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Participation of a concealed nodoventricular fiber in the genesis of paroxysmal tachycardias
Participation of a concealed nodoventricular fiber in the genesis of paroxysmal tachycardias An unusual form of tachycardia circuit is described. The circuit incorporates a concealed nodoventricular fiber that conducts in a retrograde path, connects the atrioventricular node and the right ventricle, and also includes the distal portion of the atrioventricular node, the His-Purkinje system, and the ventricle, The study patient was first seen with paroxysmal tachycardias of normal QRS duration, complete right bundle branch block, and complete left bundle branch block. Electrophysiologic studies disclosed poor anterograde atrioventricular nodal conduction with a block proximal to His deflection that occurred at an atrial paced cycle length of 600 msec with no ventriculoatrial conduction. The tachycardias were inducible with two ventricular extrastimuli, had a His deflection that preceded each QRS complex and an HV interval identical to that during sinus rhythm, and revealed ventriculoatrial dissociation. Tachycardia with QRS patterns of right bundle branch block had a cycle 30 to 35 msec longer than tachycardias with either normal QRS duration or complete left bundle branch block. Tachycardias could be entrained by appropriate right ventricular pacing at rates slightly faster than the rate of tachycardia. Tachycardias could be terminated abruptly by an intravenous bolus of either adenosine triphosphate or verapamil. (AM HEART J 1990;119:583.)
Delon Wu, MD, S a n - J o u Yeh, MD, T o s h i o Y a m a m o t o , MD, F u n - C h u n g Lin, MD, a n d N y e - J a n Cheng, MD. Tapei, Taiwan
M a h a i m fibers t h a t c o n n e c t the a t r i o v e n t r i c u l a r node or His b u n d l e to the ventricle or the right bundle b r a n c h ( n o d o v e n t r i c u l a r or fasciculo-ventricular fibers) h a v e b e e n a n a t o m i c a l l y described for the p a s t 50 years. 1 Although the physiologic significance of these fibers has been q u e s t i o n e d recently, 2, 3 the possible roles of these fibers h a v e been widely i m p l i c a t e d in the genesis of certain cardiac a r r h y t h m i a s . T M One f o r m of p a r o x y s m a l wide Q R S complex t a c h y c a r d i a with a p a t t e r n of left b u n d l e b r a n c h block has been p r o p o s e d to result f r o m a r e e n t r a n t circuit with a n o d o v e n t r i c u l a r fiber for a n t e r o g r a d e conduction a n d t h e H i s - P u r k i n j e s y s t e m for r e t r o g r a d e c o n d u c t i o n ) ' 7, 10, 12 A n o t h e r f o r m of wide Q R S complex t a c h y c a r d i a suggests t h a t the M a h a i m fibers serve as " b y s t a n d e r s " during s u p r a v e n t r i c u l a r tachycardias.6, s, 11,13,14 In this s t u d y we p r e s e n t ev-
From the Section of Cardiology, Department of Medicine, Chang Gung Memorial Hospital,Chang Gung Medical College,Taipei, Taiwan,R.O.C. Supported in part by a grant fromthe National ScienceCouncil (NSC-770412-B-182-17)ofthe Republicof China. Dr. Yamamotois an international fellowfromthe SecondDepartmentof Medicine, SaitamaMedicalSchool, Saitama, Japan. Received for publication June 27, 1989;accepted Oct. 20, 1989. Reprint requests: Delon Wu, MD, Chang Gung Memorial Hospital, 199 Tung-Hwa N. Rd, Taipei, Taiwan. 4/1/18022
idence t h a t suggests the p r e s e n c e of a concealed n o d o v e n t r i c u l a r fiber c a p a b l e of only r e t r o g r a d e conduction. Its role in the genesis of p a r o x y s m a l tachycardias a n d its p o t e n t i a l role in the genesis of certain cardiac a r r h y t h m i a s is discussed. METHODS
The patient was a 51-year-old man with recurrent attacks of palpitations over a 10-year period. The attacks were associated with dizziness and instances of cold sweating and they lasted for a couple of hours. Both the physical examination and a two-dimensional echocardiogram were normal. The resting electrocardiogram (Fig. 1, A) showed sinus rhythm at a rate of 79 beats/min, a PR interval of 0.21 second, a QRS duration of 0.09 second, and a QRS axis of +60. Three types of QRS configurations were recorded during tachycardia; incomplete left bundle branch block with a normal QRS duration, a QRS axis of +110, and a rate of 230 beats/min (cycle length of 260 msec) (Fig. 1, B); complete right bundle branch block at a rate of 214 beats/ min (cycle length of 280 msec) (Fig. 1, C); complete left bundle branch block at a rate of 222 beats/min (cycle length of 270 msec) (Fig. 1, D). These attacks could be terminated by an intravenous bolus of 5 mg verapamil. The electrophysiologic study was performed with the patient in a postabsorptive, unsedated state after written informed consent was obtained. All cardiac medications were discontinued for 5 plasma half-lives before the study. Multiple electrocatheters were positioned in the right atrium, across the tricuspid valve, and at various sites of the 583
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584
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Fig. 1. Electrocardiograms that show sinus rhythm (panel A), tachycardia with a QRS pattern of incomplete left bundle branch block (left posterior hemiblock) and normal duration (panel B); tachycardia with a QRS pattern of complete right bundle branch block (panel C), and tachycardia with a QRS pattern of complete left bundle branch block (panel D). (See text for a detailed description.)
