(Circulation. 1995;92:66-76.)
© 1995 American Heart Association, Inc.
Articles |
Electrophysiological Manifestations of the Excitable Gap of Slow-Fast AV Nodal Reentrant Tachycardia Demonstrated by Single Extrastimulation
From the Section of Cardiology, Department of Internal Medicine, Kaohsiung Medical College, Taiwan, Republic of China, and the Department of Cardiovascular Medicine, Stanford (Calif) University.
Correspondence to Wen-Ter Lai, MD, Cardiology Section, Department of Internal Medicine, Kaohsiung Medical College Hospital, 100 Shih-Chuan 1st Rd, Kaohsiung 80731, Taiwan, ROC.
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Abstract |
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Background Although AV nodal reentrant tachycardia (AVNRT) is a well-known rhythm disorder, its anatomic substrate and electrophysiological mechanism remain to be defined. Previously, the description of the excitable gap (EG) of AVNRT was based on electrical stimulation performed from sites remote from the reentrant circuit. In the present study, we characterized the EG of AVNRT by atrial extrastimulation close to the putative reentrant circuit in the AV junction.
Methods and Results In 16 patients (3 men, 13 women; mean age, 45±13 years) with inducible slow-fast AVNRT (mean cycle length, 353±52 ms), single extrastimuli with a 10-ms decrement in the premature coupling interval were delivered from the anterosuperior interatrial septum (fast pathway area) and the posteroinferior interatrial septum (slow pathway area) from late diastole until atrial refractoriness. An EG was considered present when resetting or termination of AVNRT was induced by single atrial extrastimulation. The study showed that the duration of the EG of AVNRT was wide, measuring 121±56 and 123±47 ms and occupying 33±11% and 34±9% of the tachycardia cycle length during single extrastimulation from the slow pathway area and the fast pathway area, respectively. The resetting pattern most commonly manifested as the sum of the coupling interval and the return cycle being less than a fully compensatory pause (two times the basic tachycardia cycle length). However, patterns equal to and greater than a fully compensatory pause were also observed. Of note, in 2 of the 16 patients, atrial extrastimulation from either the fast or slow pathway area also affected the preceding tachycardia cycle length (HH interval), indicating alteration of the anterograde input. In all patients, the curve derived from plotting the coupling interval of extrastimuli against the return cycle during resetting exhibited an "increasing" pattern. The mode of tachycardia termination usually occurred when the premature atrial impulse was orthodromically blocked in the anterograde slow pathway.
Conclusions The EG of slow-fast AVNRT is relatively wide, as demonstrated by single atrial extrastimulation from the interatrial septum near the AV junction. Overall, the electrophysiological manifestations of the EG of AVNRT are very similar to those described in AV reciprocating tachycardia incorporating an accessory connection. These findings lend further support to the notion that, in humans, AVNRT involves a reentrant mechanism with a wide excitable gap.
Key Words: atrioventricular node • electrophysiology • excitation • reentry
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Introduction |
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The response of a cardiac tachyarrhythmia to single extrastimulation or rapid pacing at a rate faster than that of the tachyarrhythmia provides useful information pertaining to the underlying electrophysiological mechanism.1 2 3 In the case of a reentrant tachycardia, an excitable gap is present between the tail of refractoriness of the last tachycardia impulse and the time of arrival of the next tachycardia impulse. During the excitable gap, this portion of the tissue within the reentrant circuit is capable of propagating an electrical impulse.4 5 When an appropriately timed extrastimulus is delivered during the excitable gap, it enters the reentrant circuit and may thereby activate the excitable tissue in the same pattern as the reentrant wave front. This phenomenon is called resetting.6 7 Repetitive resetting of the reentrant circuit by rapid pacing is referred to as entrainment.8 9 In addition, a critically timed extrastimulus delivered during the excitable gap may terminate the tachycardia by induction of bidirectional block.10 11 Electrophysiological manifestations of the excitable gap have been demonstrated in ventricular tachycardia,12 13 atrial flutter,8 14 AV reciprocating tachycardia involving an accessory connection,15 16 and AV nodal reentrant tachycardia17 18 (AVNRT) in humans. However, the excitable gap of AVNRT previously described was based on stimulation from sites remote from the reentrant circuit.19 20 In this study, we delivered single extrastimuli from the AV junction at sites close to the putative AVNRT circuit and systematically studied the excitable gap. Furthermore, from characterization of the excitable gap, we intended to further elucidate the electrophysiological substrate of AVNRT in humans.
