone for antidromic nodoventricularre-entrant ventricular echoes was also defined.Endocardial ventricular mapping was performed dur-ing atrial pacing with conduction through theanomalous pathway. The earliest site of activationcould not be defined, but the anterior right ventricu-lar areas (apex and anterior proximal outflow tract)were earlier than the posterior (inflow) areas.

Nodoventricular re-entrant tachycardia was readilyinduced with rapid ventricular pacing and occurredspontaneously after premature ventricular contrac-tions. The tachycardia was characterised by a leftbundle branch block pattern (identical to the one seenwith atrial pacing). The cycle length of the tachycar-dia varied between 280 and 310 msec. The His poten-tial was not visible. The retrograde atrial sequencewas normal with a ventriculoatrial conduction time of90 msec.

PHARMACOLOGICAL STUDYAfter the control studies, which showed induciblesustained nodoventricular re-entry tachycardia, serialdrug testing was performed over several days.Quinidine and procainamide were not tested becauseof previous intolerance.Ouabain (0.01 mg/kg) resulted in no change in

anterograde or retrograde block rates, nor in theanomalous pathway effective refractory period. Re-entry tachycardia was inducible and sustained with acycle length similar to that in the control study.Intravenous propranolol (0.1 mg/kg) did not affect theanomalous pathway anterograde block rate or effec-tive refractory period but decreased the retrogradeblock rate from 200 to 170 beats/min. Tachycardiacould not be induced. Disopyramide (1-2 g/day)decreased both the anterograde anomalous pathwayand retrograde atrioventricular nodal block rates from200 to 150 beats/min, resulting in lack of induction ofthe tachycardia. No pre-excited beats were seen dur-ing atrial extrastimulus testing, implying a prolongedanomalous pathway effective refractory period. The

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patient has remained asymptomatic on beta blockersfor 12 months.

Case 3

A 17 year old girl with a history of myocardial con-tusion and recurrent tachycardia was studied.Treatment with digoxin and propranolol did not alterthe frequency of palpitations. No evidence of organicheart disease was found. The resting electrocardio-gram showed possible small delta waves (Fig. 1). The12 lead electrocardiogram during tachycardia showeda wide QRS complex tachycardia at a rate of 250beats/min with a left bundle branch block pattern andleft axis deviation of -45° (Fig. 1).

ELECTROPHYSIOLOGICAL STUDIESElectrophysiological studies showed a normal AHinterval (70 msec) and variable HV interval with dif-ferent degrees of pre-excitation. Incremental atrialpacing showed a gradual but slight prolongation of theAH and AV intervals. The AV nodal Wenckebachrate was 250 beats/min. At a paced rate of 240 beats/min, after the first conducted beat the successive con-ducted beats had a left bundle branch block patternand a time between the stimulus and the onset of theQRS of 195 msec; they were not preceded by a Hispotential and were similar to the patient's spontane-ous tachycardia. Atrial extrastimulus testing showeddual atrioventricular nodal pathways. At close coupl-ing intervals on the atrioventricular nodal fast path-way, QRS conducted complexes had a left bundlebranch block appearance, were not preceded by Hispotential, and showed a 20 msec increase in atrioven-tricular conduction time. When conduction jumpedto the slow pathway the QRS complex became nar-row. The effective refractory period of the left-bundle-branch-block-like conducted beats (anomal-ous pathway conducted beats) was 255 msec whentested at sinus rhythm (cycle length of 580 msec) andincreased to 270 msec when tested at a driven atrialcycle length of 500 msec.

Ventricular pacing showed a retrograde block rateof 230 beats/min. The retrograde conduction se-quence was abnormal with coronary sinus sites pre-ceding right sided sites. Nodoventricular re-entranttachycardia was readily induced with ventricularextrastimulus testing and rapid atrial and ventricularpacing. The tachycardia had a cycle length of 300msec. It was characterised by wide QRS complexeswith a left bundle branch block and left axis deviationpattern. No His potentials were seen during thetachycardia. Endocardial ventricular mapping of thetachycardia showed the inferior basal right ventricleas the earliest area of ventricular activation. Mappingof retrograde atrial activation showed the coronary

sinus as the earliest site (130 msec), followed by theproximal and mid-coronary sinus (135 and 140 msecrespectively), the low septal right atrium (155 msec),and the high right atrium (180 msec).

PHARMACOLOGICAL STUDYAfter control studies, which revealed inducible sus-tained nodoventricular re-entry tachycardia, serialdrug testing was performed over several days.