right and left ventricles for recordings of intracardiac electrogram and pacing. Multiple surface and intracardiac electrograms were simultaneously recorded on a multichannel oscilloscopic recorder (model VR-16, PPG Biomedical Systems/Med. Electr. Div., Pleasantville, N.Y.) at paper speeds of 100 and 150 mm/sec. Stimuli were provided by a programmable digital stimulator (Bloom and Associates, DTU PC 100, Narberth, Pa.) and were approximately twice the diastolic threshold and 2 msec in duration. Anterograde and retrograde conduction properties were evaluated by means of incremental pacing and extrastimulus testing techniques. Conduction intervals, refractory periods, and echo zone were defined and measured as described by Wu et al. 15 After the initial study, all catheters were removed except the hexapolar catheter. The tip of this catheter was repositioned at the right ventricular apex (RVAP) and secured for the purpose of subsequent sequential drug studies. RESULTS
T h e recordings during sinus r h y t h m showed a cycle length of 760 msec, a PA interval of 25 msec, an AH interval of 130 msec, and an HV interval of 40 msec. Atrioventricular Wenckebach block proximal to the His bundle occurred at an atrial paced cycle length of 600 msec (Fig. 2, A). T he effective refractory period of the atrioventricular node was 560 msec. No
ventriculoatrial conduction was noted during ventricular pacing (Fig. 2, B), but concealment of the ventricular paced impulse to the atrioventricular node was present as suggested by the effect of the ventricular paced beat on the AH interval of the following sinus beat. Initiation of tachycardias. Sustained tachycardias could be induced by delivery of double ventricular extrastimuli ($2S3) from either the right or the left ventricle. When the second extrastimulus ($3) was delivered at a basic ventricular drive cycle length of 500 msec with $1S2 ($1 = basic driven stimulus; $2 = first extrastimulus) of 250 msec, tachycardias with right bundle branch block, left bundle branch block, or a narrow QRS complex were induced at $2S3 coupling intervals between 205 and 255 msec. Fig. 3 shows initiation of a tachycardia with a right bundle branch block QRS pattern by $3 t hat was delivered f r o m the high posterior left ventricle. Spontaneous initiation of tachycardia was also noted during sinus rhythm. Fig. 4 shows initiation of a tachycardia with a QRS pat t ern of incomplete left bundle branch block during sinus rhythm without a provoking atrial or ventricular premature beat. Characteristics of tachycardias. Most of the tachycardias t h a t were induced during electrophysiologic
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Number 3,
Nodoventricular/iber and tachycardias. 5 8 5
Part 1
studies had a QRS pattern of complete right bundle branch block. However; tachycardias with a pattern of incomplete left bundle branch block but of normal QRS duration or those with complete left bundle branch block also occurred. There was no difference in the mode of initiation in regard to tachycardias of different QRS patterns. Each QRS complex during tachycardia was preceded by a deflection in the His bundle (H) with an HV interval identical to that during sinus rhythm (Figs. 3 to 5). The atria and ventricles were dissociated during tachycardias. A minor alternation in cycle length of 5 to 15 msec was frequently noted during tachycardia. In general tachycardias with a right bundle branch block pattern had a cycle 30 to 35 msec longer than those of tachycardias with a normal QRS duration or a left bundle branch block pattern. Conversion from a right bundle branch block pattern to a normal QRS pattern could be achieved by ventricular pacing during tachycardia. Fig. 5, A shows conversion from a pattern of right bundle branch block to one of normal QRS duration. As shown in Fig. 5, A, the tachycardia had a pattern of right bundle branch block, and the cycle length alternated between 285 and 300 msec; the interval between His bundle deflection and the left ventricular electrogram (H-LV) was 45 msec and the interval between the left ventricular electrogram and His bundle deflection (LV-H) alternated between 240 and 255 msec; the interval between His bundle deflection and right ventricular apical electrogram (H-RVAP) was 100 msec and the RVAP-H interval alternated between 185 and 200 msec. The QRS pattern was converted to normal duration after the first ventricular paced beat that originated from the right ventricular outflow tract (RVOT). The cycle length of tachycardia shortened to 265 to 270 msec, the HRVAP shortened to 60 msec, and the RVAP-H shortened to 205 to 210 msec; the H-LV remained unchanged, whereas the LV-H shortened to 220 to 225 msec. Conversion from a left bundle branch block pattern to a normal QRS pattern occurred spontaneously. Fig. 5, B shows a tachycardia with a left bundle branch block pattern that converted spontaneously to a normal QRS pattern. The cycle length of tachycardia was between 295 and 300 msec and remained unchanged after conversion; the H-RVAP was 40 msec and the RVAP-H was 255 to 260 msec and was unchanged; the H-LV shortened from 105 to 45 msec, whereas the LV-H lengthened from 190 to 195 msec to 250 to 255 msec. The decrease in tachycardia cycle length when the QRS pattern changed from right bundle branch block to a narrow QRS configuration was tested reproducibly on five occasions, and when QRS pattern changed from left bun-
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Fig. 2. Recordings that show rapid atrial pacing at a cycle length of 600 msec that produced second-degree Wenckebach block proximal to the His bundle recording site (panel A) and no ventriculoatrial conduction with atrioventricular dissociation during right ventricular pacing at a paced cycle length of 500 msec (panel B). I, AVF, and $11, electrocardiographic leads I, AVF, and V1; RA and HBE, right atrial and His bundle electrogram L V, left ventricular electrogram recorded from high posterior interventricular septum; S, stimulus artifact; A and H, low septal right atrial and His bundle responses.
die branch block to a narrow QRS pattern an unchanged tachycardia cycle length was observed twice during the study. Entrainment of tachycardias, T h e t a c h y c a r d i a s
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be entrained by rapid ventricular pacing from the right ventricle at cycle lengths between 260 and 275 msec, depending on the coupling interval of the first paced beat. When the initiating paced beat had a longer coupling interval, it captured only a portion of the ventricles, which resulted in entrainment of the tachycardia. When the initiating paced beat had a shorter coupling interval, it captured both ventricles, which resulted in termination of tachycardias. At a ventricular paced cycle length of less than 250 msec, tachycardias were always terminated. Fig. 6, A shows entrainment of the tachycardia with right ventricular apical pacing at a paced cycle length of 265 msec.
March 1990
586
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American Heart Journal
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The cycle length of tachycardia was 280 msec (as reflected by LV-LV and RVAP-RVAP intervals); the first paced beat captured the RVAP and the right ventricular outflow tract (RRVOT); the coupling inteval of the first paced beat (RVAP-RVAP) was shortened to 185 msec. It did not capture the left ventricle (LV) and the high right ventricular septum (recorded from His bundle electrogram, [HBE]); the LV-LV interval remained at 280 msec, and the tachycardia was entrained. Note that the forms of the LV and H B E ventricular electrograms during pacing were similar to those during tachycardia, whereas the forms of RVAP and RVOT ventricular electrograms were different from those during tachycardia. Except for the first two paced beats, the QRS form was sta-
ble for the subsequent paced beats, which suggests a constant fusion. When pacing was stopped, tachycardia resumed. The time between the R-R interval and the LV-LV interval of the last ventricular paced beat to the first tachycardia beat was 265 msec, identical to the paced cycle length, whereas the time between RVAP-RVAP and the RVOT-RVOT interval was 335 msec, longer than the paced cycle, which suggests that the first returning tachycardia beat was the last captured beat. Fig. 6, B shows termination of tachycardia by right ventricular apical pacing at a cycle length of 275 msec. The paced cycle was longer than that shown in Fig. 6, A, but the first paced beat had a shorter coupling interval than that shown in Fig. 6, A. Thus the first and all subsequent paced
Volume
119
Number 3. Part
Nodoventricular fiber and tachycardias
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Fig. 6. Entrainment of tachycardia by rapid right ventricular apical pacing at a paced cycle length of 265 msec (panel A), and termination of tachycardia after termination of right ventricular apical pacing at a paced cycle length of 275 msec (panel B). Note that the coupling interval of the first paced beat in panel A was slightly later than that in panel B and that the first paced beat in panel B captured all ventricular electrograms (beat with asterisk). (See text for discussion.)
587
March 1990
Wu et al.
588
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Fig. 7. Abrupt termination of tachycardia 14 seconds after an intravenous bolus of 10 mg adenosine triphosphate (ATP). Note that marked perpetuation of cycle length with alternation of long and short intervals occurred immediately before termination. The QRS pattern changed from complete right bundle branch block to normal duration before termination, and the termination occurred when a QRS complex was not followed by an H, which suggests that the block probably occurred in the atrioventricular node.
