atypical av junctional reentrant tachycardia following av nodal modification

Journal of Electrocardiology Vol. 27 No. 1 1994

Atypical AV Junctional Reentrant Tachycardia Following AV Nodal

Modification

J e f f r e y G o l d b e r g e r , M D , F r e d e r i c k E h l e r t , M D , J e f f r e y B a e r m a n , M D ,

a n d A l a n K a d i s h , M D

Abstract: The authors present a patient who initially unde rwen t anterior approach atrioventricular (AV) nodal modification for treatment of typical AV junctional reentrant tachycardia (AVJRT) and subsequently developed clinical episodes of a previously undocumented type of supraventricular tachycardia. Findings during electrophysiologic studies suggest that this tachycardia is due to both anterograde and retrograde conduction in a slow AV nodal pathway. A "slow pathway" potential was identified and dissociated from the local atrial and ventricular depolarizations. Posterior approach AV nodal modification was successfully used to ablate this tachycardia. These findings suggest that atypical AVJRT occurring after AV nodal modification may be "slow-slow" AVJRT. Key words: supraventricular tachycardia, AV node, catheter ablation, radiofrequency.

Radiofrequency current catheter modification of the atrioventricular (AV) node has become a widely used technique for the treatment of patients with AV junctional reentrant tachycardia (AVJRT). ~-6 Two techniques have been described for performing the AV nodal modification procedure: (1) the anterior or "fast pathway" approach 2 and (2) the posterior or "slow pathway" approach. 3-6 We report a case of a patient who underwent anterior approach AV nodal modification that was complicate d by the occurrence of spontaneous clinical episodes of a new type of supraventricular tachycardia (SVT) that was likely due to atypical AV junctional reentry. Posterior approach AV nodal modification resulted in control of her symptoms. Our findings also suggest new in-

From the Department of Medicine, Division of Cardiology, Northwest- ern University Medical School, Chicago, Illinois.

Reprint requests: Jeffrey Goldberger, MD, Northwestern Memo- rial Hospital, 250 East Superior Street, Suite 524, Chicago, IL 60611.

formation regarding the physiology of this type of AVJRT.

Materials and Methods

Following clinical evaluation at our institution, the patient was admitted for electrophysiologic studies and catheter ablation. After allowing antiarrhythmic medications to wash out for greater than five half- lives, an electrophysiology study was performed in the fasting, mildly sedated state. Through the right femoral vein, standard quadripolar catheters were positioned in the high right atrium and right ventricle. A large tipped (4 mm) steerable 7 F quadripolar catheter with 2 -mm interelectrode distance (Mans- field-Webster, Watertown, MA) was initially advanced across the tricuspid valve to record a His bundle electrogram and was subsequently used for

79

80 Journal of Electrocardiology Vol. 27 No. 1 January 1994

mapping of the interatrial septum and ablation. A multipolar electrode catheter was positioned in the coronary sinus via a sheath placed in the right inter- nal jugular vein. Electrocardiographic leads I, II, III, V~, and V6 and the intracardiac electrograms (band- pass filters of 4 0 - 4 0 0 Hz) were displayed on an oscil- loscope and recorded at a paper speed of 100 mm/s (Astromed MT-96000, West Warwick, RI). Pacing was performed with a programmable stimulator (Bloom Associates, Reading, PA) using rectangular stimuli at twice the diastolic threshold with a stimu- lus duration of 2 ms. Standard atrial and ventricular pacing techniques were used to evaluate AV nodal conduction and refractoriness and to induce SVT. Ra- diofrequency energy was delivered as a continuous unmodulated sine wave output from an electrosurgi- cal unit at 350 kHz (Radionix RFG-3C Lesion Gener- ator, Burlington, MA). Atypical AVJRT was defined as SVT with the characteristics of AV junctional reentry in which the retrograde atrial activation was over a slow AV nodal pathway. This was detected when the earliest retrograde atrial activation was near the coronary sinus OS. 7

