J. ELECTROCARDIOLOGY 13 (1), 1980, 85-92

Enhanced Atrioventricular Nodal Conduction in a Patient with Dual Extranodal Pathways

BY ROLANDO GONZALEZ, M.D., MELVIN M. SCHEINMAN, M.D., JAWAHER DESAI, M.D., EDWARD KERSH, M.D. AND ROBERT W. PETERS, M.D.

SUMMARY A patient was admitted to the hospital with wide complex tachycardia and a

history of recurrent palpitations. Electrophysiologic studies showed evidence of dual atrioventricular (AV) accessory pathways. One proved to be an anteroseptal (possible right anterior) pathway probably capable of only unidirectional con- duction. The other pathway was in the posterior septum and conducted only in the retrograde direction. The tachycardia circuit involved anterograde conduc- tion via either the AV node-His axis or the anteroseptal pathway and retrocon- duction over the posteroseptal accessory pathway. In addition, enhanced AV nodal conduction (or partial AV nodal bypass) was also present. Enhanced AV nodal conduction coupled with two accessory AV nodal pathways has rarely been described in English medical literature.

Previous reports have carefully described anatomic, 1 electrocardiographic, 2,3 and electrophysiologic 4-v evidence of more than one accessory pathway in pa- tients with the Wolff-Parkinson-White syndrome. The introduction of surgical techniques for ablation of an accessory pathway s demands precision in the elec- trophysiologic evaluation of patients with ventricular preexcitation. Reported herein is a patient with the unique finding of two extranodal accessory pathways and enhanced atrioventricular (AV) nodal conduction (or AV nodal bypass).

CASE REPORT A 48-year-old man with a 3-year history of

recurrent palpitations was admitted to San Francisco General Hospital Medical Center. The episodes occurred approximately six times per year and were associated with mild precordial chest discomfort. Digoxin (0.25 mg/day orally) was prescribed in December 1977. On June 12, 1978, a 12-lead ECG (dur- ing an episode of palpitations) showed a broad complex tachycardia (Fig. 1). The tachycardia terminated spontaneously and the 12-lead electrocardiographic recording failed to show evidence of ventricular preexcitation. Elec- trophysiologic studies were performed to con- firm or negate the referr ing diagnosis of ventricular tachycardia.

All medications were terminated 3 days prior to study. Informed written consent was obtained and studies were performed in the nonsedated, postabsorptive state in the car- diac catheterization laboratory. Three quad- ripolar electrode catheters were inserted into the right femoral vein and positioned against

From the Medical Service, San Francisco General Hospi- tal Medical Center, and the Department of Medicine, University of California, San Francisco, California. The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked "advertisement" in accord- ance with 18 U.S.C. w 1734 solely to indicate this fact. Reprint requests to: Dr. Melvin M. Scheinman, Bldg. 30, Room 3301, San Francisco General Hospital Medical Center, 1001 Potrero Avenue, San Francisco, California 94110.

the high lateral r ight atrium, across the tricuspid valve, and against the apex of the right ventricle, respectively. An additional multipolar electrode catheter was inserted into a medial antecubital vein and positioned in the mid portion of the coronary sinus (CS). Surface leads X, Y, and Z of the Frank orthog- onal lead system were displayed simultane- ously with intracardiac recordings from the high right atrium, His bundle electrogram (HBE), or CS (or left atrial) electrogram, and the right ventricular apex (RV) on an Elec- tronics for Medicine DR-8 oscilloscope. The AH interval was measured from the rapid component of the low right atrial electrogram to the onset ef the initial rapid component of the His bundle deflection. The HQ interval was measured from the onset of the first rapid His deflection to the first recording of ven- tricular activation from the surface leads. Re- cordings were obtained at a paper speed of 100 or 200 mm/sec with time lines generated at 1-sec intervals.