Table
h Effects of drugs on induction of tachycardia Drug
Dosage
Tachycardia induction
Cycle length (msec)
Ability to sustain tachycardia
Digoxin Diltiazem Lidocaine Procainamide Propranolol Quinidine Verapamil
1.5 mg/day PO 240 mg/day PO 150 mg IV 1000 mg IV 160 mg/day PO 1600 mg/day PO 320 mg/day PO
Yes Yes Yes No (single beat) Yes No (3 beats) Yes
300-310 330-360 270 -280 -320-330
Yes No Yes -Yes -No
PO, oral administration; IVI intravenous administration.
beats had captured both ventricles, and the forms of all the recorded ventricular electrograms were different from those during tachycardia, indicating that the tachycardia was terminated. Effects of drugs. After the control study, sustained tachycardia was induced and observed for 2 minutes. Adenosine triphosphate (10 mg) was administered intravenously as a bolus while the patient was monitored constantly. The tachycardia was terminated 14 seconds after the bolus. The effect of adenosine triphosphate was confirmed three more times by dosing in 10-minute intervals, and the tachycardias were terminated in 5, 10, and 12 seconds, respectively. Fig. 7 shows termination of tachycardia after a bolus of adenosine triphosphate. The cycle lengthened slightly and then a striking alternation oc-
cuffed. The tachycardia was terminated with a QRS complex that was not followed by an H response. Ten minutes after t h e ' l a s t dose of adenosine triphosphate was given, sustained tachycardia was again induced. While the patient was monitored constantly, verapamil (10 mg) was administered intravenously as a bolus. The tachycardia was terminated with a QRS complex that was not followed by an H response in 36 seconds. After this, repeated electrophysiologic studies failed to induce tachycardias. The results of subsequent sequential drug studies are summarized in Table I. Oral verapamil, oral diltiazem, oral quinidine, and intravenous procainamide effectively prevented induction of sustained tachycardia; however, intravenous lidocaine, oral propranolol, and oral digoxin were ineffective in
Volume 119
Nodoventricular fiber and tachycardias
Number 3, Part 1
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Fig. 8. Diagrams that represent the proposed tachycardia circuits with different QRS patterns. Tachycardia with a normal QRS duration consists of the retrograde nodoventricular fiber, the distal portion of the atrioventricular node, the His bundle, the right bundle, and the right ventricle (panel A); tachycardia with a QRS pattern of complete right bundle branch block consists of the retrograde nodoventricular fiber, the distal atrioventricular node, the His bundle, the left bundle, the interventricular septum, and the right ventricle (panel B); tachycardia with a QRS pattern of complete left bundle branch block consists of the retrograde nodoventricular fiber, the distal atrioventricular node, the His bundle, the right bundle, and the right ventricle (panel C). Thus the circuit in tachycardia that have a QRS pattern of complete right bundle-branch block is larger than that with a normal QRS pattern or with a QRS pattern of complete left bundle branch block. preventing the induction of sustained tachycardias. The patient was discharged on a maintenance regimen of oral diltiazem (240 mg per day in four divided doses) and has been followed up for a period of 18 months without recurrence of tachycardia. DISCUSSION Mahaim fibers and paroxysmal tachycardias. Mahaim fibers with either nodoventricular or fasciculo-ventricular connections l~ave been frequently implicated in the genesis of certain types of paroxysmal tachycardias. 4-z4 In patients who have a normal PR interval, a delta wave, and a paroxysmal tachycardia with a QRS pattern of left bundle branch block, it has been proposed that the tachycardia circuit uses a nodoventricular fiber that connects the right side of the atrioventricular node to the right ventricle or to the right bundle branch for anterograde conduction and the His-Purkinje system for retrograde conduction.5, 7, 10,12Dual atrioventricular nodal pathway physiology is frequently present in these patients, and it has been suggested that the nodoventricular fibers arise from the slow atrioventricular nodal pathway. 8' 11, 13,14Paroxysmal tachycardias are usually induced during incremental atrial pacing or premature atrial stimulation when atrioventricular nodal conduction is progressively lengthened with a block that occurs distal to the atrioventricular nodal insertion of the accessory nodoventricular connection. Another form of supraventricular tachycardia suggests that the nodoventricular or the fasciculo-
ventricular fibers serve as "bystanders" in activation of the ventricles without participation in the genesis of supraventricular tachycardias, s, 11, 13, 14 These hypotheses have been challenged recently because the findings of a normal PR interval, a delta wave, and the mode of induction of paroxysmal tachycardia with a QRS pattern of left bundle branch block, which suggests participation of a nodoventricular fiber, can also be explained and have been documented in patients with the presence of a slowly conducting right-sided accessory pathway. 2' 3 Nevertheless, there were three previously reported cases in which ventriculoatrial dissociation was documented during tachycardia, a finding that excludes atria, and thereby an anterograde slow accessory pathway, as a portion of the tachycardia circuit. 7 Furthermore, reversal of the tachycardia circuit was indicated in one of these three patients although definitive evidence was not provided. 7 A recent study described a patient with evidence of anterograde nodoventricular connection in whom atrioventricular dissociation occurred during narrow QRS tachycardia, which suggested reversal of the tachycardia circuit that used the nodoventricular fiber for retrograde conduction. 16 Proposed mechanism of tachycardias. The proposed mechanism of the tachycardias that occurred in the study patient is presented schematically in the diagram in Fig. 8. The proposed tachycardia circuit incorporates a concealed nodoventricular fiber that connects the distal portion of the atrioventricular
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node to the right ventricle, which is capable of only retrograde conduction; the circuit consists of the distal portion of the atrioventricular node, the HisPurkinje system, the ventricle, and the retrograde nodoventricular fiber. This hypothesis is based on data gathered from electrophysiologic studies. First, the occurrence of ventriculoatrial dissociation during tachycardia, the absence of ventriculoatrial conduction, and the poor anterograde atrioventricular nodal conduction exclude the possibility that the atria and the upper portion of the atrioventricular node are parts of the circuit. Second, the findings that a His bundle deflection preceded each QRS complex during tachycardias and that the HV interval was identical to that during sinus rhythm suggest that the His-Purkinje system was used for anterograde conduction during tachycardias. It also suggests that the upper link (or turnaround) was likely to involve a portion of the atrioventricular node; otherwise the HV interval during tachycardia would be expected to be shorter than that during sinus rhythm and the revolution time of the circuit would probably be too short to sustain tachycardia. Third, the finding that the tachycardia cycle lengthened with the occurrence of complete right bundle branch block suggests that the right ventricle was the site of the ventricular insertion of the nodoventricular fiber. This phenomenon is similar to that of the orthodromic atrioventricular reentrant tachycardia with lengthening of the tachycardia cycle when a bundle branch block that is ipsilateral to the accessory pathway o c c u r s . 17 Fourth, the ability to induce tachycardias with a pattern of narrow QRS, complete right bundle branch block, and complete left bundle branch block that is associated with the ability to change the QRS pattern from complete right bundle branch block or complete left bundle branch to narrow QRS excludes the possibility that bundle branch or fascicular reentry was responsible for the tachycardia.18 Fifth, the demonstration of entrainment with appropriate ventricular pacing confirms that the tachycardias are of a reentrant nature, 19 which excludes the possibility of a junctional tachycardia that arises from an automatic focus. Finally, the responses of tachycardia to an intravenous bolus of either adenosine triphosphate or verapamil further support the theory that a portion of the atrioventricular node is a component of the c i r c u i t . 2~ Perpetuation of cycle length with alternation of long and short cycles that resulted in the abrupt termination of tachycardia and that occurred after a short preceeding cycle and a QRS complex that was not followed by a His bundle response is consistent with this hypothesis. However, adenosine triphosphate and verapamil may affect abnormal