Case Report

The patient is a 48-year-old woman with no significant cardiac disease who has had paroxysmal SVT since age 20. Episodes occurred every 2 months and

were associated with palpitations, lightheadedness, and occasional chest pain and shortness of breath. The patient had been treated with multiple antiarrhythmic medications, which did not successfully control her tachycardia. In December I990, she underwent electrophysiologic studies at another institution. Findings at that time included an AH interval of 75 ms and an HV interval of 45 ms. The AV nodal Wenckebach cycle length was 300 ms. The AV nodal effective refractory period was 270 ms at a drive cycle length of 500 ms. The ventriculoatrial (VA) Wencke- bach cycle length was 260 ms. During induced SVT, the atrial and ventricular electrograms were superim- posed with the earliest atrial activation in the His bundle electrogram. Tachycardia induction by atrial extrastimulation was accompanied by a jump in the AH interval. Thus, SVT was most consistent with typical AVJRT. The patient subsequently underwent an anterior or fast pa thway AV nodal modification. Ten radiofrequency lesions were administered using the technique described by Lee et al. 2 Following AV nodal modification, typical AVJRT was not inducible. Ventriculoatrial conduct ion persisted with earliest retrograde atrial activation in the proximal coronary sinus recording. Nonsustained SVT with the characteristics of atypical AV junctional reentry was inducible. During monitoring following the procedure, the patient cont inued to have symptomatic palpitations associated with nonsustained episodes of SVT. She was initially treated with flecainide, which

Fig. 1. Standard 12-lead electrocardiogram demonstrating supraventricular tachycardia with 2:1 atrioventricular block. The asterisks indicate the P waves.

subsequently was discontinued secondary to side ef- fects. She was then treated with quinidine.

The patient subsequently presented to the emergency room at another institution in May 1991 with palpitations and was noted to be in SVT. She was treated with nifedipine and verapamil and sent home. She remained on quinidine therapy. In July 1991, she first presented to our institution with palpitations and was noted to be in SVT. The tachycardia terminated spontaneously during venipuncture. An electrocardiogram during SVT is shown in Figure 1. Note the presence of 2 : 1 AV block and inverted P waves in leads II, III, and aVF. The tachycardia rate is approximately 240 beats/min.

The patient was admitted for electrophysiologic testing and potential repeat ablation after quinidine

Atypical AVJRT • Goldberger et al. 81

had been discontinued for 48 hours. Baseline findings included a sinus cycle length of 760 ms, PR interval of 250 ms, AH interval of 200 ms, and HV interval of 50 ms. The AV nodal and VA Wenckebach cycle lengths were 420 and 450 ms, respectively. The AV nodal and VA effective refractory periods were 260 and 370 ms , respectively, at a drive cycle length of 550 ms. With the application of single ventricular extrastimuli, there were no criteria for retrograde dual AV nodal physiology. Following the administration of isoproterenol at a dose of 1 p,g/min, SVT was easily inducible with ventricular pacing (Fig. 2). Note the constant VA interval on the first four paced beats and the sudden prolongation of the VA interval on the fifth paced beat that leads to initiation of the tachycardia. This sudden increase in VA time during

II

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Fig. 2. Simultaneous recordings of surface leads I, II, III, Vl, and V6, with intracardiac recordings from the high right atrium (HRA), distal (HBEd) and proximal (HBEp) His bundle electrograms (the catheter has slipped back slightly into the atrium--see Figure 3 for HBE recordings during tachycardia), proximal (CSp) and distal (CSd) coronary sinus, and right ventricular apex (RVA). The electrograms are recorded at a paper speed of 100 mm/s. During ventricular overdrive pacing at a cycle length of 280 ms, atypical atrioventricular junctional reentrant tachycardia is induced. The arrow indicates that the earliest retrograde atrial activation occurs in the proximal coronary sinus. The ventriculoatrial time for the first four beats is constant. Following the last paced beat, there is a sudden prolongation in ventriculoatrial time. Atrial (A), His bundle (H), and ventricular (V) electrograms are labeled.


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Fig. 3. Simultaneous recordings of surface leads I, II, III, V~, and V6, with intracardiac recordings from the high right atrium (HRA), distal (HBEd) and proximal (HBEp) His bundle electrograms, proximal (CSp) and distal (CSd) coronary sinus, and right ventricutar apex (RVA). The electrograms are recorded at a paper speed of 100 mm/s. (A) Recording during the first induced supraventricular tachycardia indicates that earliest retrograde atrial activation is near the coronary sinus os. (B) Recording during the second induced supraventricular tachycardia indicates that earliest retrograde atr ial activation is near the coronary sinus os.