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Methods |
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Patients
Sixteen patients in whom a reproducible and sustained slow-fast form of AVNRT could be induced during electrophysiological study were enrolled.21 22 There were 3 men and 13 women, with a mean age of 45±13 years (range, 18 to 70 years).
Electrophysiological Study
The study was performed with
patients in a fasting, unsedated
state after informed consent had been obtained and after all
antiarrhythmic medications had been discontinued for at least 5
elimination half-lives. With conventional methods,16 three
6F quadripolar electrode catheters were introduced into the right
femoral vein and advanced to the high right atrium, right AV junction,
and right ventricular apex for recording and stimulation. Additionally,
a decapolar electrode catheter was introduced into the right internal
jugular vein and placed in the coronary sinus. The intracardiac
electrograms were filtered at 30 to 500 Hz and simultaneously displayed
with three surface ECG leads (I, II, and V1) on a
multichannel oscilloscopic recorder (Electronics for Medicine VR-16)
and recorded on a photosensitive paper at a speed of 100 mm/s.
Electrical stimulation was performed with a programmable stimulator
(Bloom and Associates). Stimuli were delivered as rectangular pulses of
2-ms duration at two times diastolic threshold.
Study Protocol
During a sustained and stable AVNRT, single
extrastimuli were
synchronized to the tachycardia QRS complex and delivered from the high
right atrium, right ventricular apex, and proximal coronary sinus. In
addition, through a deflectable, 4-mm, large-tip ablation catheter
(Mansfield), single extrastimuli were also delivered from the so-called
fast pathway and slow pathway areas.23 The fast pathway
area was defined as the right anterosuperior interatrial septum just
behind the His bundle, where ablation of fast pathway conduction was
usually performed.24 The slow pathway area was defined as
the right posteroinferior interatrial septum near the coronary sinus
ostium, where ablation of slow pathway conduction was usually
applied.25 Consistent capture by stimulation of the
ablation catheter was documented during sinus rhythm, and the catheter
positions were checked by fluoroscopy during stable ANVRT rhythm. After
every 12th tachycardia beat, single extrastimuli were delivered from
each site with 10-ms decrements in the premature coupling interval
until the entire tachycardia cycle was scanned. If the tachycardia was
terminated by a single extrastimulus, the tachycardia was reinduced and
single extrastimulation was continued until scanning of the whole
cardiac cycle was completed.
Definition of Terms
Diagnoses of dual AV nodal pathway
conduction and slow-fast
AVNRT were as previously described.21 22 An increment
50
ms in the AV nodal conduction time (A2H2) after
a decrement of 10 ms in the atrial premature coupling interval
(A1A2) was attributed to failure of fast AV
nodal pathway conduction with resultant slow AV nodal pathway
conduction. A critical conduction delay in the slow AV nodal pathway
was required for initiation of slow-fast AVNRT.21
The coupling interval was measured as the interval from the local electrogram of the extrastimulus to that of the preceding tachycardia beat, and the return cycle was measured as the interval from the local electrogram of the extrastimulus to that of the following tachycardia beat.
When a single extrastimulus is delivered during AVNRT, the extrastimulus may or may not affect the tachycardia, and the following terms were defined.5 16
The zone of ineffectual impulse was defined as premature activation of the local tissue at the pacing site with no effect on the tachycardia—an impulse collision in the intervening tissue between the pacing site and reentrant circuit.
The zone of resetting was defined as premature activation of the local tissue at the pacing site causing subsequent cycle length (return cycle) to be different from that of the tachycardia without termination—interaction with the propagating wave front within the reentrant circuit without interruption of reentry. When single extrastimuli were delivered from the high right atrium, proximal coronary sinus, fast pathway area, and slow pathway area, resetting was deemed to have occurred when there was a change in the HH interval of the tachycardia beat following atrial extrastimulation. On the other hand, when single extrastimuli were delivered from the right ventricular apex, resetting was deemed to have occurred when there was a change in the AA interval of the tachycardia beat following ventricular extrastimulation.