American Heart Journal
tissue with slow channel properties other than the a t r i o v e n t r i c u l a r n o d e . 2325 Thus the possibility that a slowly conducting concealed fasciculo-ventricular connection was the fiber responsible for retrograde conduction cannot be definitively excluded. C l i n i c a l i m p l i c a t i o n s . This study has important clinical implications. First, it demonstrates that reentry that incorporates a concealed nodoventricular fiber that conducts in a retrograde path can be a mechanism of paroxysmal tachycardias. It strengthens the theory that the Mahaim fiber can play a significant role in the genesis of cardiac arrhythmias. Second, it is possible that one-to-one ventriculoatrial conduction may occur during this type of paroxysmal tachycardia. If so, then differentiation between this arrhythmia and the orthodromic atrioventricular reentrant tachycardia that incorporates a paraseptal accessory pathway, or the slow-fast form of atrioventricular nodal reentrant tachycardia, could be difficult. Furthermore, differentiation of this arrhythmia and the atypical form of junctional reciprocating tachycardia that incorporates a slowly conducting retrograde paraseptal accessory pathway could present a problem, as the retrograde atrioventricular conduction (proximal to the insertion of the nodoventricular connection) could be long. However, several guidelines could be extrapolated for differentiation from the present study: (1) During tachycardia the retrograde atrial activation sequence would be expected to be normal, and the earliest activation should be registered from the low septal right atrium (recorded from the His bundle catheter) or possibly from the orifice of the coronary sinus. (2) During tachycardia the atria may be preexcited by a properly timed premature ventricular beat when the His bundle is still refractory. (3) The atria may be dissociated when the tachycardia is entrained by a proper ventricular pacing. (4) The atria may be dissociated during tachycardia by atrial pacing at a rate faster than the tachycardia rate by an appropriate premature atrial stimulated beat or by intravenous administration of adenosine triphosphate or verapamil. REFERENCES
1. Mahaim I, Winston MR. Recherches d'anatomic compar~e et du pathologie experimentale sur les connexions du faisceau de His-Tawara. Cardiologia 1941;5:189-260. 2. Tchou P, Lehmann MH, Jazayeri M, Akhtar M. Atriofascicular connection or a nodoventricular Mahaim fiber? Electrophysiologic elucidation of the pathway and associated reent r a n t circuit. Circulation !988;77:837-48. 3. Klein GJ, Guiraudon GM, Kerr CR, Sharma AD, Yee R, Szabo T, Yeung Lai Wah JA. "Nodoventricular" accessory pathway: evidence for a distinct accessory atrioventricular pathway with atrioventricular node-like properties. J Am Coll Cardiol 1988;11:1035-40.
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4. Tonkin AM, Dugan FA, Svenson RH, Sealy WC, Wallace AG, Gallagher JJ. Coexistence of functional Kent and Mahaimtype tracts in the pre-excitation syndrome. Circulation 1975;52:193-200. 5. Touboul P, Vexler RM, Chatelain MT. Reentry via Mahaim fibers as a possible basis for tachycardia. Br Heart J 1978;40:806-11. 6. Ward DE, Camm AJ, Spurrell RAJ. Ventricular preexcitation due to anomalous nodo-ventricular pathways: report of 3 Patients. Eur J Cardiol 1979;9:111-27. 7. Gallagher J J, Smith WM, Kasell JH, Benson DW Jr, Sterba R, Grant AO. Roles of Mahaim fibers in cardiac arrhythmias in man. Circulation 1981;64:176-89. 8. Morady F, Scheinman MM, Gonzalez R, Hess D. His-ventricular dissociation in a patient with reciprocating tachycardia and a nodoventricular bypass tract. Circulation 1981;64:83944. 9. Lerman BB, Waxman HL, Proclemer A, Josephson ME. Supraventricular tachycardia associated with nodoventricular and concealed atrioventricular bypass tracts. AM HEART J 1982;104:1097-1102. 10. Bhandari A, Morady F, Shen EN, Schwartz AB, Botvinick E, Scheinman MM. Catheter-induced His bundle ablation in a patient with reentrant tachycardia associated with a nodoventricular tract. J Am Coll Cardiol 1984;4:611-16. 11. Bardy GH, German LD, Packer DL, Coltorti F, Gallagher JJ. Mechanism of tachycardia using a nodofascicular Mahaim fiber. Am J Cardiol 1984;54:1140-1. 12. Ellenbogen KA, O'Callaghan WG, Colavita PG, Packer DL, Gilbert MR, German LD. Catheter atrioventricular junction ablation for recurrent supraventricular tachycardia with nodoventricular fibers. Am J Cardiol 1985;55:1227-9. 13. Murabit I, Sosa E, Pileggi F, Denes P. Multiple reentry tachycardia in patients with ventricular preexcitation: report of three cases. AM HEARTJ 1986;111:69-80. 14. Deng Z, Gang ES, Rosenthal ME, Oseran D, Mandel WJ, Peter T. Wide QRS tachycardia due to AV nodal reentry and a "bystander" bypass tract with slow conduction properties. PACE 1986;9:188-95. 15. Wu D, Denes P, Amat-y-Leon F, Dhingra R, Wyndham CRC, Bauernfeind R, Latif P, Rosen KM. Clinical, electrocardio-
- - --N o- d -o v e n t r i c u l a- -r f i b e r
--
and tachycarclias 5 9 1
graphic and eleetrophysiological observations in patients with paroxysmal supraventricular tachycardia. Am J Cardiol 1978;41:1045-51. 16. Shimizu A, Ohe J, Takaki H, Kamakura S, Matsuhisa M, Sato I, Shimomura K. Narrow QRS complex tachycardia with atrioventricular dissociation. PACE 1988;11:384-93. 17. Coumel P, Attual P. Reciprocating tachycardia in overt and latent preexcitation. Influence of functional bundle branch block on the rate of the tachycardia. Eur J Cardio11974;1:42336. 18. Caceres J, Jazayeri M, McKinnie J, Avitall B, Denker ST, Tchou P, Aktar M. Sustained bundle branch reentry as a mechanism of clinical tachycardia. Circulation 1989;79:25670. 19. Henthorn WR, Okumura K, Olshansky B, Plumb VJ, Hess PG, Waldo AL. A fourth criterion for transient entrainment: the electrogram equivalent of progressive fusion. Circulation 1988;77:1003-12. 20. Belardinelli L, Fenton RA, West A, Linden J, Althaus JS, Berne RM. Extracellular action of adenosine and the antagonism by aminophylline on the atrioventricular conduction of isolated perfused guinea pig and rat hearts. Circ Res 1982;51:569-79. 21. Lerman BB, Greenberg M, Overholt ED, Swerdlow CD, Smith RTJ, Sellers TD, DiMarco JP. Differential electrophysiologic properties of decremental retrograde pathways in long RP' tachycardia. Circulation 1987;76:21-31. 22. Wit AL, Cranefield PF. Effect of verapamil on the sinoatrial and atrioventricular nodes of the rabbit and the mechanism by which it arrests reentrant atrioventricular nodal tachycardia. Circ Res 1974;35:413-25. 23. Lerman BB, Belardinelli L, West A, Berne RM, DiMarco JP. Adenosine-sensitiveventricular tachycardia: evidence suggestive cyclic AMP-medicated triggered activity. Circulation 1986;74:270-80. 24. Wu D, Kou HC, Hung JS. Exercise-triggered paroxysmal ventricular tachycardia. Ann Intern Med 1981;95:410-14. 25. Lin FC, Finley CD, Rahimtoola SH, Wu D. Idiopathic paroxysmal ventricular tachycardia with a QRS pattern of right bundle branch block and left axis deviation: a unique clinical entity with specific properties. Am J Cardiol 1983;52:95-100.