f ixed ra te pac ing suggests the p re sence of r e t rog rade dua l AV n o d a l phys io logy . Two types of SVT w e r e i n d u c e d (Fig. 3); the i r character is t ics are s h o w n in Table 1. Earl ies t a t r ia l ac t iva t ion is n o t e d in the p rox i - ma l c o r o n a r y s inus r eco rd ing for b o t h t achycard ias . Figure 4A d e m o n s t r a t e s r ecord ings m a d e du r ing s inus r h y t h m a p p r o x i m a t e l y 1 c m pos te r io r to the

c o r o n a r y s inus os (MAPd) . Record ings at this site are d i sp l ayed for the first SVT in F igure 4B. M a p p i n g of a t r ia l ac t iva t ion r evea led tha t the ear l ies t a tr ial acti- v a t i o n occu r red at this site w i t h a VA t ime of 200 ms. F igure 5A d e m o n s t r a t e s the record ings m a d e dur ing s inus r h y t h m pr ior to i n d u c t i o n of the second type of SVT. Once again , these record ings w e r e m a d e ap-

Tab le 1. Characteristics of the Two Types of Supraventr icular Tachycardia Induced in the Patient (ms)

TCL AH HA VAHBE VAearly A-SP

First supraventricular tachycardia 415 140 275 235 200 20 Second supraventricular tachycardia 380 260 120 80 45 - 25

TCL = tachycardia cycle length; VAHBE = ventriculoatrial time during supraventricular tachycardia in the His bundle recording; VAearly = earliest ventriculoatrial time recorded during supraventricular tachycardia, which was approximately 1 cm posterior to the coronary sinus os in both tachycardias; A-SP = time from the atrial depolarization to the slow pathway potential recorded on the mapping catheter.

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Fig. 4. Simultaneous recordings of surface electrocardiographic leads I, II, III, V1, and V6, with intracardiac recordings from the high right atrium (HRA), distal (MAPd) and proximal (MAPp) mapping catheter located 1 cm posterior to the coronary sinus os, proximal (CSp) and distal (CSd) coronary sinus, and right ventricular apex (RVA). All tracings are recorded at a paper speed of 100 mm/s. (A) Recording during sinus rhythm. The atrial (A), slow pathway (SP), and ventricular (V) electrograms are labeled on the MAPd tracing. (B) Recording during supraventricular tachycardia.

proximately 1 cm posterior to the coronary sinus os. Although there are minor differences be tween the sinus rhy thm electrograms recorded f rom the mapping catheter (MAPd) in Figures 4A and 5A, the mapping catheter was fluoroscopically in the same location for both recordings. Recordings at this site are displayed for the second SVT in Figure 5B. Again, mapping of atrial activation revealed that the earliest atrial activation was near the coronary sinus os with a VA time of 45 ms. Atrioventricular reentrant tachycardia utilizing a concealed accessory pa thway was ruled out by the clinical occurrence of 2 : 1 AV block and the induction of two tachycardias with the same atrial activation sequence but with markedly different VA times (Table 1, Figs. 4, 5). In addition, premature ventricular extrastimuli did not advance the suc- ceeding atrial electrogram, making AV reentrant tachycardia utilizing a posteroseptal accessory pathway unlikely. 8 Atrial tachycardia was ruled out by the ability to dissociate the earliest atrial activation

from the tachycardia as described below. In addition, the tachycardia was induced by ventricular pacing that resulted in a prolonged VA interval (Fig. 2). Be- cause the earliest retrograde atrial activation occurred 1 cm posterior to the coronary sinus os, both SVTs were most consistent with atypical AVJRT.

The sinus rhy thm recordings in Figures 4A and 5A demonstrate clear atrial and ventricular electrograms. Between the atrial and ventricular electrograms is a discrete potential that has been suggested to be a slow pa thway potential reflecting activation of either the atrial connection with the slow pa thway 6 or perhaps other nodal/perinodal tissue. During the first SVT (Fig. 4B), the sequence of activation on the mapping catheter recording is atrial-slow pathway, with the atrial-slow pa thway interval being 20 ms. During the second SVT (Fig. 5B), there is fusion of atrial, slow pathway, and ventricular electrograms. Single ventricular extrastimuli were introduced in order to advance the ventricular


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Fig. 5. Simultaneous recordings of surface electrocardiographic leads I, II, IIl, Vl, and V6, with intracardiac recordings from the high right atrium (HRA), distal (MAPd) and proximal (MAPp) mapping catheter located 1 cm posterior to the coronary sinus os, proximal (CSp) and distal (CSd) coronary sinus, and right ventricular apex (RVA). All tracings are recorded at a paper speed of 100 mnfs. (A) Recording during sinus rhythm. The atrial (A), slow pathway (SP), and ventricular (V) electrograms are labeled on the MAPd tracing. (B) Recording during supraventricular tachycardia. There is fusion of the A, SP, and V electrograms, preventing detailed identification of the morphology of these potentials. A premature ventricular extrastimulus is applied that advances the ventricular electrogram in the MAPd recording allowing visualization of two discrete potentials (SP and A).

