(Circulation. 1999;100:621-627.)
© 1999 American Heart Association, Inc.
Clinical Investigation and Reports |
Electrophysiological Delineation of the Tachycardia Circuit in Atrioventricular Nodal Reentrant Tachycardia
Presented in part at the 70th Scientific Sessions of the American Heart Association, Orlando, Fla, November 9–12, 1997, and published in abstract form (Circulation. 1997;96[suppl I]:I-703).
From the Division of Cardiology, Kumamoto City Hospital, Kumamoto, Japan.
Correspondence to Hiroshige Yamabe, MD, Division of Cardiology, Kumamoto City Hospital, 1-1-60 Kotoh, Kumamoto, 862-8505 Japan.
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Abstract |
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Background—The exact boundaries of the reentry circuit in atrioventricular nodal reentrant tachycardia (AVNRT) have not been convincingly defined.
Methods and Results—To define the tachycardia circuit, single extrastimuli were delivered during AVNRT to 8 sites of the right intra-atrial septum: 3 arbitrarily divided sites of the AV junction extending from the His bundle (HB) site to the coronary sinus ostium (CSOS) (sites S, M, and I) and the superior (S-CSOS), inferior (I-CSOS), posterior (P-CSOS), and posteroinferior (PI-CSOS) portions of the CSOS and the CSOS in 18 patients. The mean tachycardia cycle length (TCL) was 368±52 ms. Retrograde earliest atrial activation was observed at the HB site in all patients. The longest coupling intervals of single extrastimuli that reset AVNRT at sites S, M, I, I-CSOS, CSOS, S-CSOS, P-CSOS, and PI-CSOS were 356±51, 356±51, 355±52, 357±51, 318±47, 305±53, 311±56, and 312±56 ms, respectively, and the following return cycles at these sites were 368±52, 368±53, 367±53, 367±53, 407±66, 431±73, 415±55, and 412±56 ms, respectively. The longest coupling intervals at sites S, M, I, and I-CSOS did not differ from each other and were longer than those at CSOS and S-, P-, and PI-CSOS (P<0.0001). The return cycles at sites S, M, I, and I-CSOS did not differ from the TCL, whereas those at CSOS and S-, P-, and PI-CSOS were longer than the TCL (P<0.0001).
Conclusions—The perinodal atrium extending from the HB site to I-CSOS was involved in the tachycardia circuit. I-CSOS was thought to be the entrance of the slow pathway.
Key Words: atrioventricular node • mapping • reentry
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Introduction |
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TopAbstractIntroductionMethodsResultsDiscussionReferences |
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The prevailing clinical understanding of atrioventricular nodal reentrant tachycardia (AVNRT) is based on a model of dual AV node pathways that are functionally and anatomically distinct.1 2 However, the exact boundaries of the reentry circuit in AVNRT have not been convincingly defined. The purpose of the present study was to define the tachycardia circuit in AVNRT. Single extrastimulus testing is useful for determining the location of the pacing site relative to the reentry circuit.3 4 Using this diagnostic tool to identify the location of the reentry circuit, we examined whether the tachycardia involves the atrium in the circuit, in particular to determine the extent of the atrial myocardium involved in the reentry circuit in AVNRT.
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Methods |
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Patients
Eighteen patients with typical AVNRT (7 men and 11 women; mean age 56 years, range 22 to 82 years) were included. All drugs were discontinued 3 days before the ablation procedure. All patients gave written informed consent. The protocol was approved by the hospital Human Research Committee. The inclusion criteria for patients were (1) induction of a sustained slow-fast form of AVNRT and (2) a stable tachycardia cycle length that varied by no more than 10 ms over 20 consecutive beats.
Electrophysiological Study
The study was performed with patients in a fasting, unsedated
state. Three 6F quadripolar electrode catheters (USCI) were inserted
percutaneously via the right femoral and subclavian
veins and positioned in the His bundle (HB) region, right
ventricular apex, and coronary sinus ostium (CSOS).
