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The mechanism of AV junctional reentryRole of the atrio-nodal junction.

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THE ANATOMICAL RECORD 201:179-188 (1981)
The Mechanism of AV Junctional Reentry: Role of the AtrioNodal Junction
Departments of Medicine and Physiology of the Jefferson Medical College of the Thomas
Jefferson University and the Lankenav-Hospital, Philadelphia, Pennsyfvania
Mapping of atrial-AV nodal (AVN)activation patterns was performed in 10 superfused rabbit AVN preparations utilizing 3 bipolar electrodes
placed simultaneously a t the crista terminalis (CT),interatrial septum (IAS) and
His bundle (H) regions in close proximity to the AVN, along with two or three
microelectrodes in the AN, N and NH regions of the AVN. Basic and premature
stimuli were introduced a t either or both the CT and IAS regions of the AVN.
The timing of the premature stimuli was varied to induce close interaction of
inputs to the AVN. Summation andlor cancellation, as evidenced by changes in
the morphology of the action potentials and alteration of Hl-HZ intervals, were
observed. Apparent reentry phenomena could be induced or terminated by appropriately timed stimulation a t the CT and IAS inputs. Reentry was critically
related to both the patterns and timing of the spread of excitation within AVN
and surrounding atrial tissue. Slow conduction and unidirectional block were
observed in various portions of the reentry circuit. It is concluded that 1) interaction between input waves engaging the AVN produced either summation or
fragmentation; 2 ) slow conduction and reentry resulted from a critical collision
of wavefronts; 3) in this preparation, AVN reentry circuits always appeared to
involve conduction through atrial tissue immediately surrounding AVN; and 4)
remarkably, reentry confined to the intranodal region was never observed.
Recently, the factors controlling impulse
transmission within the atrioventricular (AV)
junctional tissues have been extensively reviewed (Watanabe and Dreifus, '77). Delay in
conduction of the cardiac excitatory wave is
thought to occur predominantly within the N
region of the AV node, as originally suggested
by Paes de Carvalho and de Almeida ('60) and
others (Billette et al., '76).
Early evidence for a dual AV transmission
system was suggested by Mendez and Moe
('66). This concept was used to explain sudden,
marked alterations in AV conduction intervals, which were attributed to either anatomically or functionally independent AV nodal
pathways (Mendez and Moe, '66; Hoffman et
al., '63; Denes, '73; Ogawa and Dreifus, '77).
Alternatively, these observations were also
explained by different degrees of fragmentation and inhomogeneous conduction at several
levels within the AV node (Watanabe and
Dreifus, '65; Janse et al., '71).
Janse et al. ('71) presented experimental evidence that possible reentry circuits could occur
within the AV node, whereas Watanabe and
Dreifus ('65) demonstrated concealed reentry
within the AV node resulting from inhomogeneous conduction, particularly within the N
fibers. Later experimental work by Janse et al.
('76) and Zipes et al. ('73) indicated that AV
nodal transmission was also dependent on the
pattern of AV nodal input. For example, although the crista terminalis (CT)was the dominant nodal input, AV nodal activation
changed when the interatrial septum was
stimulated. These authors concluded that the
site of the atrial pacemaker could be a decisive
factor in AV nodal transmission. It became
clear that, using the concept of a dual AV nodal
input, the presence of unidirectional block in
one of the inputs could predispose to a reentry
movement as the wavefront from the other input invaded the blocked route retrogradely and
engendered a circus movement.
The present studies confirm the importance
of a dual input into the AV node and the imReceived January 26, 1981; accepted April 30, 1981
Address reprint requests to Dr. Leonard M. Dreifus. Lankenau
Hospital, Lancaster and City Line, Philadelphia, PA 19151.
portance of the perinodal fibers of the atrium,
which surround the AV node and could participate in AV junctional reentry mechanisms.
We studied in vitro preparations from the
hearts of 10 young adult New Zealand white
rabbits (weight 2.5-3.5 kg), and successful experiments were completed in 6 preparations.
Figures 1-5 are representative of the electrophysiological responses resulting from the various interventions.