The zone of termination was defined as premature activation of the local tissue at the pacing site causing immediate termination of the tachycardia—induction of bidirectional (orthodromic and antidromic) block within the reentrant circuit that interrupted reentry.
The zone of local refractoriness was defined as the inability of a premature extrastimulus to activate local tissue at the pacing site because of local tissue refractoriness. During tachycardia, the shortest coupling interval that could activate the local tissue was limited by the functional refractory period of that local tissue. Thus, the functional refractory period of the local tissue was given as the upper limit of the zone of local refractoriness at each extrastimulation site.
The excitable gap was defined as the sum of the duration of the resetting zone and termination zone measured at each extrastimulation site.
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Results |
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The baseline electrophysiological data of those 16 patients are summarized in Table 1
. The mean tachycardia cycle length
was 353±52 ms. In all but 3 patients, induction of slow-fast AVNRT was
associated with typical anterograde dual AV nodal pathway conduction
curves during atrial extrastimulation. In the 3 patients without
typical anterograde dual AV node pathway conduction curves, slow-fast
AVNRT could be induced either by double atrial extrastimuli or by rapid
high right atrial pacing.
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Excitable Gap of AVNRT
As shown in Table 2,
the excitable gap of AVNRT
(the sum of the zone of resetting and zone of termination) was also
calculated as percentage of the tachycardia cycle length from different
pacing sites. The excitable gap could be exposed in all 16 patients
when extrastimuli were delivered from the slow pathway area, fast
pathway area, and proximal coronary sinus. In contrast, the excitable
gap could be demonstrated in only 6 and 5 patients when single
extrastimuli were delivered from the right ventricular apex and high
right atrium, respectively. The mean duration of the excitable gap was
121±56, 123±47, 91±50, 16±28, and 12±19 ms,
which occupied
33±11%, 34±9%, 24±11%, 4±6%, and 3±5% of
the
tachycardia cycle length, when single extrastimuli were delivered from
the slow pathway area, fast pathway area, proximal coronary sinus,
right ventricular apex, and high right atrium, respectively. Of note,
the excitable gap exposed by single extrastimuli from the right
ventricular apex and high right atrium was seen only in patients whose
tachycardia had a relatively long cycle length (>360 ms). There was no
difference in the resetting and termination behavior between patients
with and those without typical anterograde dual AV nodal pathway
conduction curves.
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Responses to Single Extrastimulation From the Slow Pathway and Fast
Pathway Areas
When single extrastimuli were delivered from these two
areas, the
extrastimuli could reset the tachycardia almost at the moment when they
began to depolarize the intervening atrial tissue (Fig 1A).
This phenomenon accounted for the observed wide
excitable gap.
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During the resetting of AVNRT from the slow pathway
area,
characteristically there was a 10- to 60-ms (mean, 28±14 ms) duration
during which single extrastimuli were capable of prematurely
depolarizing the atrial tissue in the posteroinferior interatrial
septum and the proximal coronary sinus while leaving the atrial tissue
in the His bundle region and the high right atrium depolarized by the
preceding impulse of the reentrant tachycardia. As shown in Fig
1B
, in
a patient with a tachycardia cycle length of 410 ms, a single
extrastimulus was delivered from the slow pathway area with a premature
coupling interval of 380 ms. The premature beat reset the AVNRT as it
shortened the following HH' interval from 410 to 380 ms. The AA'
interval of the recording sites from the slow pathway area and the
proximal coronary sinus was 380 ms, whereas that from the high right
atrium and the His bundle area remained unchanged at the tachycardia
cycle length of 410 ms. This finding indicated that the extrastimulus
from the slow pathway area prematurely depolarized the local atrial
tissue on the posteroinferior interatrial septum and reset the
reentrant circuit of the tachycardia, whereas the atrial tissue of the
anterosuperior interatrial septum and high right atrium was still
excited by the preceding tachycardia impulse conducting from the
retrograde fast pathway.
Commonly, resetting of AVNRT was characterized
by a change in the HH
interval of the tachycardia beat following atrial extrastimulation.