electrogram, starting in late diastole and then at 10- ms decrements until ventricular refractoriness. Fig- ure 5B demonstrates that when the ventricular electrogram is advanced, the slow pathway potential pre- cedes the atrial electrogram with an atrial-slow pathway interval of - 2 5 ms (note that the onset of the atrial electrogram on the MAPd recording occurs at the same time as the onset of the atrial electrogram recorded from the proximal electrodes of the mapping catheter). Subsequently, single ventricular and atrial extrastirnuli were introduced simultaneously, starting in late diastole and then at 10-ms decrements. Figure 6 demonstrates a typical recording in which the local ventricular and atrial electrograms are advanced in front of the remaining slow pathway potential (the slow pa thway potential following the premature atrial and ventricular depolarizations is actually delayed by 15 ms). Thus, the local atrial depolarization was dissociated from the slow pathway potential for this beat. On the following beat, the atrial depolarization is again advanced with a "high- low" atrial activation sequence, presumably origi-

nating from an intraatrial echo or the sinus node. The tachycardia nevertheless continues.

Six radiofrequency lesions were administered at this site. Energy was delivered for 30 -100 seconds at 16-36 W. Electrograms at the final ablation site recorded prior to and following ablation are displayed in Figure 7. Prior to ablation (Fig. 7A), a large slow pathway potential is noted on the MAPd recording. There is a small atrial deflection on this tracing that occurs at the same time as the atrial deflection recorded from the proximal pair of electrodes on the same catheter. Following ablation (Fig. 7B), a slow pathway potential is no longer seen. On electrophysiologic testing 2 days after the procedure, SVT was not inducible. Electrophysiologic testing 4 months after the procedure revealed a sinus cycle length of 720 ms, PR interval of 265 ms, AH interval of 200 ms, and HV interval of 40 ms. The AV nodal and VA Wenckebach cycle lengths were 520 and 470 ms, respectively. The AV nodal effective refractory period was 530 ms at a drive cycle length of 600 ms. No SVT could be induced at baseline or after the


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Fig. 6. Simultaneous recordings of surface electrocardiographic leads I, II, III, VI, and V6, with intracardiac recordings from the high right atrium (HRA), distal (MAPd) and proximal (MAPp) mapping catheter located 1 cm posterior to the coronary sinus os, proximal (CSp) and distal (CSd) coronary sinus, and right ventricular apex (RVA). All tracings are recorded at a paper speed of 100 mm/s. Premature atrial (PAC) and ventricular (PVC) extrastimuli are applied during supraventricular tachycardia.

administration of isoproterenol. The patient has had no clinical recurrences of atypical AVJRT for 24 months since the procedure.

Discussion

This is the first documented report of spontaneous clinical episodes of atypical AVJRT occurring following anterior approach AV nodal modification in which atypical AVJRT was induced during electrophysiologic studies. Our findings suggest that at least one of the two induced tachycardias is due to both anterograde and retrograde conduction in a slow

pa thway representing "s low-s low" AVJRT. Second, while the origin of slow pa thway potentials remains uncertain, this case provides further evidence that these potentials can be dissociated f rom both local atrial and ventricular depolarizations, suggesting that they may in fact represent recordings f rom a perinodal/nodal slow pathway.

Recognizing atypical AVJRT as a potential compli- cation of anterior approach AV nodal modification may be important in terms of decisions regarding further ablative therapy. Because the anterograde pathway of this tachycardia is not clearly established but appears to be a "s low AV nodal pa thway ," further AV nodal modification should be directed toward the retrograde limb of this tachycardia. While the risk


A

V6

B

HRA

MAPd

MAPp

Y

Fig. 7. Simultaneous recordings of surface electrocardiographic lead V6 with intracardiac recordings from the high right atrium (HRA) and distal (MAPd) and proximal (MAPp) mapping catheter located 1 cm posterior to the coronary sinus os. (A) Recording during sinus rhythm showing a small atrial (A) deflection, a large slow pathway (SP) potential, and a large ventricular electrogram (V) made prior to the sixth and final radiofrequency energy application. (B) Recording during sinus rhythm showing a small atrial deflection, no slow pathway potential, and a large ventricular electrogram (V) made following the sixth and final radiofrequency energy application at the same site.

of developing complete AV block when performing posterior approach AV nodal modification in patients who have already undergone anterior approach AV nodal modification is unknown, posterior approach AV nodal modification was successfully performed in this patient without development of AV block. Ja- zayeri et al. 5 reported that further attempts at ablation of the anterograde limb of these u n c o m m o n AV3RTs using the anterior approach were unsuccess- ful and that the posterior approach was successfully used in two patients (heart block was not reported). Extreme caution and careful review of the risk for AV block should be under taken when performing such a procedure. However, at this time, it is not clear whether patients with atypical AVJRT following anterior approach AV nodal modification require further ablative therapy as the incidence of new clinical episodes of atypical AVJRT following anterior approach AV nodal modification is unknown.