Delon Wu, MD, S a n - J o u Yeh, MD, T o s h i o Y a m a m o t o , MD, F u n - C h u n g Lin, MD, a n d N y e - J a n Cheng, MD. Tapei, Taiwan
M a h a i m fibers t h a t c o n n e c t the a t r i o v e n t r i c u l a r node or His b u n d l e to the ventricle or the right bundle b r a n c h ( n o d o v e n t r i c u l a r or fasciculo-ventricular fibers) h a v e b e e n a n a t o m i c a l l y described for the p a s t 50 years. 1 Although the physiologic significance of these fibers has been q u e s t i o n e d recently, 2, 3 the possible roles of these fibers h a v e been widely i m p l i c a t e d in the genesis of certain cardiac a r r h y t h m i a s . T M One f o r m of p a r o x y s m a l wide Q R S complex t a c h y c a r d i a with a p a t t e r n of left b u n d l e b r a n c h block has been p r o p o s e d to result f r o m a r e e n t r a n t circuit with a n o d o v e n t r i c u l a r fiber for a n t e r o g r a d e conduction a n d t h e H i s - P u r k i n j e s y s t e m for r e t r o g r a d e c o n d u c t i o n ) ' 7, 10, 12 A n o t h e r f o r m of wide Q R S complex t a c h y c a r d i a suggests t h a t the M a h a i m fibers serve as " b y s t a n d e r s " during s u p r a v e n t r i c u l a r tachycardias.6, s, 11,13,14 In this s t u d y we p r e s e n t ev-
From the Section of Cardiology, Department of Medicine, Chang Gung Memorial Hospital,Chang Gung Medical College,Taipei, Taiwan,R.O.C. Supported in part by a grant fromthe National ScienceCouncil (NSC-770412-B-182-17)ofthe Republicof China. Dr. Yamamotois an international fellowfromthe SecondDepartmentof Medicine, SaitamaMedicalSchool, Saitama, Japan. Received for publication June 27, 1989;accepted Oct. 20, 1989. Reprint requests: Delon Wu, MD, Chang Gung Memorial Hospital, 199 Tung-Hwa N. Rd, Taipei, Taiwan. 4/1/18022
idence t h a t suggests the p r e s e n c e of a concealed n o d o v e n t r i c u l a r fiber c a p a b l e of only r e t r o g r a d e conduction. Its role in the genesis of p a r o x y s m a l tachycardias a n d its p o t e n t i a l role in the genesis of certain cardiac a r r h y t h m i a s is discussed. METHODS
The patient was a 51-year-old man with recurrent attacks of palpitations over a 10-year period. The attacks were associated with dizziness and instances of cold sweating and they lasted for a couple of hours. Both the physical examination and a two-dimensional echocardiogram were normal. The resting electrocardiogram (Fig. 1, A) showed sinus rhythm at a rate of 79 beats/min, a PR interval of 0.21 second, a QRS duration of 0.09 second, and a QRS axis of +60. Three types of QRS configurations were recorded during tachycardia; incomplete left bundle branch block with a normal QRS duration, a QRS axis of +110, and a rate of 230 beats/min (cycle length of 260 msec) (Fig. 1, B); complete right bundle branch block at a rate of 214 beats/ min (cycle length of 280 msec) (Fig. 1, C); complete left bundle branch block at a rate of 222 beats/min (cycle length of 270 msec) (Fig. 1, D). These attacks could be terminated by an intravenous bolus of 5 mg verapamil. The electrophysiologic study was performed with the patient in a postabsorptive, unsedated state after written informed consent was obtained. All cardiac medications were discontinued for 5 plasma half-lives before the study. Multiple electrocatheters were positioned in the right atrium, across the tricuspid valve, and at various sites of the 583
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Fig. 1. Electrocardiograms that show sinus rhythm (panel A), tachycardia with a QRS pattern of incomplete left bundle branch block (left posterior hemiblock) and normal duration (panel B); tachycardia with a QRS pattern of complete right bundle branch block (panel C), and tachycardia with a QRS pattern of complete left bundle branch block (panel D). (See text for a detailed description.)