However, an uncommon resetting pattern could occasionally be observed
when single extrastimuli were delivered from the slow pathway area or
fast pathway area. An atrial extrastimulus not only reset the
tachycardia by changing the subsequent HH interval but also shortened
the preceding HH interval of the tachycardia beat. This unusual
phenomenon was observed in 2 of the 16 patients, as shown in Figs
2 and 3. In 1 patient (patient 16) with a
tachycardia cycle length of 450 ms, a single extrastimulus from the
slow pathway area with a premature coupling interval of 280 ms reset
the reentrant tachycardia by shortening the subsequent HH' interval
from 450 to 420 ms (Fig 2A). When the premature coupling
interval was
shortened by 10 ms (to 270 ms), the extrastimulus not only reset the
subsequent tachycardia impulse by shortening the H'H'' interval
from 450
to 430 ms but also affected the preceding tachycardia beat by
shortening of the HH' interval from 450 to 440 ms (Fig
2B). As the
premature coupling interval of the extrastimulus was shortened to 210
ms, the unusual resetting phenomenon described above remained
discernible (Fig 2C). In another patient (patient 12) with a
tachycardia cycle length of 420 ms, a single extrastimulus was
delivered from the fast pathway area (Fig 3A) and the slow
pathway area
(Fig 3B), respectively, with a premature coupling interval of
240 ms.
Both extrastimuli could encroach on the preceding as well as the
subsequent HH intervals of the tachycardia.
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Responses to Single Extrastimulation From the Proximal Coronary
Sinus
The excitable gap could be demonstrated in all 16 patients when
single extrastimuli were delivered from the proximal coronary sinus
(Table 2). In late diastole, extrastimuli capable of resetting
the
tachycardia could prematurely depolarize the local atrial tissue of the
proximal coronary sinus and the posteroinferior interatrial septum
(slow pathway area) while the atrial tissue of the anterosuperior
interatrial septum (fast pathway area) and high right atrium was still
excited by the preceding tachycardia impulse. The electrophysiological
manifestations of the excitable gap were very similar to those observed
when single extrastimuli were delivered from the slow pathway area.
Nevertheless, the zone of ineffectual impulse was wider (26±22 versus
1.0±3.5 ms) and, consequently, the width of the excitable gap
was narrower (91±50 versus 121±56 ms) compared with
extrastimulation from the slow pathway area. Furthermore, the unusual
resetting phenomenon in which extrastimulation affected both the
preceding and subsequent HH intervals of the tachycardia was not
observed.
Responses to Single Extrastimulation From the Right Ventricular
Apex and High Right Atrium
The excitable gap could be exposed by
single extrastimuli from the
right ventricular apex and high right atrium in only 6 and 5 patients,
respectively. When single extrastimuli were delivered from the right
ventricular apex, the zone of resetting lasted 10 to 60 ms (mean,
32±18 ms) in 6 patients, whereas the zone of termination lasted 10 to
30 ms (mean, 18±10 ms) in 4 patients. When single extrastimuli were
delivered from the high right atrium, the zone of resetting lasted 10
to 50 ms (mean, 33±17 ms) in 4 patients, whereas the zone of
termination was present in only 1 patient and lasted 30 ms. Of
note, resetting and termination of AVNRT resulting from
extrastimulation from these two pacing sites (distant from the
reentrant circuit) could be observed only in AVNRT with a cycle length
>360 ms (Table 2).
Patterns of Tachycardia Resetting in Response to Single
Extrastimulation
When single extrastimuli were delivered from the slow
pathway
area, fast pathway area, and proximal coronary sinus, the zone of
resetting was widely accessible. Three patterns of tachycardia
resetting were observed. Most commonly, the sum of the coupling
interval and the return cycle was less than a fully compensatory pause
(two times the basic tachycardia cycle length) (Fig 4A).
Less commonly, it was equal to or greater than a fully compensatory
pause (Fig 4B and 4C). Regardless of the pacing
site, the resetting
pattern could change from being less than to greater than a fully
compensatory pause as the premature coupling interval of
extrastimulation was progressively shortened. The resetting pattern was
determined primarily by the length of the return cycle, which was
affected by the extrastimulation-induced conduction delay in the
anterograde slow pathway.