Atrial or ventricular pacing was performed through the distal electrode pairs. Pulses of 2 msec dura t ion at 2-3 t imes diastolic threshold were delivered by means of a pro- grammable st imulator (Bloom Associates, Narbeth, Pennsylvania). Overdrive right atrial or left atrial pacing was performed at cycle lengths 480, 430,380, 330, 290, 280, and 260 msec. Anterograde refractory periods using the extrastimulus technique s were ob- tained at a paced cycle length of 480 msec (the entire atrial diastolic interval was scanned

85

86 GONZALEZ ET AL

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Fig. 1 Wide complex tachycardia (with left bundle branch configura- tion) with ventricular rate of ap- proximately 270 beats/min.

with extrast imuli introduced at 10 msec de- crements) from the right and left atria. Simi- larly, right ventricular overdrive pacing (at similar cycle length) and right ventricular re- fractory periods were obtained by the extra- stimulus technique.

Retrograde atrial activation was recorded during both tachycardia and right ventricular pacing using the method described by Gal- lagher et al. 1~ In brief, the high right atrial catheter was replaced by a modified Brocken- b rough ca the t e r t h a t enab led d i rec t iona l orientation and detailed exploration of the tricuspid annulus. In addition, retrograde left atrial activation sequence was determined by gradual withdrawal of the CS catheter to the orifice of the CS. Enhanced AV Nodal Conduction.

Control recordings revealed an AH of 55 msec while the HQ was 50 msec, and yen-

t r icular preexcitat ion was occasionally re- corded (Fig. 2). Overdrive atrial pacing from either the right or left a t r ium revealed 1:1 AV conduction up to a paced cycle length of 290 msec. The AH interval at this paced cycle length showed only 55 msec prolongation from control recordings. The last two com- plexes of these series showed prolongation of t h e A H to 150 m s e c , b u t AV n o d a l Wenckeback conduction was not observed. Both right and left atrial overdrive pacing at a cycle length of 260 msec resulted in a 6:5 AV nodal Wenckebach conduc t ion sequence . Overdrive pacing from either the right or left a t r ium was never associated with ventricular preexcitation. Unidirectional Retroconduction Via a Post- eroseptal Pathway.

Cri t ical ly t imed a t r ia l p rema tu re beats were used to initiate and terminate bouts of

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87 DUAL SEPTAL PATHWAYS

Fig. 2 Simultaneous recordings of surface leads X, Y, and Z of the Frank orthogona] system and from high right atrium (HRA), coronary sinus (CS), His bundle electrogram (HBE) and right ventricular apex (RVA). The first two complexes are conducted solely via the AV node-His axis with an AV nodal (A-H) conduction time of 55 msec and infranodal conduction time (H-Q) of 50 msec. The last complex shows a delta wave in the surface leads and shortening of the H-Q interval and results from simultaneous ventricular activation via the normal and accessory pathway.

s u p r a v e n t r i c u l a r t a c h y c a r d i a . D u r i n g tachycardia, anterograde conduction usually occurred via the AV node-His axis, whereas retroconduction always occurred via a post- eroseptal accessory pathway. Two lines of evidence support the contention that a post- eroseptal bypass was present and was capable of only retrograde conduction.

1) Overdrive atrial pacing near the bypass site failed to produce ventricular preexcita- tion. 11,~2

2) Supravent r icu lar tachycardia was as- soc i a t ed w i t h t h r e e d i f f e r e n t QRS mor- phologies: normal, right, or left bundle branch block configurations. Regardless of QRS mor- phology during tachycardia , the CS atr ial electrogram always preceded that from either the right atrial septum (HBE) (Fig. 3) or from any other site along the tricuspid annulus (Fig. 4), thus establishing a posteroseptal ac- cessory pathway. 13 Sole ut i l iza t ion of the posteroseptal pa thway dur ing tachycard ia was also suggested by the differences in re- trograde ventricular-to-atrial activation dur- ing tachycardia. The interval from the initial vent r icular deflection to re t rograde spetal atrial activation was longer during left bun- dle branch block tachycardia (160 msec! (Fig.

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5) than during either the narrow (130 msec) or r ight bund le branch block (130 msec) (not shown) forms of the tachycardia. The longer V-A 1 d u r i n g l e f t b u n d l e b r a n c h b l o c k tachycardia suggests incorporation of the left bundle branch in the tachycardia circuit. 14,15 On the other hand, there was no evidence of r i gh t - s ided b y p a s s p a r t i c i p a t i o n in ven- triculoatrial conduction. Anterograde Conduction Via an Anteroseptal Pathway.