One 7F large-tip (4-mm-long), deflectable quadripolar electrode
catheter with a 2-mm interelectrode distance (Cordis Webster) was
introduced into the right femoral vein and advanced to the right
intra-atrial septum for atrial mapping, pacing, and ablation. Bipolar
electrograms from the CSOS, HB region, right ventricular
apex, and sequential right intra-atrial septum were filtered at 50 to
600 Hz and recorded along with the surface ECG (leads II and
V1) with the use of a polygraph (RMC-2000, Nihon
Kohden). The right atrium was paced at an output of 2 times the
diastolic threshold and a pulse width of 2 ms with a
cardiac stimulator (SEC-3102, Nihon Kohden). Dual AV nodal physiology
was identified by an increment of 
50 ms in the
A2H2 interval in response
to a decrement of 10 ms in the
A1A2 interval during
programmed atrial stimulation. AVNRT was defined by the previously
published standard criteria.5
Study Protocol
To define the retrograde atrial activation sequence during
AVNRT, atrial mapping was performed at 8 sites of the right
intra-atrial septum: 3 arbitrarily divided sites of the AV junction
extending from the HB site to CSOS (sites S [superior], M [middle],
and I [inferior third of atrioventricular
junction of septal leaflet between HB region and CSOS,
respectively]) and the superior (S-CSOS), inferior
(I-CSOS), posterior (P-CSOS), and posteroinferior (PI-CSOS)
portions of the CSOS and the CSOS (Figure 1
).
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Single extrastimuli were delivered to these 8 sites during AVNRT beginning with the tachycardia cycle length and decreasing by 10 ms until the next His potential was advanced. The catheter positions during pacing were checked by biplane fluoroscopy. The pacing protocol was performed at least twice at each site. The longest coupling interval of the single extrastimulus that reset the tachycardia and the following return cycle at each site were measured. Extrastimuli that advanced the atrial potential in the HB region were excluded from the analysis. When resetting was confirmed, the coupling interval of the single extrastimulus was not shortened further to perform the single extrastimulation during the same tachycardia. If the tachycardia was terminated, it was reinitiated and the stimulation protocol was performed again from the start.
Catheter Ablation
Radiofrequency (RF) energy was delivered by the RF energy
generator (CAT 500, Central Inc) as a continuous, unmodulated sine
waveform at 500 kHz in a unipolar mode between the tip of the ablation
catheter and a large skin electrode placed under the patient's back.
Slow pathway ablation was instituted in a stepwise fashion. RF energy
(20 W for 30 seconds at each site) was delivered along the tricuspid
annulus, starting at the level of the PI-CSOS with the ablation
catheter positioned to record an atrial-to-ventricular
electrogram ratio 
0.5. If tachycardia was induced after
the energy application, the catheter tip was then advanced more
superiorly to the next adjacent site in a stepwise fashion.
Statistics
Values are expressed as mean±SD. Differences between
electrophysiological parameters
were analyzed with Student's t test. A value of
P<0.05 was considered statistically significant.
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Results |
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The slow-fast form of AVNRT was induced in association with typical antegrade AV duality (jump >50 ms in the AH interval with a 10-ms decrement in A1A2) in all patients. The mean tachycardia cycle length was 368±52 ms.
Retrograde Atrial Activation Sequence During AVNRT
The retrograde atrial exit from the fast pathway during AVNRT was
located at the HB site in all patients. The intra-atrial conduction
intervals between the earliest atrial electrogram at the HB site and
that at each mapping site are shown in Figure 2.
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Response to Single Extrastimuli
In all patients, resetting of the AVNRT was observed at all sites.
The longest coupling intervals of a single extrastimulus that reset the
tachycardia at sites S, M, I, I-CSOS, CSOS, S-CSOS, P-CSOS,
and PI-CSOS were 356±51, 356±51, 355±52, 357±51, 318±47, 305±53,
311±56, and 312±56 ms, respectively (Table 1). The longest coupling intervals
at sites S, M, I, and I-CSOS were significantly longer than those at
CSOS, S-CSOS, P-CSOS, and PI-CSOS (P<0.0001) (Table 1). There was no significant difference in the longest coupling
interval among sites S, M, I, and I-CSOS. The return cycles at sites S,
M, I, I-CSOS, CSOS, S-CSOS, P-CSOS, and PI-CSOS were 368±52, 368±53,
367±53, 367±53, 407±66, 431±73, 415±55, and 412±56 ms,
respectively (Table 2). The return cycles
at sites S, M, I, and I-CSOS were significantly shorter than those at
CSOS, S-CSOS, P-CSOS, and PI-CSOS (P<0.0001) (Table 2). The return cycles at sites S, M, I, and I-CSOS were not
different from the tachycardia cycle length, whereas those
at CSOS, S-CSOS, P-CSOS, and PI-CSOS were longer than the
tachycardia cycle length (P<0.0001) (Table 2). Thus, sites S, M, I, and I-CSOS were concluded to be located
within the tachycardia circuit, whereas CSOS, S-CSOS,
P-CSOS, and PI-CSOS were not. Because the retrograde atrial exit site
was located at the HB site in all patients, atrial tissue extending
from the HB site to I-CSOS was concluded to be involved in the
tachycardia circuit. I-CSOS was considered to be the
entrance of the slow pathway, because it was located most distally to
the retrograde atrial exit site.