Intravenous propranolol decreased the anterogradeatrioventricular nodal block rate from 250 to 210beats/min and decreased the anomalous pathwayanterograde block rate from 240 to 200 beats/min.The retrograde block rate decreased from 230 to 180beats/min. Re-entry tachycardia was not inducible.Intravenous procainamide (1 g over 20 min) was givenduring an episode of induced tachycardia. After sevenminutes of infusion the tachycardia stopped spon-taneously, with the site of block occurring in theanterograde limb (anomalous pathway). After com-pletion of the procainamide infusion, repeat studiesshowed that procainamide did not alter the antero-grade atrioventricular nodal block rate and that theretrograde block rate decreased to 190 beats/min.Anomalous pathway beats were not seen either duringincremental atrial pacing or during atrial extra-stimulus testing. With ventricular extrastimulus test-ing non-sustained nodoventricular tachycardia (10beats) was induced, but subsequently sustainedtachycardia was induced with an increase in cyclelength from 300 to 320 msec. The procainamide con-centration measured at that time was 6-8 mg/100 ml.Oral quinidine (1-6 g/day) and disopyramide (0.8 g/day) decreased the anterograde atrioventricular blockrate to 190 beats/min, and no pre-excited beats wereobserved (total anomalous pathway block). Theretrograde block rate decreased to 170 and 130beats/min respectively. No tachycardia could beinduced.The patient was discharged and prescribed oral

propranolol and has remained free of arrhythmias fortwo and a half years.

Discussion

Re-entry tachycardia due to nodoventricular fibres isrelatively uncommon compared with the number ofreported cases of the Wolff-Parkinson-White syn-drome with re-entrant tachycardia. Nevertheless,there are enough reported cases to suggest certaincharacteristics of this type of fibre and of the re-entrytachycardia related to it.

Gallagher et al.I reported six patients with sus-pected nodoventricular pathways, all with re-entranttachycardia. In addition, a review of the publishedwork regarding this type of arrhythmia showed that

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the resting electrocardiogram could be normal orshow pre-excitation. QRS complexes duringtachycardia showed a left bundle branch block pat-tern. This distinct electrocardiographic pattern sug-gested a right ventricular insertion of the nodoven-tricular fibre.

In most of the reported cases the re-entry circuithas been characterised by anterograde conductionover the accessory pathway (producing a wide QRScomplex) and retrograde conduction over the His-Purkinje atrioventricular node axis.

In one of the cases of Gallagher et al. an inversere-entry circuit was postulated. In other reports, thenodoventricular pathway has been considered as abystander for the first beat of a re-entry circuit or forthe entire length of the tachycardia with the atrioven-tricular node considered as the site of re-entry(atrioventricular nodal re-entry).2-4Our patients presented with characteristics similar

to those reported in previous cases. They were youngand had no evidence of organic heart disease. Theywere referred for evaluation of rapid wide QRS com-plex tachycardia with ventricular tachycardia diag-nosed in two of them. The basal electrocardiogramwas normal in two patients, while a possible deltawave (with narrow QRS complex) was present in theother.

Electrophysiological studies showed normal basicconduction intervals in two patients while the thirdpatient had variable HV intervals according to thedegree of pre-excitation. Ventricular pre-excitationbecame clearly evident when atrial pacing or atrialextrastimulus testing induced enough (critical)atrioventricular nodal delay to allow greater ventricu-lar depolarisation through the anomalous pathway.Two of our patients (cases 2 and 3) showed dualanterograde atrioventricular nodal pathways withconduction through the nodoventricular pathwayrelated only to conduction via the atrioventricularnodal fast pathway. This contrasts with previousobservations where the nodoventricular pathway wasrelated to the atrioventricular nodal slow pathway.2 3 5In case 1 conduction through the nodoventricularpathway was also related to the fast pathway, but asthe refractory period of the accessory pathway waslonger than the refractory period of the atrioventricu-lar nodal fast pathway we cannot establish with cer-tainty if the conduction was related only to the fastpathway. It is not clear in our patients why all threehad dual atrioventricular nodal pathways and whethertheir occurrence relates to the occurrence of nodoven-tricular connections. It is also not clear why nodoven-tricular activation occurred only when the fast path-way was used and not when the slow pathway wasused. The results imply an anatomical discontinuitywithin the atrioventricular node, with a nodoventricu-

lar pathway being in partial series at least with theatrioventricular nodal fast pathway and not the slowpathway. Since the anatomical locations of fast andslow atrioventricular nodal pathways are not known(if there is an anatomical basis for dual atrioventricu-lar nodal pathways), it would only be speculative totry to explain this relation.

Reciprocating tachycardia was induced in all threepatients. Ventricular stimulation (rapid pacing orextrastimulus) allowed the easiest induction of thetachycardia. The tachycardia had a left bundle branchblock pattern in three patients; it had a 1:1 ven-triculoatrial relation and conducted back to the atriumthrough the His-Purkinje atrioventricular node axis intwo patients and was a concealed accessory pathway inthe third patient.The effect of antiarrhythmic agents on the proper-

ties of nodoventticular fibres and the associated re-entry tachycardia has not been closely examined. Dif-ferent drugs such as digoxin, verapamil, quinidine,and disopyramide (in low doses) have been describedas ineffective.6-8 Gallagher et al.' suggested thatquinidine was effective in preventing tachycardia butthey did not present any electrophysiological data insupport of this.