Intermit tent ventricular preexcitation was occasionally present during sinus rhythm or tachycardia but was never ~inducible" by either right or CS atrial overdrive, or progres- sively premature atrial extrastimulation. The reasons for these findings remain obscure. We believe that these complexes represent t rue ventricular preexcitation rather than fu- sion wi th r andom p r e m a t u r e ven t r i cu la r depolarizations because 1) typical concertina progression ~6 was observed (Fig. 6); and 2) ventricular premature depolarizations unas- sociated with preceding atrial activation were never observed throughout the study.

Anterograde conduction via an anterosep- tal pathway is strongly suggested by orienta- tion of the initial forces posteriorly, inferiorly

88 GONZALEZ ET AL

Fig. 3 "Anterior" is the atrial electrogram recording from a straight anterior position along the tricuspid annulus; see Fig. 2 for other abbreviations. The figure shows a supraventricular tachycardia with cycle length of 285 msec. The first, second and fourth complexes are conducted via the AV node-His axis while the third and fifth complexes (arrows) represent fusion beats from normal and accessory pathways. The CS atrial electrogram precedes that from the septum or anterior right atrium. Ventricular preexcitation during tachycardia with left atrial retrograde preexcitation proves the existence of two extranodal accessory path- ways. The time from ventricular activation (surface leads) to local atrial activation is given (160, 110 and 125 msec). The interval from ventricular depolarization to the atrial septal electrogram is 130 msec. This interval lengthens when the tachycardia shows a left bundle branch block configuration (see Fig. 6). The lines in front of the last four complexes denote onset of QRS in the surface recordings.

and leftward (Fig. 6). These initial forces have never been described for posteroseptal acces- sory pa thways . 17,1s Moreover , m a x i m a l l y preexcited complexes showed a shortening of the initial ventr icular activation from surface leads to r ight septal ventr icular activation as recorded from the HBE, and a lengthening of the right septal electrogram to ei ther the high

posterobasal left ventr icular electrogram (re- corded from the CS catheter) or r ight ven- t r icular apical e lec t rogram compared with normally conducted beats (Figs. 2, 3 and 6). 19 The presence of dual extranodal pathways is proved by vent r icular preexci tat ion during tachycardia associated wi th retrograde left atrial preexcitat ion (Figs. 3 and 5).

RETROGRADE ATRIAL EXCITATION DURING RIGHT VENTRICULAR PACING (CL= 330)

Mitral. / valve I Tricuspid

valve

Coronary sinu~ O ~ Annulus 10

O Bundle of His

Fig. 4. Pictorial designation of retrograde atrial activation excita- tion sequence along tricuspid and mitral annulus (modified from Gallagher et al TM) during right ventricular pacing (cycle length = 330 msec). The earliest area of atrial preexcitation occurs near the coronary sinus orifice. A simi- lar atrial map was recorded during supraven t r i cu la r tachycardia . During tachycardia, the coronary sinus atrial electrogram always preceded that from any other right atrial site.

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DUAL SEPTAL PATHWAYS 89

Fig. 5. Supraventricular tachycardia with left bundle branch block contour that is similar in form and rate to the spontaneous tachycardia (Fig. 1). The interval from ventricular depolarization to the septal atrial electrogram is 160 msec. The last beat of this figure is probably a fusion complex (partial preexcitation). See Fig. 2 for definitions of abbreviations.