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To investigate the return cycle dynamics with
increasing degrees of
prematurity, we plotted the coupling interval of the extrastimulus
during resetting against the return cycle. One example is shown in Fig
5. Regardless of the pacing site, an "increasing"
pattern was always observed during the resetting of AVNRT.
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Modes of Tachycardia Termination in Response to Single
Extrastimulation
When single extrastimuli were delivered from the slow
pathway
area, fast pathway area, and proximal coronary sinus, AVNRT could be
terminated in 7 of 16, 7 of 16, and 6 of 16 patients with a mean
duration of the termination zone of 33±29, 32±30, and
43±33
ms, respectively. The atrial extrastimuli always induced orthodromic
impulse conduction block in the anterograde slow pathway, whereas the
antidromic impulse collided with the preceding tachycardia beat in the
fast pathway (Fig 6). The inner border of the
termination zone was limited by the refractory period of the
intervening tissue of the pacing site. With regard to the
electrophysiological mechanism of termination, there was no difference
whether atrial extrastimuli were delivered from the slow or from the
fast pathway area.
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When single extrastimuli were delivered from the
right ventricular
apex, the tachycardia could be terminated in only 4 of 16 patients,
with a mean duration of the termination zone of 18±10 ms. Two modes of
tachycardia termination were observed. Premature ventricular beat could
terminate AVNRT by inducing orthodromic impulse conduction block either
in the anterograde slow pathway after premature atrial depolarization
through the retrograde fast pathway (Fig 7A) or in the
retrograde fast pathway without premature atrial depolarization (Fig
7B).
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When single extrastimuli were delivered from the high right atrium, the tachycardia could be terminated in only 1 of 16 patients with orthodromic impulse conduction block in the anterograde slow pathway.
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Discussion |
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TopAbstractIntroductionMethods Results Discussion References |
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Moe et al26 first demonstrated the presence of a dual AV transmission system in animal hearts and suggested a possible mechanism for an arrhythmia involving this dual AV transmission system. Since then, a large body of literature concerning AVNRT has accumulated.27 28 29 30 However, the anatomic substrate and the electrophysiological mechanism of AVNRT in humans remain to be determined.31 32 In this study, we delivered single extrastimuli from the high right atrium, right ventricular apex, proximal coronary sinus, the fast pathway area (anterosuperior interatrial septum near the His bundle), and the slow pathway area (posteroinferior interatrial septum near the coronary sinus orifice)23 during the sustained slow-fast form of AVNRT. The results showed that single extrastimulation from either the fast or slow pathway area close to the putative AVNRT circuit could widely expose the excitable gap of AVNRT. The electrophysiological characteristics of the excitable gap so exposed were very similar to those of AV reciprocating tachycardia involving an accessory connection.15 16 These findings provide further support for a reentrant mechanism in AVNRT in humans.
Factors Affecting Exposure of the Excitable Gap in AVNRT
In a
reentrant tachycardia, the closer the pacing site to the
reentrant circuit, the easier it is to expose the excitable
gap.33 Since the putative reentrant circuit of AVNRT is
confined to the AV junctional region, the duration of the excitable gap
of AVNRT as disclosed by single extrastimulation from the high right
atrium and right ventricular apex is expected to be relatively short.
Our findings are in agreement with those of previous
studies.18 19 In the present study, however,
extrastimulation was further delivered from the fast and slow pathway
areas in the AV junction. The excitable gap of AVNRT, so exposed, was
wide, and it occupied 33% to 34% of the tachycardia cycle length. The
excitable gap started just about when the extrastimulus was able to
depolarize the intervening tissue as represented by the
zone of resetting (Fig 1A). The zone of resetting was followed
either
by the zones of termination and refractoriness or directly by the zone
of refractoriness alone. The excitable gap could thus be estimated by
the difference between the AVNRT cycle length and the intervening
tissue refractoriness. We realize that the true excitable gap may be
even wider than we measured because of the limitation of the
intervening tissue refractoriness. Therefore, delivery of double
extrastimuli may further extend the width of the excitable gap by
losing the time interval required for the impulse to travel from
the tachycardia circuit to the site of stimulation and by shortening
the local tissue refractoriness of the pacing site.