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The tracings during resetting of the AVNRT in patient 5 are shown in
Figures 3, 4, and 5. The
extrastimulus delivered from site S with a coupling interval of 340 ms
shortened the interval between His potentials before and after the
extrastimulus to 340 ms, and the following return cycle was identical
to the tachycardia cycle length (Figure 3A). A
single extrastimulus delivered from site M with a coupling interval of
340 ms also reset the tachycardia, and the following return
cycle was identical to the tachycardia cycle length
(Figure 3B).
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Figure 4
shows the recordings
during delivery of a single extrastimulus from I-CSOS. A single
extrastimulus with a coupling interval of 340 ms reset the
tachycardia, and the following return cycle was identical
to the tachycardia cycle length (Figure 4A). When
the coupling interval of the single extrastimulus was shortened to 320
ms, the interval between the His potentials before and after the
extrastimulus shortened further to 330 ms (Figure 4B).
Figure 5 shows the
recordings during delivery of a single extrastimulus from
PI-CSOS. A single extrastimulus with a coupling interval of 340 ms was
unable to reset the tachycardia (Figure 5A). Single
extrastimuli with coupling intervals of 330, 320, and 310 ms were also
unable to reset the tachycardia. The
tachycardia was reset initially when the coupling interval
was shortened to 300 ms; however, the return cycle after the
extrastimulus was longer than the tachycardia cycle length
(Figure 5B).
Catheter Ablation
RF ablation was successful in eliminating inducible AVNRT in all
patients. The mean number of RF applications required for successful
ablation was 3±3. The atrial-to-ventricular electrogram
amplitude ratio at the successful ablation site was 0.2±0.1. RF energy
application along the tricuspid annulus at the level of PI-CSOS was not
efficacious in any of the patients. The successful ablation site was
located at the level of I-CSOS in 14 patients (78%) and at the level
of site I in 4 patients (22%). There were no complications associated
with ablation.
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Discussion |
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TopAbstractIntroductionMethodsResultsDiscussionReferences |
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The exact anatomic tachycardia circuit in typical AVNRT has not been convincingly defined. Mendez and Moe,6 and more recently, Iinuma et al7 demonstrated that the perinodal tissue was a necessary link in the AV node reentrant circuit in their model. Alternatively, another experimental study provided evidence in favor of an intra-AV nodal reentry circuit.8 Also, some recent descriptions of the AV node have suggested that the slow and fast pathways exist within the AV node.9 10 Clinically, Josephson and Miller11 proposed the concept of intra-AV nodal reentry. However, several studies have confirmed that surgical procedures could cure AVNRT without significantly impairing AV nodal conduction.12 13 This suggests that cure is achieved by damaging the putative atrial part of the reentrant circuit.13 The involvement of the atrial tissue in the reentry circuit of AVNRT was also demonstrated electrophysiologically.14 Also, it was shown that RF energy application near the CSOS inferior to the AV node can selectively eliminate the slow pathway conduction.1 15 In addition, Keim et al16 demonstrated the location of the site of the antegrade slow pathway using ice mapping techniques. Histological findings in patients also have provided evidence that the AV node itself does not participate in the slow pathway conduction.17 18 These findings strongly suggest that the tissue inferior to the compact AV node is used in the reentry circuit of the AVNRT.
Atrial Myocardium Participated in the Reentry
Circuit
Resetting of AVNRT by the atrial extrastimulus without advancing
the atrial potential at the HB site indicates that the atrial
myocardium participates in the tachycardia
circuit in AVNRT. Lai et al19 reported that the single
extrastimulus delivered from the posteroinferior
interatrial septum during late diastole began to reset the
AVNRT once the extrastimulus started to depolarize the intervening
tissue. In the present study, the extrastimulus began to reset the
AVNRT as soon as it was delivered during late diastole at
sites S, M, I, and I-CSOS. Furthermore, the return cycles at these
sites were almost uniformly identical to the tachycardia
cycle length. These results strongly suggest that sites S, M, I, and
I-CSOS are involved in the tachycardia circuit of the
AVNRT.
