(Circulation. 1999;99:143-155.)
© 1999 American Heart Association, Inc.
Basic Science Reports |
Longitudinal Dissociation Within the Posterior AV Nodal Input of the Rabbit
A Substrate for AV Nodal Reentry
From the Department of Medicine, College of Medicine, University of Oklahoma Health Sciences Center (B.J.S., E.P.) and Department of Veterans Affairs Medical Center (B.J.S., E.P.), Oklahoma City, Okla.
Correspondence to Eugene Patterson, PhD, Research Service 151-F, DVA Medical Center, 921 NE 13th St, Oklahoma City, OK 73104. E-mail eugene-patterson{at}uokhsc.edu
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Abstract |
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Background—Longitudinal dissociation of an anatomic pathway into 2 electrophysiologically distinct pathways has been hypothesized as a basis for localized AV nodal reentry and supraventricular arrhythmias.
Methods and Results—Extracellular bipolar and intracellular
microelectrodes were used to record activation in the superfused
rabbit AV junction. A subset of rabbit hearts (n=19 of 72) demonstrated
dissociation of the posterior AV nodal input into 
2 functional
pathways. Antegrade AH conduction was maintained by a pathway just
inferior to the tendon of Todaro. Rate-dependent conduction
block was observed in a second pathway just superior to the tricuspid
annulus, allowing retrograde activation of the distal portion of the
inferior posterior AV nodal input and leading to the
formation of apparent "dead-end" pathways. The superior (antegrade)
and inferior (retrograde) pathways were separated by a band
of well-polarized but poorly excitable transitional cells. Additional
decreases in the atrial cycle length progressively increased the AH
interval, further delaying retrograde activation of the
inferior pathway, and progressively moved the site of
conduction block in the inferior pathway proximally, thus
extending the length of the retrograde conduction pathway and allowing
circus movement within the transitional cells of the posterior AV nodal
connection.
Conclusions—Longitudinal dissociation within the posterior AV nodal input can give rise to localized reentry and AV nodal reentrant tachycardia.
Key Words: atrioventricular node • arrhythmia • tachycardia, atrioventricular nodal reentry • action potentials
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Introduction |
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Atrioventricular nodal reentrant tachycardias (AVNRTs) are a common cause of supraventricular arrhythmia. Electrode catheter recordings and atrial pacing demonstrate dual AV conduction pathways in a majority of patients with this arrhythmia.1 2 The cellular electrophysiology, tissue composition, and anatomic location of the dual AV pathways are less certain.
Early evidence for a dual AV transmission system as a basis for reentrant arrhythmia was provided by Moe et al3 in the canine heart and by Mendez and Moe4 in the superfused rabbit AV junction. Both experiments demonstrated 2 functional pathways communicating with a final common pathway above the HB. The presumed site of longitudinal dissociation and reentrant atrial echo beats was the upper AV node. Further experiments using the superfused rabbit AV junction have demonstrated echo beats and even sustained supraventricular arrhythmia within the posterior-inferior right atrium, with the reentrant pathway contained either within or partially outside of Koch's triangle.5 6 7 8 Little information concerning the anatomic site and functional basis for echo beats and sustained supraventricular arrhythmia has been provided, a result of a complicated 3-dimensional anatomy and the absence of an accepted definition for the dimensions and location of the AV node. Both the mechanism and the site for AVNRT in humans have been presumed to be intra-AV nodal for 20 to 30 years, with a paucity of clinical data supporting this hypothesis.9 10 11
Clinical concepts of the basis for AVNRTs have recently been rent asunder by electrode catheter recordings from the posterior-inferior right atrium and localized radiofrequency lesioning.9 10 11 Consistent electrograms can be obtained from tissues remote from the compact AV node, demonstrating decremental conduction and/or block in association with AVNRT. Radiofrequency lesions at critical extranodal sites eradicate 1 excitation pathway without abolishing AV transmission. Atrial extrastimuli no longer initiate sustained AVNRT, and the clinical AVNRT is eliminated.
During the course of study of AV transmission in 72 superfused rabbit AV preparations, 19 preparations demonstrated longitudinal dissociation within transitional cells comprising the posterior input of the compact AV node, commonly termed the slow pathway. Rate-dependent longitudinal dissociation within posterior transitional cells comprising input to the compact AV node was the basis for antegrade and retrograde activation pathways leading to apparent "dead-end" pathways. With additional rate-dependent delays, however, localized reentry in these dissociated pathways resulted in single echo beats and supraventricular tachycardia.