The extent of the excitable gap is related not only to the site of stimulation but also to the tachycardia cycle length. The shorter the tachycardia cycle length, the narrower the width of the excitable gap in the reentrant circuit.5 13 34 However, the present study showed that regardless of the tachycardia cycle length, the excitable gap of AVNRT could be broadly displayed until tissue refractoriness when pacing was from either the fast or the slow pathway area.
Patterns of Tachycardia Resetting in AVNRT
When a slow-fast
form of AVNRT is reset, the impulse of the
extrastimulus antidromically collides with the preceding tachycardia
beat and orthodromically propagates through the anterograde slow AV
nodal pathway (when pacing was from the interatrial septum or proximal
coronary sinus) or the retrograde fast pathway (when pacing was from
the right ventricular apex) for maintaining the same direction of
reentry.16 17 18 19 35
When an extrastimulus was delivered from the posteroinferior
interatrial septum during late diastole, once the extrastimulus began
to depolarize the intervening tissue, it started to reset AVNRT. The
premature impulse orthodromically propagated through the anterograde
slow pathway, resulting in alteration of the subsequent HH' interval,
whereas it antidromically collided with the preceding tachycardia beat
coming from the retrograde fast pathway in the atrial tissue
beyond the fast pathway exit site. As the coupling interval of
the premature beat shortened, it continued to reset the tachycardia
while antidromically colliding with the preceding tachycardia beat
within the fast pathway rather than the atrial tissue (Fig 1).
When an
extrastimulus was delivered from the proximal coronary sinus, the
resetting behavior was similar to that when extrastimulation was from
the posteroinferior interatrial septum. The premature impulse
antidromically collided with the preceding tachycardia beat in the
atrial tissue beyond the fast pathway exit site in late diastole. As
the coupling interval of the premature beat progressively shortened,
antidromic impulse collision then occurred within the fast pathway.
When an extrastimulus was delivered from the anterosuperior interatrial
septum near the retrograde fast pathway exit site, the extrastimulus
also started to reset AVNRT at the moment when it began to depolarize
the intervening tissue. However, the premature beat depolarized all the
atrial tissue of the four representative intracardiac recording
sites, because it antidromically collided with the preceding
tachycardia beat within the fast pathway instead of the atrial tissue
during the early zone of tachycardia resetting.36 This
finding suggests that part of the atrial tissue near the anterosuperior
interatrial septum may be involved in the reentry circuit and may
constitute a part of the upper turnaround tissue of
AVNRT.37 38
During the excitable gap of AVNRT, no matter how premature the extrastimuli were, the premature beats usually affected only the subsequent HH' interval but not the preceding HH interval. This finding suggests that the atrial premature beats do not interfere with the impulse propagation of the preceding tachycardia beat conducting from the anterograde slow pathway to the lower turnaround tissue (distal common pathway) before reaching the His bundle. Hence, the site of antidromic impulse collision should be located within the reentry circuit where the tachycardia beat has already conducted thoroughly across the anterograde slow pathway and has entered the retrograde fast pathway. When the premature coupling interval is very short, the time required for the tachycardia impulse conducting through the anterograde slow pathway and turning around into the retrograde fast pathway should be brief enough for the impulse collision to consistently take place in the retrograde fast pathway. This finding suggests that the lower turnaround tissue (distal common pathway) may be located within the AV node proper (the compact node). Alteration of the subsequent HH' interval indicates that the atrial premature beat orthodromically conducts through the anterograde slow pathway, which is still in a partially recovered state produced by the preceding tachycardia impulse (manifesting as prolongation of the AH interval corresponding to atrial extrastimulation).
It was of interest to
observe a previously undescribed resetting
phenomenon in which critically timed single extrastimuli delivered from
the interatrial septum reset AVNRT and affected not only the subsequent
HH interval but also the preceding HH intervals in two patients (Figs
2 and 3). The atrial premature beat conducted
orthodromically through the
anterograde slow pathway, thereby affecting the subsequent HH interval.