Retrograde Conduction. Vent r i cu l a r overdr ive pacing at longer

p a c e d c y c l e l e n g t h s s h o w e d n e a r - s imul taneous re t rograde act ivat ion of the septal and CS atrial electrograms (Fig. 7). This finding is compatible with retrograde atrial fusion from impulses arriving from the posteroseptal and ei ther His-AV node (en- hanced conduction) or anteroseptal pathways. Progressively earlier premature ventr icular d e p o l a r i z a t i o n s r e s u l t e d in a c o n s t a n t s t imulus to the CS atrial electrogram, but with progressive prolongation of the st imulus to the septal atrial electrogram (Fig. 7). Right ventr icular overdrive pacing at shorter cycle lengths (Fig. 4) resulted in exclusive retro- grade conduction via the posteroseptal acces- sory pathway. At a right ventricular paced cycle length of 280 msec, Mobitz II retrograde ventriculoatrial block was observed (Fig. 8). The atrial septal electrogram showed gradual lengthening prior to retrograde ventriculo- atrial block. Because the CS electrogram re- mained in a relatively fixed relationship to ventr icular depolarization, it is l ikely that retroconduction proceeded via the posterosep- tal pa thway and the delayed atrial electrog- ram from the septum was due to progressive interatrial conduction delay. It is highly un- l ike ly t ha t s imul t aneous re t rograde ven- triculoatrial Wenckebach conduction occurred over the His-AV node axis (or anterospetal pathway) because in such a case one would have to postulate universal simultaneous ret- rograde block in both pathways. Of further interest was the sequence of retrograde atrial depolarization following the pause (Fig. 8).

The septal electrogram always preceded that from the CS which in turn usual ly preceded the high right a t r ium electrogram. However, on occasion (Fig. 8) the high right a tr ium e l e c t r o g r a m p receded t h a t f rom the CS suggest ing re t rograde conduction over the normal AV node-His axis or via a septal or right-sided accessory AV nodal pathway.

DISCUSSION Previous reports have shown anatomic, 1

e lec t rocard iographic 2'3 and electrophysio- logic 4-7 ev idence for m u l t i p l e accessory pathways in patients with preexcitation. Gal- lagher et al., 7 for example, found that five of 135 patients with the Wolff-Parkinson-White syndrome had evidence of two accessory AV pathways and an additional 12 had a single pa thway with enhanced AV conduction. Simi- larly, unidirectional conduction in an acces- sory pathway has been described previously in a number of reports. 4'6'2~ The case pre- sented in this report appears to be unique in tha t dual septal accessory pathways and en- hanced AV nodal conduction were present in this patient. In searching for an anatomic model to explain our findings, one might en- vision mult iple septal accessory pa thways which functionally serve as partial (enhanced AV nodal conduction) or complete AV node bypass tracts. It is well appreciated, however, t ha t the anatomic basis for enhanced AV nodal conduction is still uncertain. Discrete atrio-His bundle tracts appear to be rare 22 and rapid AV nodal conduction may conceiva-

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90 GONZALEZ ET AL

Fig. 6. The surface recordings show progressive increases in ventricular preexcitation that are associated with a gradual decrease of the H-Q interval (55 --* 5 msec). The last complex shows near-maximal preexcita- tion with initial forces oriented posteriorly, inferiorly and leftward. See Fig. 2 for definitions of abbrevia- tions.

bly result from functional changes in a nor- mal node or a smal l or undeve loped AV node. 23 The only somewhat similar case de- scribed in the l i terature was the patient re- ported by Gallagher et al. v This patient (Case No. 6) showed evidence of enhanced AV nodal conduction, a septal accessory pathway and Mahaim tracts (fasciculoventricular tracts). This constellation of findings again raises the possibility of multiple septal accessory path- ways with differing functional roles depend- ing on origin and insertion. One other patient (Case No. 1) has evidence of both enhanced AV nodal conduction and two free wall acces- sory pathways. 7 Pat ients with dual septal ac- cessory pathways with or without enhanced AV nodal conduction have not, to our knowl- edge, been described previously.

Several important limitations of our con- clusion merit emphasis. First, the most re- l i ab le p r e s e n t t e c h n i q u e for loca t ion of accessory pathway involves retrograde atrial m a p p i n g dur ing e i t he r s u p r a v e n t r i c u l a r tachycardia or r ight ventr icular overdrive pacing. In our patient, location of the antero- grade conducting accessory pathway was in- ferred on the basis of the orientation of the delta wave. In addition, a septal pathway is suggested by the earlier activation of the high RV septum during maximal preexcitation. 19 Because the pat tern of retrograde atrial acti- vation via a septal pathway cannot be distin- guished from tha t proceeding via the AV node-His axis, 24 difficulty was encountered in defining the pathways involved in retrocon- duct ion (especial ly in the presence of en- hanced AV nodal conduction) during right ventricular overdrive pacing. The pat tern of response during right ventricular overdrive pacing at longer cycle lengths suggests atrial