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Methods |
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Adult rabbits of both sexes weighing 2.5 to 4 kg were anesthetized with intravenous sodium pentobarbital (30 to 40 mg/kg). The heart was removed and rinsed in modified Tyrode's solution (in mmol/L: NaCl 130, KCl 4.05, MgCl2 1.0, NaHCO3 20, NaH2PO4 1.0, glucose 5.5, and CaCl2 1.35) bubbled with 0.95 O2/0.05 CO2 at 36°C to 37°C. The AV junction (containing the entire right atrium and interatrial septum and the base of the posterior right ventricle and interventricular septum) was exposed (Hoffman et al12). The tissue was pinned to a 20-mL Lucite chamber and superfused at 20 mL/min with modified Tyrode's solution. Bipolar electrode recordings (0.10-mm-diameter Teflon-coated silver wires, 1 mm apart) were obtained from the following locations: (1) inferior to the tendon of Todaro and superior to the tricuspid annulus midway between the coronary sinus os and apex of the triangle of Koch (posterior input to the compact AV node), commonly termed the slow pathway [SP]); (2) halfway between the fossa ovalis and the apex of the triangle of Koch along the anterior limbus of the fossa ovalis (anterior input to the compact AV node), commonly termed the fast pathway [FP]); and (3) from the HB anterior to the central fibrous body. Pacing was performed from the high right atrium, the base of the crista terminalis, or the HB with 2-ms-duration square wave pulses at 1 to 3 times middiastolic threshold voltage.
Bipolar electrograms were individually amplified and filtered at 1 to
5000 Hz. Intracellular recordings were obtained with
conventional 10- to 25-M
resistance glass microelectrodes filled
with 3 mol/L KCl and a World Precision Instruments model 773
electrometer. A custom-made differentiator with linear peak-and-hold
capability over a range of 10 to 800 V/s was used to determine
dV/dtmax. Permanent records of intracellular
and extracellular recordings were obtained with a Gould
Windograf recorder. Electrophysiological
measurements were determined from recordings taken at a paper
speed of 100 mm/s. Individual microelectrode recordings
were obtained during incremental atrial pacing. Composite illustrations
were reconstructed from identical pacing protocols producing identical
bipolar electrogram activation patterns in 19 rabbit preparations that
demonstrated longitudinal dissociation and in 10 normal rabbit AV
preparations.
Statistics
Data are expressed as mean±SEM. Differences within groups were
determined by an ANOVA followed by Scheffé's test. Differences
between normal and dissociated posterior AV nodal input properties were
determined by Student's t test for unpaired data. The
criterion for significance was P
0.05.
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Results |
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Rate-dependent longitudinal dissociation within the posterior AV nodal input was observed in 19 of 72 consecutive rabbit hearts. Dead-end pathways13 14 15 (transitional cells contained within Koch's triangle having summed antegrade and retrograde conduction times >120% of the AH conduction time) were observed in 3 preparations at a spontaneous cycle length of 497±23 ms. These dead-end pathways provided the substrate for echo beats and nonsustained AVNRT when subjected to rapid atrial pacing.
SP Gradient Between the Tendon of Todaro and the Tricuspid
Annulus
The region between the tendon of Todaro (SP-1) to the tricuspid
annulus (SP-5) was arbitrarily divided into 5 evenly spaced bands.
Intracellular potentials were recorded from each tissue band during
incremental high right atrial pacing. At paced cycle lengths >600 ms,
uniform activation from the tendon of Todaro to the valve annulus (SP-1
to SP-5) was observed. At shorter cycle lengths, 2 different conduction
patterns were apparent: (1) a uniform Wenckebach cycle length for
transitional cells of the posterior AV nodal input (Figure 1
) (normal SP) and (2) dissociation of
the SP into 2 or more pathways with different Wenckebach cycle lengths
(Figure 2) (dissociated SPs). In each
experiment, only 1 of the pathways maintained HB activation: the
superior pathway just inferior to the tendon of Todaro
(n=17) or the inferior pathway immediately superior to the
tricuspid annulus (n=2). Pacing from the base of the crista terminalis
did not alter dissociation within the posterior AV nodal input versus
high right atrial pacing.
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The AH Wenckebach cycle length did not differ in rabbit hearts with normal (205±8 ms; n=10) and dissociated (207±11 ms; n=19) posterior AV nodal inputs. In addition, the cycle length that produced 2:1 block within transitional cells of the anterior AV nodal input (FP) was not different for hearts with normal (132±3 ms; n=10) and dissociated (134±8 ms; n=19) posterior AV nodal inputs.