right and left ventricles for recordings of intracardiac electrogram and pacing. Multiple surface and intracardiac electrograms were simultaneously recorded on a multichannel oscilloscopic recorder (model VR-16, PPG Biomedical Systems/Med. Electr. Div., Pleasantville, N.Y.) at paper speeds of 100 and 150 mm/sec. Stimuli were provided by a programmable digital stimulator (Bloom and Associates, DTU PC 100, Narberth, Pa.) and were approximately twice the diastolic threshold and 2 msec in duration. Anterograde and retrograde conduction properties were evaluated by means of incremental pacing and extrastimulus testing techniques. Conduction intervals, refractory periods, and echo zone were defined and measured as described by Wu et al. 15 After the initial study, all catheters were removed except the hexapolar catheter. The tip of this catheter was repositioned at the right ventricular apex (RVAP) and secured for the purpose of subsequent sequential drug studies. RESULTS
T h e recordings during sinus r h y t h m showed a cycle length of 760 msec, a PA interval of 25 msec, an AH interval of 130 msec, and an HV interval of 40 msec. Atrioventricular Wenckebach block proximal to the His bundle occurred at an atrial paced cycle length of 600 msec (Fig. 2, A). T he effective refractory period of the atrioventricular node was 560 msec. No
ventriculoatrial conduction was noted during ventricular pacing (Fig. 2, B), but concealment of the ventricular paced impulse to the atrioventricular node was present as suggested by the effect of the ventricular paced beat on the AH interval of the following sinus beat. Initiation of tachycardias. Sustained tachycardias could be induced by delivery of double ventricular extrastimuli ($2S3) from either the right or the left ventricle. When the second extrastimulus ($3) was delivered at a basic ventricular drive cycle length of 500 msec with $1S2 ($1 = basic driven stimulus; $2 = first extrastimulus) of 250 msec, tachycardias with right bundle branch block, left bundle branch block, or a narrow QRS complex were induced at $2S3 coupling intervals between 205 and 255 msec. Fig. 3 shows initiation of a tachycardia with a right bundle branch block QRS pattern by $3 t hat was delivered f r o m the high posterior left ventricle. Spontaneous initiation of tachycardia was also noted during sinus rhythm. Fig. 4 shows initiation of a tachycardia with a QRS pat t ern of incomplete left bundle branch block during sinus rhythm without a provoking atrial or ventricular premature beat. Characteristics of tachycardias. Most of the tachycardias t h a t were induced during electrophysiologic
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Number 3,
Nodoventricular/iber and tachycardias. 5 8 5
Part 1
studies had a QRS pattern of complete right bundle branch block. However; tachycardias with a pattern of incomplete left bundle branch block but of normal QRS duration or those with complete left bundle branch block also occurred. There was no difference in the mode of initiation in regard to tachycardias of different QRS patterns. Each QRS complex during tachycardia was preceded by a deflection in the His bundle (H) with an HV interval identical to that during sinus rhythm (Figs. 3 to 5). The atria and ventricles were dissociated during tachycardias. A minor alternation in cycle length of 5 to 15 msec was frequently noted during tachycardia. In general tachycardias with a right bundle branch block pattern had a cycle 30 to 35 msec longer than those of tachycardias with a normal QRS duration or a left bundle branch block pattern. Conversion from a right bundle branch block pattern to a normal QRS pattern could be achieved by ventricular pacing during tachycardia. Fig. 5, A shows conversion from a pattern of right bundle branch block to one of normal QRS duration. As shown in Fig. 5, A, the tachycardia had a pattern of right bundle branch block, and the cycle length alternated between 285 and 300 msec; the interval between His bundle deflection and the left ventricular electrogram (H-LV) was 45 msec and the interval between the left ventricular electrogram and His bundle deflection (LV-H) alternated between 240 and 255 msec; the interval between His bundle deflection and right ventricular apical electrogram (H-RVAP) was 100 msec and the RVAP-H interval alternated between 185 and 200 msec. The QRS pattern was converted to normal duration after the first ventricular paced beat that originated from the right ventricular outflow tract (RVOT). The cycle length of tachycardia shortened to 265 to 270 msec, the HRVAP shortened to 60 msec, and the RVAP-H shortened to 205 to 210 msec; the H-LV remained unchanged, whereas the LV-H shortened to 220 to 225 msec. Conversion from a left bundle branch block pattern to a normal QRS pattern occurred spontaneously. Fig. 5, B shows a tachycardia with a left bundle branch block pattern that converted spontaneously to a normal QRS pattern. The cycle length of tachycardia was between 295 and 300 msec and remained unchanged after conversion; the H-RVAP was 40 msec and the RVAP-H was 255 to 260 msec and was unchanged; the H-LV shortened from 105 to 45 msec, whereas the LV-H lengthened from 190 to 195 msec to 250 to 255 msec. The decrease in tachycardia cycle length when the QRS pattern changed from right bundle branch block to a narrow QRS configuration was tested reproducibly on five occasions, and when QRS pattern changed from left bun-
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die branch block to a narrow QRS pattern an unchanged tachycardia cycle length was observed twice during the study. Entrainment of tachycardias, T h e t a c h y c a r d i a s
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The cycle length of tachycardia was 280 msec (as reflected by LV-LV and RVAP-RVAP intervals); the first paced beat captured the RVAP and the right ventricular outflow tract (RRVOT); the coupling inteval of the first paced beat (RVAP-RVAP) was shortened to 185 msec. It did not capture the left ventricle (LV) and the high right ventricular septum (recorded from His bundle electrogram, [HBE]); the LV-LV interval remained at 280 msec, and the tachycardia was entrained. Note that the forms of the LV and H B E ventricular electrograms during pacing were similar to those during tachycardia, whereas the forms of RVAP and RVOT ventricular electrograms were different from those during tachycardia. Except for the first two paced beats, the QRS form was sta-
ble for the subsequent paced beats, which suggests a constant fusion. When pacing was stopped, tachycardia resumed. The time between the R-R interval and the LV-LV interval of the last ventricular paced beat to the first tachycardia beat was 265 msec, identical to the paced cycle length, whereas the time between RVAP-RVAP and the RVOT-RVOT interval was 335 msec, longer than the paced cycle, which suggests that the first returning tachycardia beat was the last captured beat. Fig. 6, B shows termination of tachycardia by right ventricular apical pacing at a cycle length of 275 msec. The paced cycle was longer than that shown in Fig. 6, A, but the first paced beat had a shorter coupling interval than that shown in Fig. 6, A. Thus the first and all subsequent paced
Volume
119
Number 3. Part
Nodoventricular fiber and tachycardias
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Fig. 6. Entrainment of tachycardia by rapid right ventricular apical pacing at a paced cycle length of 265 msec (panel A), and termination of tachycardia after termination of right ventricular apical pacing at a paced cycle length of 275 msec (panel B). Note that the coupling interval of the first paced beat in panel A was slightly later than that in panel B and that the first paced beat in panel B captured all ventricular electrograms (beat with asterisk). (See text for discussion.)
587
March 1990
Wu et al.
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American Heart Journal
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Fig. 7. Abrupt termination of tachycardia 14 seconds after an intravenous bolus of 10 mg adenosine triphosphate (ATP). Note that marked perpetuation of cycle length with alternation of long and short intervals occurred immediately before termination. The QRS pattern changed from complete right bundle branch block to normal duration before termination, and the termination occurred when a QRS complex was not followed by an H, which suggests that the block probably occurred in the atrioventricular node.
Table
h Effects of drugs on induction of tachycardia Drug
Dosage
Tachycardia induction
Cycle length (msec)
Ability to sustain tachycardia
Digoxin Diltiazem Lidocaine Procainamide Propranolol Quinidine Verapamil
1.5 mg/day PO 240 mg/day PO 150 mg IV 1000 mg IV 160 mg/day PO 1600 mg/day PO 320 mg/day PO
Yes Yes Yes No (single beat) Yes No (3 beats) Yes
300-310 330-360 270 -280 -320-330
Yes No Yes -Yes -No
PO, oral administration; IVI intravenous administration.