In our patients disopyramide (0-8-1.2 g/day) wastested in all three patients, and proved to be the mosteffective drug, depressing both limbs of the re-entrycircuit. Quinidine (1.6 g/day) seemed as effective asdisopyramide for preventing tachycardia induction,but was tested in only two patients and its effects onthe re-entry circuit were not as pronounced as diso-pyramide. Procainamide was ineffective in the twopatients tested; the reason for this is unclear as pro-cainamide shows similar type I antiarrhythmic actionsto quinidine and disopyramide.Ouabain was tested in only one patient and proved

ineffective. Intravenous propranolol was effective intwo patients, acting on the retrograde limb of thetachycardia. In one of the patients who responded topropranolol the retrograde limb of the re-entry circuitwas the His-Purkinje-atrioventricular nodal axis whilethe second patient had an eccentric retrograde con-duction, suggesting a retrogradely conductinganomalous pathway with atrioventricular node likeproperties.The electrophysiological studies and drug

responses in our patients provide some understandingof the properties of nodoventricular pathways. In twoof the patients the nodoventricular pathways had elec-trophysiological and pharmacological properties simi-lar to those observed in typical Kent bundles(decreased refractoriness with decreased cycle length,increased refractoriness after administration of type Iantiarrhythmic drugs, and no change in refractorinessafter administration of drugs that act on atrioventricu-

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lar node like tissue-for example, ouabain and prop-anolol). In our last patient the nodoventricular path-way had some atrioventricular node like properties.Refractory periods increased with decreasing cyclelengths and propranolol decreased the block rate by40 beats/min. Nevertheless, the effects of type I anti-arrhythmic drugs were similar to the effects observedin the other two patients. The atrioventricular nodelike properties seen in the last patient could be relatedto properties of the anomalous pathway, presentingatrioventricular node like properties similar to someanomalous pathways of the Kent type or to propertiesof the atrioventricular nodal tissue adjacent to theemergence of the nodoventricular pathway from theatrioventricular node and not related to the nodoven-tricular pathway itself.There is clearly a group of patients with relatively

distinct characteristics including a tendency towards anormal electrocardiogram during sinus rhythm,paroxysmal tachycardia with a left bundle branchblock pattern, and a capability for anterograde con-duction with identical QRS complex pattern, whenappropriate atrioventricular nodal delay and longanomalous pathway conduction times are achieved.These patients can now be identified on clinical

grounds. In addition, our electrophysiological studiesshowed appreciable sensitivity to at least some type Iagents and sporadic sensitivity to atrioventricularnode like depressant drugs for preventing paroxysmaltachycardia. These data should be useful to other doc-tors concerned with the management of patients withthis unusual variety of paroxysmal tachycardia.

This study was supported in part by an InstitutionalTraining Grant from the National Heart, Lung, andBlood Institute, Bethesda, Maryland, and Research

Grants from the Eleanor B Pillsbury Resident TrustFund, Chicago, Illinois, and a grant from the BanesEstate, Chicago, Illinois.

References

1 Gallagher JJ, Smith WM, Kasell JH, Benson DW Jr,Sterba R, Grant AO. Role of Mahaim fibres in cardiacarrhythmias in man. Circulation 1981M64: 176-89.

2 Wellens HJJ. Electrical stimulation of the heart in the studyand treatment of tachycardias. Baltimore: University ParkPress, 1971: 97.

3 Ward DE, Camm AJ, Spurrell RAJ. Ventricular preexci-tation due to anomalous nodoventricular pathways:report of 3 patients. EurJ Cardiol 1979; 9: 111-27.

4 Morady F, Scheinman MM, Gonzalez R, Hess D. His-ventricular dissociation in a patient with reciprocatingtachycardia and a nodoventricular bypass tract. Circula-tion 1981; 64: 83944.

5 Sung RJ, Styperek JL. Electrophysiologic identificationof dual atrioventricular nodal pathway conduction inpatients with reciprocating tachycardia using anomalousbypass tracts. Circulation 1979; 60: 1464 76.

6 Ward DE, Camm J, Cory-Pearce R, Fuenmayor I, ReesGM, Spurrell RAJ. Ebstein's anomaly in association withanomalous nodoventricular conduction. Pre-operativeand intra-operative electrophysiological studies. 7 Elec-trocardiol 1979; 12: 227-33.

7 Mark AL, Basta LL. Paroxysmal tachycardia withatrioventricular dissociation in a patient with a variant ofpreexcitation syndrome.7Electrocardiol 1974; 7: 355-64.

8 Heddle WF, Tonkin AM. Atrial and His bundle stimula-tion with an accessory nodo-ventricular connection.PACE 1980; 3: 286-91.

Requests for reprints to Dr Boris Strasberg, CoronaryCare Unit, Beilinson Medical Center, Petah Tiqva49100, Israel.

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