In the normal posterior AV nodal input, a gradient of decreasing
resting potential, action-potential amplitude, and
dV/dtmax was present from the tendon of
Todaro (SP-1) to the tricuspid annulus (SP-5)
(Table). A different pattern was
observed with longitudinal dissociation (Table). A decrease in resting
potential, action-potential amplitude, and
dV/dtmax was observed from SP-1 to SP-3. Cells
near the valve annulus were hyperpolarized, with an increasing gradient
of action-potential amplitude and dV/dtmax
observed from SP-3 to SP-5 (Table). An inexcitable tissue band (SP-3 or
SP-4) was present when longitudinal dissociation produced dual
pathways with different Wenckebach cycle lengths (superior to
SP-3=227±16 ms versus inferior to SP-3=327±23 ms;
P=0.00001).
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Dissociated Posterior AV Nodal Inputs at Slow Heart Rates
Two distinct deflections in the local bipolar electrogram
were observed in 9 of 19 preparations and correlated temporally with
intracellular recordings from the 2 pathways. An example is
shown in Figures 3 and 4. Microelectrode and extracellular
recordings are shown at paced cycle lengths of 450 and 167 ms
for sites SP-2, SP-3, SP-5 proximal (P), SP-5 mid (M), SP-5 distal (D),
midposterior AV nodal input (BP-SP), HB (BP-HB), and anterior AV nodal
input (BP-FP) (Figure 3). The locations of the recording and
stimulation sites are also shown. At a cycle length of 450 ms (Figure 3A), the posterior AV nodal input near the valve annulus was
activated retrogradely after HB activation and is reflected as
a deflection in the local electrogram. With a decrease in the paced
cycle length to 167 ms (Figure 3B), the site of block moved posteriorly
along the valve annulus to site SP-5M. SP-3 demonstrated only
electrotonic interactions with the 2 SPs. An additional decrease in the
cycle length to 150 ms (Figure 4A) produced 5:4 Wenckebach in SP-2,
mediating 5:4 AH conduction. Progressive conduction block (beats 1, 2,
3, and 4) and then a reentrant beat were observed at SP-5P (beat 5).
With a further decrease in the cycle length to 134 ms (Figure 4B), 3:2
Wenckebach block at SP-2 mediated 3:2 AV conduction. Retrograde
activation of SP-5, SP-5M, and SP-5P is not observed in Figure 4B
because AH conduction block prevented retrograde reexcitation of the
inferior pathway.
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Activation of Apparent Dead-End Pathways
Post-Hisian activation of cells near the tricuspid annulus (SP-5)
was recorded during sinus rhythm (n=3) and high right atrial pacing
at cycle lengths 300 ms (n=5). The location of the cells along the
valve annulus posterior to the central fibrous body is
consistent with type B dead-end
pathways.13 Extracellular potentials were
observed coincident with intracellular dead-end recordings
(n=2).
In Figure 5, dead-end pathway cell
activation correlated with an extracellular potential recorded in
the HB electrogram. At cycle lengths 275 ms, the intracellular (SP-5)
and extracellular potentials occurred before AV nodal and HB
activation. An abrupt change from pre-Hisian/pre-AV nodal activation to
post-Hisian/post-AV nodal activation occurred at a cycle length of 250
to 275 ms (Figure 5). Conduction block 2:1 of the dead-end action
potential occurred at a longer cycle length (200 ms) than that which
was necessary to produce 2:1 A-H conduction block (155 ms) (Figure 5).
When a 1- to 2-mm-long incision perpendicular to the posterior AV nodal
input was made immediately superior to the tricuspid annulus (3 to
4 mm posterior to the central fibrous body) (Figure 6, bottom), activation of the dead-end
pathway at cycle lengths >275 ms was observed only subsequent to HB
activation (Figure 6). In Figure 7, the
response of an apparent dead-end cell to premature stimuli is shown.
Before the inferior incision, activation occurred before HB
activation at a basic cycle length of 400 ms. Extrastimuli <275 ms
shifted dead-end cell activation. After the incision, activation
occurred only after AV nodal (Figure 6) and HB activation.