fusion (from pos te rosepta l and e i ther AV node-His or an t e rosep t a l pathways) , while shorter paced cycles (or during tachycardia) were associated with exclusive posteroseptal conduction. At paced cycle lengths shorter than the tachycardia cycle length, retrograde Mobitz II ventriculoatrial block was observed and on occasion the retrograde atrial activa- tion sequence was compatible with either an- teroseptal or a right-sided accessory pathway. In summary, our location of the anterograde accessory pa thway remains inferential and we cannot completely exclude the possibility that this pa thway is, in fact, located in the anterior free wall of the right ventricle. Clinical Significance.

Current laboratory techniques enable both location of accessory pathway site(s) and im- plication of a given accessory pathway during reentrant tachycardia. The present study was of a clinica! value in determining that the presenting wide complex tachycardia was re- lated to anterograde conduction down the AV node-His pathways with associated left bun- dle branch block. In addition, we found that anterograde accessory pa thway conduction was not an essential link in the tachycardia circuit. The patient described in this report is presently asymptomatic on a regimen includ- ing digoxin and quinidine and is not a candi- date for surgical ablation of the accessory pathways. The surgical approach to a pat ient with these e!ectrophysiologic findings, how- ever, poses several interesting considerations. Ablation of the posteroseptal pathway alone may not be cura t ive in that retroconduction might conceivably be possible via the an- t e r o s e p t a l p a t h w a y b u t w i t h a s l o w e r tachycardia rate. Similarly, His bundle sec- t i o n a l o n e m i g h t n o t p r o t e c t a g a i n s t

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D UAL SE PTAL PATHWAYS 91

N N

Fig. 7. Ventricular overdrive pacing during refractory period determination at a basic drive rate (S, S1) of 470 msec shows near-simultaneous depolarization of CS and septal atrial electrograms ($1 - A = 115 msec). A ventricular extrastimulus ($2) introduced 290 msec after the last driven complex reveals constant stimulus to CS atrial electrogram ($2A2 = 115 msec) with lengthening of stimulus to septal atrial electro- gram ($2A2 = 130 msec). The pattern of retrograde atrial preexcitation on drive represents atrial fusion between the left atrial depolarization and that from either His-AV node axis or via a septal accessory pathway. Premature ventricular depolarizations block in the later pathway and proceed via the posterior- septal pathway. See Fig. 2 for definitions of abbreviations.

t a c h y c a r d i a u t i l i z ing a c ircui t composed of an- t e rog rade conduction over a r i g h t accessory (or an te rosep ta l ) p a t h w a y and re t roconduc- t ion via the pos te rosep ta l bypass . A to ta l ly cu ra t i ve ope ra t ive p rocedure would involve sect ion of two of th ree ava i l ab l e AV p a t h w a y s w i t h p e r m a n e n t v e n t r i c u l a r pac ing if the His bund le was sacrificed.

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92 GONZALEZ ET AL

Fig. 8. Continuous recordings dur- ing r igh t ven t r i cu la r overdrive pacing at a cycle length of 270 msec. The interval from stimulus to CS atrial electrogram remains relatively constant (150-160 msec) proximate to blocked atr ial de- p o l a r i z a t i o n s ( d e n o t e d by *), characteristic of retrograde Mobitz II block in the posterior accessory pa thway . There is p rogress ive lengthening of the interval from stimulus to septal atrial and HRA electrograms, which is probably due to interatrial conduction delay during rapid overdrive. The septal a t r ia l e lec t rogram usual ly pre- cedes that of the CS in the com- plexes following the blocked atrial depolarization. The HRA electro- gram precedes or is coincident with that from the HBE which in turn precedes that from the CS for the second atrial complex in strip B and is associated with clear-cut shortening of the stimulus to His bundle a t r ia l e lec t rogram (120 msec). The early HRA electrogram is strongly suggestive of retrocon- duction over a right-sided or septal pathway. See Fig. 2 for definitions of abbreviations.

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