However, shortening of the preceding HH interval could be accounted for
by three possible different routes for the transmission of the
antidromic impulse of the atrial premature beat. First, the antidromic
impulse could conduct through the anterograde fast pathway to collide
with the previous tachycardia impulse from the anterograde slow pathway
at the lower turnaround tissue (distal common pathway). The impulse
collision at the lower turnaround tissue produced an effect of impulse
summation39 40 that consequently shortened the
preceding
HH interval [Fig 2B(b)]. Second, the antidromic
impulse not only
prematurely depolarized the whole anterograde fast pathway but also
passed the lower turnaround tissue to activate the His bundle and
simultaneously to collide with the previous tachycardia wave front from
the anterograde slow pathway within the slow pathway. Activation of the
His bundle by the antidromic impulse from the anterograde fast pathway
resulted in shortening of the preceding HH interval. Third, the
antidromic impulse conducted through an additional AV nodal
pathway41 42 with a relatively short AH interval,
thereby
reducing the preceding HH interval [Fig 2C(c)]. The
third mechanism
is in accordance with the propensity for multiple inputs (pathways)
demonstrated in the rabbit AV node.43 This rare resetting
phenomenon implies that there may be more than two anterograde inputs
(pathways) for the impulse propagation through the AV node in
humans.
When single extrastimuli are delivered from the right ventricular apex, the resetting ventricular premature beat always antidromically collides with the preceding tachycardia beat at the anterograde slow pathway and orthodromically is conducted through the retrograde fast pathway to reset the tachycardia.
In this study, the curve of the return cycle against the premature coupling interval of the extrastimuli showed an "increasing" response pattern. Previous studies have suggested that an increasing pattern of resetting is more compatible with a reentrant mechanism compared with either a "decreasing" or "flat" resetting pattern.44 45 An increasing resetting pattern of AVNRT suggests that the resetting premature impulse encounters a partially recovered tissue in part of the circuit, mainly at the anterograde slow pathway, which results in progressive conduction delay as the premature coupling interval shortens.45
Modes of Tachycardia Termination
In this study, we have
demonstrated that the site of orthodromic
conduction block of the extrastimuli during AVNRT was usually in the
anterograde slow pathway. Uncommonly, the site of orthodromic
conduction block was located in the retrograde fast pathway when single
extrastimuli were delivered from the right ventricular apex. Thus,
refractoriness of the anterograde slow pathway is the major determinant
of tachycardia termination during single extrastimulation—the
weak link of AVNRT. This finding is in keeping with the clinical
experience that antiarrhythmic drugs with depressive effects on AV
nodal slow pathway conduction are efficacious for acute termination of
AVNRT.46 Since the site of orthodromic conduction block
can occur in the retrograde fast pathway, classes Ia and Ic agents are
also able to terminate AVNRT by creating conduction block in the
retrograde fast pathway.47 48
Electrophysiological Implications
Judging from observations
made in the present study, there
seem to be no significant differences in the mode of termination of the
slow-fast AVNRT when single extrastimulation is delivered from either
the slow or fast pathway area. Therefore, the mode of termination by
extrastimulation cannot be used as a reliable guide for selective
ablation of slow pathway conduction.49 Nevertheless, the
rather wide excitable gap as exposed by such an extrastimulation
technique from either the slow or fast pathway area close to the
putative reentrant circuit may be used as a means for assessing effects
of antiarrhythmic drugs on AVNRT.
The complexity of the anatomic structure and functional properties of the AV junction is well appreciated.50 The present study has demonstrated that electrophysiological manifestations of the excitable gap of slow-fast AVNRT are similar to those of AV reciprocating tachycardia involving an accessory connection.16 Thus, reentry with a microreentrant circuit is the most likely underlying mechanism for AVNRT. However, whether reentry is anatomic or functional or a combination of both remains debatable. Specifically, it has been demonstrated that the AV junction does possess anisotropic conduction properties, particularly in the slow pathway area.51 The direction in which an atrial impulse approaches the AV margin may have an influence on the conduction of the impulse in the AV node.52 The presence of anisotropy may predispose to functional reentry associated with dual pathway conduction.53 54 Furthermore, the phenomenon of resetting and termination in response to electrical stimulation can also be demonstrated in a functional reentrant circuit.55 Further studies with more detailed mapping techniques are needed to elucidate the exact reentrant mechanism of AVNRT.
Received November 21, 1994; accepted December 20, 1994.
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