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Rate-Dependent Longitudinal Dissociation Within the Posterior AV
Nodal Input: A Basis for Localized Reentry
Rate-dependent longitudinal dissociation within the posterior AV
nodal input (Figure 2
) led to localized reentry incorporating the
compact AV node (n=9). Antegrade conduction to the compact AV node at
fast atrial pacing rates (n=8) was maintained by a pathway immediately
inferior to the tendon of Todaro. Rate-dependent block was
observed in a pathway located immediately superior to the tricuspid
annulus. With AH prolongation, retrograde activation was then observed
immediately superior to the valve annulus. The AH interval for the
antegrade limb was 117±14 ms, with an HA interval of 96±12 ms for the
retrograde limb (n=8). In only 1 example was antegrade AV nodal
activation maintained in the pathway adjacent to the tricuspid annulus
and rate-dependent block with retrograde activation observed in the
pathway adjacent to the tendon of Todaro. Rate-dependent block in the
superior pathway and antegrade conduction in the inferior
pathway produced reentrant beats with early activation of the anterior
AV nodal input (FP) (AH=123 ms, HA=15 ms; not shown).
An example of localized reentry incorporating dissociated posterior AV
nodal inputs and the compact AV node is shown in Figure 8. SP-2 served as the antegrade
conduction pathway. SP-4 and SP-5 served as the retrograde conduction
pathway. SP-3 (Figure 9) remained well
polarized but inexcitable except via intracellular stimulation.
Conduction through the posterior input remained associated during the
first 2 beats of the pacing sequence (Figure 8). The third beat of the
pacing sequence blocked between the distal site SP-4D and the more
proximal site SP-4P, and site SP-4D was then retrogradely
activated, after SP-4P and HB activation. With the sixth and
seventh beats of the pacing train, the site of block moved retrogradely
to SP-4P, as evidenced by dual activation of the cell by antegrade and
retrograde wave fronts. With the eighth beat, SP-4D activation preceded
SP-4P activation. Cessation of pacing after the ninth paced beat
produced a reentrant SP beat as seen in the action potential from SP-2
(but not in extracellular recordings). The delay necessary to
produce reentry with dissociated SPs resulted from a rate-dependent
slowing of conduction within the antegrade SP, slowing of conduction
within the compact AV node, and lengthening of the reentrant pathway by
posterior movement of the site of conduction block within the
retrograde activation pathway. Reactivation of the proximal superior
(antegrade) pathway by retrograde activation of the
inferior pathway occurred before activation of cells at the
base of the crista terminalis (n=5 of 5 preparations tested), which
suggests that the turnaround for the reentrant pathway occurred
anterior to the coronary sinus os.
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The response of the dissociated SP to premature beats is shown in
Figures 10 and 11. In Figure 10 (top), a premature
stimulus is introduced that splits the local posterior AV input
electrogram into 2 components, prolonging the AH interval and producing
a nonstimulated atrial beat. Multiple impalements along the tricuspid
annulus (inferior pathway) demonstrated a decrementing
retrograde impulse that reexcited the SP only and failed to reexcite
atrial tissue (Figure 11). Conduction block in the compact AV node (no
HB activation) prevented retrograde activation (Figure 10, bottom). A
2-mm transection across the inferior posterior AV nodal
input (immediately superior to the valve annulus) prevented echo beats
(n=8), nonsustained AVNRT (n=5), and sustained AVNRT (n=2) in 8 of 8 AV
preparations.
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Sustained AVNRT
An example of sustained AVNRT is shown in Figure 12. Intracellular recordings
are shown for 5 sites, in conjunction with bipolar recordings
from the anterior AV nodal input, posterior AV nodal input, and
HB. Double potentials representing antegrade and
retrograde conduction pathways are a common finding in microelectrode
recordings from the posterior AV nodal input during sustained
reentry. The smaller and slower upstroke represents the distant
wave front, with the rapid upstroke representing local
activation. A poorly excitable tissue band with 2 slow upstrokes
representing distant antegrade and retrograde activation
wave fronts is also present in Figure 12. The AH interval during
sustained tachycardia was 90 ms, and the HA interval was 87
ms. Activation times were measured relative to the atrial electrogram.
Conduction from SP-5P to SP-5D represents retrograde conduction
down the inferior pathway. The close timing of the
antegrade and retrograde wave fronts in the SP-2P and SP-5P
electrograms suggests that these sites are near the posterior
turnaround for the tachycardia, whereas the prolonged
separation of the SP and SP' electrograms of the bipolar
recording suggests a site nearer the center of the reentrant
loop. The activation times inferior to the coronary
sinus os (23 ms) and within the proximal antegrade pathway are similar,
which suggests that activation inferior to the sinus os is
a spur from the reentrant pathway.