While several reports 2"5"9 have described the presence of new types of induced SVT following anterior approach AV nodal modification for the treatment of patients with AVJRT, their clinical significance remains uncertain. In one report, 9 a clinical episode of a previously undocumented type of SVT was noted in one patient. Because this tachycardia was not in-

ducible during follow-up electrophysiology studies, the mechanism of this previously undocumented type of SVT was not known. In another reportfl one patient who had undergone anterior approach AV nodal modification was reported to require posterior approach AV nodal modification 4 weeks following recurrent episodes of " u n c o m m o n AVJRT," but no recordings are provided. This report establishes that previously undocumented SVT, namely atypical AVJRT, may be a clinical problem following fast pa thway or anterior AV nodal modification. Al- though the patient's clinical tachycardia was faster than the tachycardias induced in the electrophysiology laboratory, this may be due to the vagolytic ef- fects of quinidine that the patient was taking at the time of her clinical episode or to other u nknown fac- tors. Prior to her last ablation, the patient had two episodes of SVT that required emergency room visits and, since ablation has had no recurrent SVT over a 2-year follow-up period, provided strong supportive evidence that her clinical tachycardia was atypical AVJRT.

The mechanism of new types of SVT occurring following anterior approach AV nodal modification is not clear. Previous studies have suggested that SVT in this setting may be due to AV junctional reentry

with retrograde upper common pathway delay, retrograde conduction delay in a damaged fast AV nodal pathway, or atypical AV junctional reentry with retrograde conduction in a slow pathway. 2'9 While evidence is accumulating 1° that these tachycardias are due to atypical AV junctional reentry with a slow AV nodal pathway serving as the retrograde limb, it is difficult to identify the anterograde limb because no criteria exist for separation of anterograde slow pathway conduction from damaged fast pathway conduction. The two tachycardias observed in this study confirm that these tachycardias are due to atypical AV junctional reentry and suggest that both the anterograde and retrograde limbs of these tachycardias are slow AV nodal pathways. The AH and HA times of the two tachycardias (Table 1) have a reciprocal relationship, suggesting that these SVTs may represent the same tachycardia circuit manifesting in the orthodromic and antidromic directions. Since the retrograde limb of both tachycardias is a slow AV nodal pathway, this would imply that the anterograde limb is also a slow AV nodal pathway. Further support for this concept may be obtained by exami- nation of the electrograms. Because the slow pathway potential that was recorded in this patient followed the atrial electrogram in the first SVT and preceded the atrial electrogram in the second SVT, it is highly probable that this slow pathway served as the anterograde limb of the tachycardia in the first instance and the retrograde limb of the second tachycardia (Fig. 8). In the first tachycardia where the slow pathway, whose activation was recorded, served as the anterograde limb, the retrograde limb must also have been a slow pathway because the earliest atrial activation occurred posteriorly. Because the reported incidence of multiple slow pathways is greater than 30%, 11 it is not surprising that following successful ablation of a fast AV nodal pathway there may re- main multiple slow pathways capable of mediating atypical (slow-slow) AVJRT. In addition, the tachycardias observed in this patient have similar properties to the tachycardias described by Baerman et a1.12 that were due to AV nodal reentry with an anterograde slow pathway and a retrograde slow pathway.

The origin of the slow pathway potential is un- clear. Most recently, Jackman et al. 6 have suggested that it represents activation of the atrial insertion of the slow pathway. They showed that the local atrial and ventricular electrograms could be dissociated from the slow pathway potential, supporting the concept that these potentials do not arise from the atrium or ventricle. In the two tachycardias in this study, dissociation from the atrial electrogram was shown in two ways. In the first tachycardia, the slow pathway potential followed the atrial electrogram by


20 ms and in the second tachycardia, the slow pathway potential preceded the atrial electrogram by 25 ms. These findings suggest that the slow pathway depolarization is not consistently linked to the atrial depolarization. In the second tachycardia, where the atrial depolarization followed the slow pathway potential (Fig. 5B), an atrial premature extrastimulus advanced the local atrial electrogram so that it preceded the slow pathway potential (Fig. 6), again suggesting that the atrial electrogram can be dissociated from the slow pathway potential. Similarly,.ventricular extrastimuli applied during the second tachycardia clearly demonstrate that the ventricular electrogram is not linked to the slow pathway potential. Given the above findings and the fact that ablation at this site resulted in the loss of inducibility of atypical AVJRT, it seems highly probable that this potential is related to activation of the (atrial insertion of the) slow pathway.