Anatomy of the AV Nodal Region
Tawara20 first described a superior dense network of
nodal tissue and an inferior, more open part of the AV node
into which atrial bands gradually merged. The anatomic area in which
the compact AV node is situated is quite complex. The compact AV node
is surrounded by transitional cells whose structure and function are
intermediate between those of atrial and compact nodal
cells.20 21 22 The connections between atrial and
transitional cells are so gradual that no clear anatomic demarcations
can be detected. Thus, sites S, M, I, and I-CSOS, which were considered
to be within the tachycardia circuit, may contain the
transitional cells. If one considers the compact AV node and the
surrounding transitional cells as a functional AV node unit, then the
AV nodal reentry is confined to the AV node. Therefore, the
disagreement about the presence or absence of an upper common pathway
may be related to this definition of the anatomy.
Tachycardia Circuit in AVNRT
The present study demonstrated that the reentrant impulse
during AVNRT initially exits into the atrium at the HB site, then
propagates the atrial component, and finally enters the slow pathway at
the I-CSOS. This circuit is consistent with the findings
previously reported. In the study by Iinuma et al,7 the
reentrant circuit included the so-called sinus septum, which would be
equivalent to sites P- and S-CSOS where they were not part of the
circuit in the present study. This may be a result of the
difference in the anatomic structure between humans and rabbits. Also,
it is possible that the reentrant circuit for single echo beats in the
study by Iinuma et al is not the same as for sustained AVNRT.
Recently, Inoue and Becker23 reported the presence of a rightward inferior extension of the AV node and suggested that this extension may represent the anatomic substrate for the slow pathway. Their results strongly suggest that the entrance of the slow pathway is anatomically defined and is usually located at the inferior margin of the CSOS. The findings of the present report are consistent with their anatomic findings. However, the ablation lesions of the slow pathway were found to be in the atrial myocardium in the cases in which histology was done.17 18 Thus, it remains debatable whether or not the destruction of the inferior extension of the AV node is required for the cure of AVNRT. Meanwhile, other substrates for the slow pathway have been suggested. An experimental study has demonstrated that AV nodal conduction is determined by discrete anteroseptal and posteroseptal atrionodal inputs that are associated with differential functional properties.24 Clinically, Markowitz et al25 suggested that successful slow pathway ablation is achieved by selective ablation of the posterior atrionodal input. McGuire et al,26 however, suggested that transitional, rather than atrial, tissues are the major constituents of the slow pathway. Also, several investigators proposed an anatomic expansion of the AV node, which included the transitional zone tissue, thus maintaining the intra-AV nodal concept of AVNRT.27 28
The results of single extrastimulation revealed that I-CSOS was the entrance of the slow pathway. Indeed, RF energy application along the tricuspid annulus near the I-CSOS was successful in most patients. This result is consistent with those previously reported.1 15 However, a more superior energy application was required in 4 patients. This may depend on a difference in the width of the slow pathway along its course. Supposing that the tachycardia circuit is partially formed functionally, the width of the slow pathway at the entrance may be wider than that at the other more superior sites. Furthermore, the site of application of energy was not the atrium, where the extrastimulation was performed, but rather the site along the tricuspid annulus, where the atrial electrogram was smaller than the ventricular electrogram to avoid the risk of AV block. Thus, an application of energy to the entrance might not be sufficient.
Recently, a variety of retrograde atrial exits from the AV node has been reported.29 Although such a variant retrograde atrial activation was not observed in the present study, it is likely that in some patients the atrionodal inputs to the fast pathway may be anatomically displaced more inferiorly. Similarly, the presence of multiple antegrade slow AV nodal pathways has been reported.30 These observations suggest that dual AV nodal pathways may not exist as a discrete entity, but rather that the proximal AV node may include several pathways with varying electrophysiological properties.31
Conclusions
This study shows that perinodal atrium extending from the HB
region to I-CSOS is an integral limb of the reentry circuit in AVNRT
and that the entrance of the slow pathway is situated at the
I-CSOS.
Study Limitations
First, our findings do not completely rule out the possibility of
confinement of the reentry circuit to the AV node. It is possible that
in some patients, the circuit is entirely intranodal and that in
others, it involves the perinodal atrium. Moreover, the
electrophysiological evidence suggestive of
an upper common pathway does not necessarily imply that the circuit is
entirely intranodal. It is possible that perinodal atrial tissue is
necessary to the circuit but becomes uncoupled from the rest of the
atrium. Second, a previous study showed that there was no structural
difference between patients with and without AVNRT, which suggests that
the defect causing AVNRT is physiological rather
than anatomic.32 Because we studied only AVNRT patients,
we cannot determine the difference between patients with and without
AVNRT. The physiological substrate that causes
reentry in AVNRT, especially in relation to the anatomic structure,
needs to be elucidated.
Received October 14, 1998; revision received April 29, 1999; accepted May 19, 1999.
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