beats had captured both ventricles, and the forms of all the recorded ventricular electrograms were different from those during tachycardia, indicating that the tachycardia was terminated. Effects of drugs. After the control study, sustained tachycardia was induced and observed for 2 minutes. Adenosine triphosphate (10 mg) was administered intravenously as a bolus while the patient was monitored constantly. The tachycardia was terminated 14 seconds after the bolus. The effect of adenosine triphosphate was confirmed three more times by dosing in 10-minute intervals, and the tachycardias were terminated in 5, 10, and 12 seconds, respectively. Fig. 7 shows termination of tachycardia after a bolus of adenosine triphosphate. The cycle lengthened slightly and then a striking alternation oc-
cuffed. The tachycardia was terminated with a QRS complex that was not followed by an H response. Ten minutes after t h e ' l a s t dose of adenosine triphosphate was given, sustained tachycardia was again induced. While the patient was monitored constantly, verapamil (10 mg) was administered intravenously as a bolus. The tachycardia was terminated with a QRS complex that was not followed by an H response in 36 seconds. After this, repeated electrophysiologic studies failed to induce tachycardias. The results of subsequent sequential drug studies are summarized in Table I. Oral verapamil, oral diltiazem, oral quinidine, and intravenous procainamide effectively prevented induction of sustained tachycardia; however, intravenous lidocaine, oral propranolol, and oral digoxin were ineffective in
Volume 119
Nodoventricular fiber and tachycardias
Number 3, Part 1
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Fig. 8. Diagrams that represent the proposed tachycardia circuits with different QRS patterns. Tachycardia with a normal QRS duration consists of the retrograde nodoventricular fiber, the distal portion of the atrioventricular node, the His bundle, the right bundle, and the right ventricle (panel A); tachycardia with a QRS pattern of complete right bundle branch block consists of the retrograde nodoventricular fiber, the distal atrioventricular node, the His bundle, the left bundle, the interventricular septum, and the right ventricle (panel B); tachycardia with a QRS pattern of complete left bundle branch block consists of the retrograde nodoventricular fiber, the distal atrioventricular node, the His bundle, the right bundle, and the right ventricle (panel C). Thus the circuit in tachycardia that have a QRS pattern of complete right bundle-branch block is larger than that with a normal QRS pattern or with a QRS pattern of complete left bundle branch block. preventing the induction of sustained tachycardias. The patient was discharged on a maintenance regimen of oral diltiazem (240 mg per day in four divided doses) and has been followed up for a period of 18 months without recurrence of tachycardia. DISCUSSION Mahaim fibers and paroxysmal tachycardias. Mahaim fibers with either nodoventricular or fasciculo-ventricular connections l~ave been frequently implicated in the genesis of certain types of paroxysmal tachycardias. 4-z4 In patients who have a normal PR interval, a delta wave, and a paroxysmal tachycardia with a QRS pattern of left bundle branch block, it has been proposed that the tachycardia circuit uses a nodoventricular fiber that connects the right side of the atrioventricular node to the right ventricle or to the right bundle branch for anterograde conduction and the His-Purkinje system for retrograde conduction.5, 7, 10,12Dual atrioventricular nodal pathway physiology is frequently present in these patients, and it has been suggested that the nodoventricular fibers arise from the slow atrioventricular nodal pathway. 8' 11, 13,14Paroxysmal tachycardias are usually induced during incremental atrial pacing or premature atrial stimulation when atrioventricular nodal conduction is progressively lengthened with a block that occurs distal to the atrioventricular nodal insertion of the accessory nodoventricular connection. Another form of supraventricular tachycardia suggests that the nodoventricular or the fasciculo-
ventricular fibers serve as "bystanders" in activation of the ventricles without participation in the genesis of supraventricular tachycardias, s, 11, 13, 14 These hypotheses have been challenged recently because the findings of a normal PR interval, a delta wave, and the mode of induction of paroxysmal tachycardia with a QRS pattern of left bundle branch block, which suggests participation of a nodoventricular fiber, can also be explained and have been documented in patients with the presence of a slowly conducting right-sided accessory pathway. 2' 3 Nevertheless, there were three previously reported cases in which ventriculoatrial dissociation was documented during tachycardia, a finding that excludes atria, and thereby an anterograde slow accessory pathway, as a portion of the tachycardia circuit. 7 Furthermore, reversal of the tachycardia circuit was indicated in one of these three patients although definitive evidence was not provided. 7 A recent study described a patient with evidence of anterograde nodoventricular connection in whom atrioventricular dissociation occurred during narrow QRS tachycardia, which suggested reversal of the tachycardia circuit that used the nodoventricular fiber for retrograde conduction. 16 Proposed mechanism of tachycardias. The proposed mechanism of the tachycardias that occurred in the study patient is presented schematically in the diagram in Fig. 8. The proposed tachycardia circuit incorporates a concealed nodoventricular fiber that connects the distal portion of the atrioventricular
March 1990
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Wu et al.
node to the right ventricle, which is capable of only retrograde conduction; the circuit consists of the distal portion of the atrioventricular node, the HisPurkinje system, the ventricle, and the retrograde nodoventricular fiber. This hypothesis is based on data gathered from electrophysiologic studies. First, the occurrence of ventriculoatrial dissociation during tachycardia, the absence of ventriculoatrial conduction, and the poor anterograde atrioventricular nodal conduction exclude the possibility that the atria and the upper portion of the atrioventricular node are parts of the circuit. Second, the findings that a His bundle deflection preceded each QRS complex during tachycardias and that the HV interval was identical to that during sinus rhythm suggest that the His-Purkinje system was used for anterograde conduction during tachycardias. It also suggests that the upper link (or turnaround) was likely to involve a portion of the atrioventricular node; otherwise the HV interval during tachycardia would be expected to be shorter than that during sinus rhythm and the revolution time of the circuit would probably be too short to sustain tachycardia. Third, the finding that the tachycardia cycle lengthened with the occurrence of complete right bundle branch block suggests that the right ventricle was the site of the ventricular insertion of the nodoventricular fiber. This phenomenon is similar to that of the orthodromic atrioventricular reentrant tachycardia with lengthening of the tachycardia cycle when a bundle branch block that is ipsilateral to the accessory pathway o c c u r s . 17 Fourth, the ability to induce tachycardias with a pattern of narrow QRS, complete right bundle branch block, and complete left bundle branch block that is associated with the ability to change the QRS pattern from complete right bundle branch block or complete left bundle branch to narrow QRS excludes the possibility that bundle branch or fascicular reentry was responsible for the tachycardia.18 Fifth, the demonstration of entrainment with appropriate ventricular pacing confirms that the tachycardias are of a reentrant nature, 19 which excludes the possibility of a junctional tachycardia that arises from an automatic focus. Finally, the responses of tachycardia to an intravenous bolus of either adenosine triphosphate or verapamil further support the theory that a portion of the atrioventricular node is a component of the c i r c u i t . 2~ Perpetuation of cycle length with alternation of long and short cycles that resulted in the abrupt termination of tachycardia and that occurred after a short preceeding cycle and a QRS complex that was not followed by a His bundle response is consistent with this hypothesis. However, adenosine triphosphate and verapamil may affect abnormal
American Heart Journal
tissue with slow channel properties other than the a t r i o v e n t r i c u l a r n o d e . 2325 Thus the possibility that a slowly conducting concealed fasciculo-ventricular connection was the fiber responsible for retrograde conduction cannot be definitively excluded. C l i n i c a l i m p l i c a t i o n s . This study has important clinical implications. First, it demonstrates that reentry that incorporates a concealed nodoventricular fiber that conducts in a retrograde path can be a mechanism of paroxysmal tachycardias. It strengthens the theory that the Mahaim fiber can play a significant role in the genesis of cardiac arrhythmias. Second, it is possible that one-to-one ventriculoatrial conduction may occur during this type of paroxysmal tachycardia. If so, then differentiation between this arrhythmia and the orthodromic atrioventricular reentrant tachycardia that incorporates a paraseptal accessory pathway, or the slow-fast form of atrioventricular nodal reentrant tachycardia, could be difficult. Furthermore, differentiation of this arrhythmia and the atypical form of junctional reciprocating tachycardia that incorporates a slowly conducting retrograde paraseptal accessory pathway could present a problem, as the retrograde atrioventricular conduction (proximal to the insertion of the nodoventricular connection) could be long. However, several guidelines could be extrapolated for differentiation from the present study: (1) During tachycardia the retrograde atrial activation sequence would be expected to be normal, and the earliest activation should be registered from the low septal right atrium (recorded from the His bundle catheter) or possibly from the orifice of the coronary sinus. (2) During tachycardia the atria may be preexcited by a properly timed premature ventricular beat when the His bundle is still refractory. (3) The atria may be dissociated when the tachycardia is entrained by a proper ventricular pacing. (4) The atria may be dissociated during tachycardia by atrial pacing at a rate faster than the tachycardia rate by an appropriate premature atrial stimulated beat or by intravenous administration of adenosine triphosphate or verapamil. REFERENCES
1. Mahaim I, Winston MR. Recherches d'anatomic compar~e et du pathologie experimentale sur les connexions du faisceau de His-Tawara. Cardiologia 1941;5:189-260. 2. Tchou P, Lehmann MH, Jazayeri M, Akhtar M. Atriofascicular connection or a nodoventricular Mahaim fiber? Electrophysiologic elucidation of the pathway and associated reent r a n t circuit. Circulation !988;77:837-48. 3. Klein GJ, Guiraudon GM, Kerr CR, Sharma AD, Yee R, Szabo T, Yeung Lai Wah JA. "Nodoventricular" accessory pathway: evidence for a distinct accessory atrioventricular pathway with atrioventricular node-like properties. J Am Coll Cardiol 1988;11:1035-40.