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Discussion |
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Reentry in the AV Junction
Single reentrant beats, nonsustained AVNRT, and sustained AVNRT were observed in the superfused rabbit AV preparation. Localized reentry was dependent on the following: (1) longitudinal dissociation and the formation of 2 functional pathways within the posterior AV nodal input, (2) block within a refractory pathway and maintenance of AH conduction in a second pathway, (3) retrograde conduction in a long refractory period pathway, and (4) reexcitation of the proximal posterior AV nodal input. Conduction block terminating reentry was observed in the compact AV node, the retrograde conduction pathway, or the antegrade conduction pathway. A band of well-polarized but poorly excitable transitional cells (SP-3) was observed that separated the 2 dissociated pathways. The reentrant pathway appeared to be contained anterior to the coronary sinus os.
Sustained AVNRT (>30 seconds) was observed 8 times in 3 rabbit AV preparations. Sustained AVNRT could not be reproducibly initiated or terminated, which prevented a systematic study of AVNRT initiation. All 3 rabbit AV preparations that generated sustained AVNRT also demonstrated longitudinal dissociation within the posterior AV nodal input and single reentrant beats or nonsustained AVNRT.
Rate-dependent longitudinal dissociation has been a frequently
proposed mechanism for dual AV transmission and AVNRTs in the
rabbit,4 5 canine,3 and
human heart.1 2 Initial demonstrations of
longitudinal dissociation3 4 14 and
AVNRT5 6 in the rabbit were assumed to be limited
to the AV node. Each study, however, included AN (transitional) cells,
4 mm posterior to the compact AV node, as a part of the AV node.
A minimal mass of atrial myocardium was also suggested as a
necessary component for sustained AVNRT.6
Subsequent studies with superfused rabbit AV preparations by Watanabe
and Dreifus15 and Mazgalev and
coworkers7 8 recognized the role of perinodal
fibers in the formation of echo beats and sustained AVNRT. Mazgalev and
coworkers7 8 also described an obligatory role of
atrial myocardium superior to the coronary sinus os
and tendon of Todaro in AVNRT, stating "in this preparation, AVN
reentry circuits always appeared to involve atrial tissue surrounding
AVN ... Remarkably, reentry confined to the intranodal region
was never observed." The reentrant pathways
outlined8 9 contrast with the present studies
in which antegrade and retrograde conduction limbs remained
inferior to the tendon of Todaro and anterior to the
coronary sinus os. As evidenced in Figure 10, a single
reentrant echo beat could be observed within the posterior AV nodal
input, without right atrial activation. AVNRT, however, demonstrated
1:1 capture of the right atrium.
In the present studies, we distinguish between the compact AV node (knoten) described by Tawara16 and posterior transitional (AN) cells otherwise termed the open node14 or the posterior AV nodal input.17 Dissociation of the posterior AV nodal input providing retrograde and antegrade conduction pathways was observed within transitional (AN) cells. The compact AV node (N cells) was a necessary component of the reentrant circuit but did not need to demonstrate dual-pathway electrophysiology. The posterior AV nodal input was longitudinally divided by a band of well-polarized but poorly excitable transitional cells (SP-3). This is a salient finding because it provides a basis for the division of the posterior AV nodal input into 2 functional pathways. With an anterior or posterior extension to the line of block, the substrate within the posterior AV nodal input could produce early or late activation of the anterior AV nodal input and reproduce AVNRT termed slow/slow, fast/slow, or slow/fast. In subsequent experiments, we have observed 13 rabbit preparations that used the inferior pathway as an antegrade pathway, with rate-dependent block and retrograde conduction in the superior pathway, producing sustained AVNRT with early activation of the anterior AV nodal input (FP). Atrial myocardium was not necessary for single echo beats, although 1:1 atrial capture was observed for both nonsustained and sustained AVNRT. High right atrial stimuli failed to reset the tachycardia, although resetting was observed with stimuli introduced into the posterior AV nodal input (not shown).
Cellular Bases for Longitudinal Dissociation and Functional
Block
Conduction block in dissociated posterior AV nodal inputs occurs
at paced heart rates inconsistent with action-potential
duration in transitional (AN) cells of the posterior input.