Significant controversy still exists regarding whether the perinodal atrial tissue is part of the tachycardia circuit in patients with AVJRT. The strongest evidence that the reentrant circuit is com- pletely intranodal is the ability to dissociate both the atrial and ventricular depolarizations from the tachycardia.13"14 The best evidence that the reentrant circuit includes the perinodal atrium is surgical ablation of the perinodal atrium and atrial inputs to the AV node leading to a cure of the tachycardia.15-is How- ever, separation of the AV node from its atrial inputs is not well demarcated, 17.~9 and damage to the AV node with surgical dissection or ablative lesions can- not be definitely excluded. It has also been suggested that the perinodal atrium must participate in the tachycardia based on the disparate atrial activation sequences in patients with both typical and atypical AVJRTs. 2°'21 While this finding appears to provide strong evidence that there is no upper common pathway, it is certainly possible that the atrial exit sites for typical and atypical AVJRT do differ while the tachycardia circuit remains intranodal. The finding in our patient that the local atrial and ventricular electrograms could be dissociated from the slow pathway potential (which is presumably a critical portion of the tachycardia circuit) suggests that the local atrial and ventricular tissues are not required to participate in the tachycardia circuit. On the other hand, as the slow pathway potential may represent activation of perinodal (atrial) tissue, it is possible that this specialized region can be dissociated from the rest of the atrium, particularly when it is engaged in the tachycardia; this hypothesis is consistent with all previous observations.

Despite the findings during this single electrophysiologic study, one must be careful in generalizing

SVT #1 SINUS RHYTHM


SVT #2

Fig. 8. Schematic representations of atrioventricular nodal activation in sinus rhythm, during the first supraventricular tachycardia (Fig. 5B, Table 1 ), and during the second one (Fig. 6B, Table 1). The posterior portion of the atrioventricular node is at the bottom of the figure. In sinus rhythm, the perinodal atrium is activated prior to the slow pathway potential and leads to the recordings in Figures 5A and 6A. During the first supraventricular tachycardia, the slow pathway potential serves as the anterograde limb of the tachycardia, thus the atrial electrogram is recorded prior to the slow pathway potential. During the second supraventricular tachycardia, the Slow pathway potential serves as the retrograde limb of the tachycardia, thus the atrial electrogram is recorded following the slow pathway potential. The presence of an upper common pathway, though illustrated for clarity purposes, is not suggested by any of the data presented. Also, whether the slow pathway potential represents activation of perinodal or nodal tissue is not known.

these results to all patients with AVJRT: t t is possible that the slow pa thway potential we recorded was not part of the tachycardia circuit but served as an innocent bystander. This seems unlikely because: ( 1 ) it was recorded at the site of earliest retrograde atrial activation; (2) it was closely coupled to the earliest atrial activation whether it was activated in the anterograde or retrograde direction; (3) ablation at this site prevented induction of tachycardia. More gener- ally, despite the fact that dual AV nodal physiology, indicating the presence of fast and slow AV nodal pathways, is noted frequently in patients with AVJRT, anatomic documenta t ion of the existence of distinct fast and slow AV nodal pa thways has never

b e e n obtained. Further studies attempting to record AV nodal activation are required to elucidate in bet- ter detail the physiology of the AV node and its anatomic correlates.

In summary, this case report documents that atypical AVJRT may occur in patients following anterior approach AV nodal modification for t reatment of typical AVJRT. In this patient, slow pa thway potentials were recorded 1 cm posterior to the coronary sinus os and were shown to be distinct f rom the local atrial and ventricular electrograms. Finally, it is likely that the anterograde and retrograde limbs of the two types of atypical AVJRTs that were observed in this patient are both slow AV nodal pathways. While it is impossible to generalize the findings from one pa-

tient to all patients with AVJRT, m a n y of these findings concur with currently accepted, though un- proven, concepts regarding the physiology of the AV node in AVJRT.

References

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