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4. Tonkin AM, Dugan FA, Svenson RH, Sealy WC, Wallace AG, Gallagher JJ. Coexistence of functional Kent and Mahaimtype tracts in the pre-excitation syndrome. Circulation 1975;52:193-200. 5. Touboul P, Vexler RM, Chatelain MT. Reentry via Mahaim fibers as a possible basis for tachycardia. Br Heart J 1978;40:806-11. 6. Ward DE, Camm AJ, Spurrell RAJ. Ventricular preexcitation due to anomalous nodo-ventricular pathways: report of 3 Patients. Eur J Cardiol 1979;9:111-27. 7. Gallagher J J, Smith WM, Kasell JH, Benson DW Jr, Sterba R, Grant AO. Roles of Mahaim fibers in cardiac arrhythmias in man. Circulation 1981;64:176-89. 8. Morady F, Scheinman MM, Gonzalez R, Hess D. His-ventricular dissociation in a patient with reciprocating tachycardia and a nodoventricular bypass tract. Circulation 1981;64:83944. 9. Lerman BB, Waxman HL, Proclemer A, Josephson ME. Supraventricular tachycardia associated with nodoventricular and concealed atrioventricular bypass tracts. AM HEART J 1982;104:1097-1102. 10. Bhandari A, Morady F, Shen EN, Schwartz AB, Botvinick E, Scheinman MM. Catheter-induced His bundle ablation in a patient with reentrant tachycardia associated with a nodoventricular tract. J Am Coll Cardiol 1984;4:611-16. 11. Bardy GH, German LD, Packer DL, Coltorti F, Gallagher JJ. Mechanism of tachycardia using a nodofascicular Mahaim fiber. Am J Cardiol 1984;54:1140-1. 12. Ellenbogen KA, O'Callaghan WG, Colavita PG, Packer DL, Gilbert MR, German LD. Catheter atrioventricular junction ablation for recurrent supraventricular tachycardia with nodoventricular fibers. Am J Cardiol 1985;55:1227-9. 13. Murabit I, Sosa E, Pileggi F, Denes P. Multiple reentry tachycardia in patients with ventricular preexcitation: report of three cases. AM HEARTJ 1986;111:69-80. 14. Deng Z, Gang ES, Rosenthal ME, Oseran D, Mandel WJ, Peter T. Wide QRS tachycardia due to AV nodal reentry and a "bystander" bypass tract with slow conduction properties. PACE 1986;9:188-95. 15. Wu D, Denes P, Amat-y-Leon F, Dhingra R, Wyndham CRC, Bauernfeind R, Latif P, Rosen KM. Clinical, electrocardio-
- - --N o- d -o v e n t r i c u l a- -r f i b e r
--
and tachycarclias 5 9 1
graphic and eleetrophysiological observations in patients with paroxysmal supraventricular tachycardia. Am J Cardiol 1978;41:1045-51. 16. Shimizu A, Ohe J, Takaki H, Kamakura S, Matsuhisa M, Sato I, Shimomura K. Narrow QRS complex tachycardia with atrioventricular dissociation. PACE 1988;11:384-93. 17. Coumel P, Attual P. Reciprocating tachycardia in overt and latent preexcitation. Influence of functional bundle branch block on the rate of the tachycardia. Eur J Cardio11974;1:42336. 18. Caceres J, Jazayeri M, McKinnie J, Avitall B, Denker ST, Tchou P, Aktar M. Sustained bundle branch reentry as a mechanism of clinical tachycardia. Circulation 1989;79:25670. 19. Henthorn WR, Okumura K, Olshansky B, Plumb VJ, Hess PG, Waldo AL. A fourth criterion for transient entrainment: the electrogram equivalent of progressive fusion. Circulation 1988;77:1003-12. 20. Belardinelli L, Fenton RA, West A, Linden J, Althaus JS, Berne RM. Extracellular action of adenosine and the antagonism by aminophylline on the atrioventricular conduction of isolated perfused guinea pig and rat hearts. Circ Res 1982;51:569-79. 21. Lerman BB, Greenberg M, Overholt ED, Swerdlow CD, Smith RTJ, Sellers TD, DiMarco JP. Differential electrophysiologic properties of decremental retrograde pathways in long RP' tachycardia. Circulation 1987;76:21-31. 22. Wit AL, Cranefield PF. Effect of verapamil on the sinoatrial and atrioventricular nodes of the rabbit and the mechanism by which it arrests reentrant atrioventricular nodal tachycardia. Circ Res 1974;35:413-25. 23. Lerman BB, Belardinelli L, West A, Berne RM, DiMarco JP. Adenosine-sensitiveventricular tachycardia: evidence suggestive cyclic AMP-medicated triggered activity. Circulation 1986;74:270-80. 24. Wu D, Kou HC, Hung JS. Exercise-triggered paroxysmal ventricular tachycardia. Ann Intern Med 1981;95:410-14. 25. Lin FC, Finley CD, Rahimtoola SH, Wu D. Idiopathic paroxysmal ventricular tachycardia with a QRS pattern of right bundle branch block and left axis deviation: a unique clinical entity with specific properties. Am J Cardiol 1983;52:95-100.