Preferential block in the inferior pathway is not provided
by reductions in dV/dtmax or action-potential
amplitude or by prolongation of the action potential (Table) compared
with tissue adjacent to the tricuspid annulus in normal SPs. Instead,
in the inferior pathway, there is a more rapid loss of
source current (dV/dtmax and action-potential
amplitude) with incremental pacing. Rate-dependent dissociation of
cellular activation/uncoupling of cellular activation (as observed in
the HB after anterior septal coronary artery
ligation18) is capable of providing for both a
decrease in dV/dtmax at decreasing paced cycle
lengths and a progressive movement of the site of conduction block from
distal to proximal in the inferior pathway.
The type and extent of intercellular connections in transitional cells of the posterior AV nodal input are unknown. Only 25% of transitional cells in the posterior AV nodal input respond to a maximal 5-µA, 4-ms duration intracellular stimulus (unpublished experiments). dV/dtmax and action-potential amplitude for individual transitional cells in associated pathways is identical when stimulated longitudinal to fiber orientation (42±5 V/s, 74±4 mV) or transverse to fiber orientation (42±5 V/s, 74±4 mV) (unpublished observations).
The posterior input as described by Tawara16 consists of an anterior "knoten" and a posterior input comprising small cells running in small bundles separated by connective tissue and gradually merging with atrial myocardium.14 16 17 Racker19 describes a proximal AV nodal bundle, "small fascicles that ran parallel to the AV ring and are contiguous with the AV node," separate from atrial myocardium. The parallel bundles and physical separation of cells could lead to poor anatomic and physiological coupling of individual lateral muscle bundles and fascicles, potentiating dissociation parallel to fiber axis. The parallel fiber orientation in the posterior AV nodal input close to the tricuspid annulus has also been postulated as an AV nodal bypass tract20 and has been suggested as an anatomic basis for dead-end pathways.14
Dead-End Pathways
The present studies suggest that dead-end
pathways13 14 (transitional cells having summed
antegrade and retrograde conduction times >120% of AH conduction
time) share a functional
electrophysiological origin with
rate-dependent longitudinal dissociation and reentry. Dead-end pathways
may be present at very slow rates such that rate dependence remains
unrecognized. Each of the superfused rabbit AV preparations that
demonstrated dead-end pathways at spontaneous rates also demonstrated
reentrant echo beats (n=3) or nonsustained AVNRT (n=1) with high right
atrial pacing.
Clinical Implications
Three different forms of AVNRT can be demonstrated in humans:
slow/fast, fast/slow, and slow/slow. The location of the reentrant
pathway and the presence of multiple SPs described for slow/slow AVNRT
in humans21 are mimicked in the present
experiments that used the superfused rabbit AV preparation. Both the
antegrade (AH) and retrograde (HA) limbs of echo beats and nonsustained
AVNRT of the present experiments are prolonged. Dual SP
electrograms were present in a majority of the rabbit AV
preparations that demonstrated AVNRT. The failure to observe FP block
in association with the initiation of echo beats or nonsustained
tachycardia does not suggest a requirement for block in the
anterior input. We22 have observed examples of
sustained AVNRT consistent with fast/slow (n=4) and slow/fast
(n=11) AVNRTs in the same experimental preparation, using the same
reentrant circuit, with clockwise rather than counterclockwise
activation of 2 dissociated pathways within the posterior input. In 1
preparation, both slow/slow (counterclockwise) and slow/fast
(clockwise) AVNRTs could be observed, with a reversal of dissociated
antegrade and retrograde SPs for the 2 AVNRTs.
The reentrant pathways in the present experiments had a long axis of 1.0 to 1.2 cm and were contained within the posterior AV nodal input, anterior to the coronary sinus os. The reentrant circuits were consistent with sustained AVNRT previously described by Janse et al5 and Wit et al6 but clearly differed from Mazgalev et al7 and Iinuma et al.8 The larger (incorporating the coronary sinus os and lying superior to the tendon of Todaro) and slower (cycle lengths >250 ms) reentrant circuits described by Mazgalev et al7 and Iinuma et al8 appear to be more consistent with the clinical entity described as slow/slow AV nodal tachycardia despite the presence of both limbs of the reentrant pathway within the posterior AV input (SP and SP'), antegrade AV conduction down the physiological SP, and the absence of involvement of the anterior AV nodal input in initiating or sustaining AVNRT in the present experiments.
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Acknowledgments |
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This research study was supported by a grant from the American Heart Association, Oklahoma Affiliate, and research funds from the Department of Veterans Affairs. The authors would like to thank Dr Ralph Lazzara for his review of the manuscript and his helpful critique.
Received March 31, 1998; revision received August 19, 1998; accepted September 2, 1998.
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