The preparution
Each rabbit was anesthetized with sodium
pentobarbital (30 mglkg, intravenously) and
heparinized (1,000 units, intravenously). The
chest was opened by a midsternal incision, and
the heart was rapidly excised. After quick removal of apical tissue to ensure more thorough
superfusion of the ventricular cavities, the
heart was placed in a room temperature modified Tyrode's solution of the following composition (concentrations are in units of mM1
liter: NaCL 128.2; KC1 4.7; CaC1, 1.3; MgCl,
1.05; NaHCO, 20.1; NaHPO, 4.7; and glucose
11.1).The solution was constantly gassed with
a mixture of 95% 02/5% C02.
After the tissue was fixed to a paraffin block,
a probe was passed through the apical end of
the right ventricle (RV), through the tricuspid
valve (TCV), into the right atrium (RA) and
out through the superior vena cava (SVC).
Using the probe as a guide, the right heart was
opened by an incision through the RV and RA
margin to the interatrial septum (IAS), to expose the endocardia1 surface. Following resection of the RV, LV and LA, the preparation
consisting of the right atrial appendage, sinus
node (SN) and atrioventricular node (AVN)
was fixed to the bottom of a tissue bath (volume
45 ml) and superfused with a constantly oxygenated solution at a rate of 10 mllmin. A temperature of 37 '.1" C was maintained by means
of a Hakke circulating water bath with thermostat.
Electrical recordings
Surface electrograms were obtained from
Teflon-insulated silver bipolar electrodes
placed in the CT, the interatrial septum (IAS)
and the bundle of His (H). Bipolar stimulating
electrodes were placed at SN, CT and IAS.
Rectangular pulses twice diastolic threshold
and 1 msec in duration were delivered by a
programmable digital stimulator (Bloom As-
sociates, Narberth, PA). Tissue response was
amplified by using either a differential amplifier (Bloom Associates) or a Hewlett-Packard
bioelectric amplifier (model 8811A) prior to
being displayed on a Tektronix memory oscilloscope (model D15).
Standard glass microelectrodes (1.0 mm outside diameter) were filled with 3.0 m KCl and
were used to monitor cellular responses within
the preparations. Tissue and cellular responses
were recorded on Kodak Ortho paper at a paper
speed of 500 m d s e c using either a Grass Kymographic camera or a Polaroid camera after
being displayed on the oscilloscope screen.
The stimulating and recording electrodes
were placed close to the CT and IAS input regions to the AV node and arranged in a manner
that would record both spontaneous and electrically induced impulses a t their respective
input regions. The recording electrodes were
always placed most proximal at each input region (Figs. 1-5).
Simultaneous transmembrane potentials
were recorded from 3 microelectrodes in each
preparation. At least one microelectrode was
used as a reference, and the others were moved
to the various areas of the AN, N and NH regions to map the course of impulse transmission through the AV node. Microelectrodes
were mounted on micromanipulators (Stoelting-Prior) for precise impalements into the
various regions of the AV node. Several coordinates drawn from the superior-anterior and
right and left portions of the AV node were
noted to localize the area of recording of the
impaled cells. The terminology of Paes de Carvalho ('60) as applied to the zones of the AV
node was used throughout the study, but the
location of the N region was more closely identified with the findings of Janse et al. ('76).
Perinodal fibers were identified by typical
atrial action potential configuration and their
location at the border of the AV node.
The location and timing of a particular fiber
was identified both by the initial inscription
and contour of the action potential (e.g. AN,
N or NH). The basic drive was from either the
CT or IAS. Several types of premature and/or
conditioning stimuli were applied at the inputs
of the CT or IAS to preexcite or induce block
at a particular site, as indicated in the figures.
Block and reentry could then be reproduced in
order to carry out the mapping techniques. In
4 experiments, precisely reproducible intervals could not be achieved, and these 4 rabbit
heart preparations were eliminated from further study.
r ”.
Fig. l.A. AV junctional reentry utilizing perinodal atrial fibers. B. concealed reentry is rnonstrated. See text for
details. Analog records are organized from top to bottom as follows: CT and IAS = bipolar electrograms from the crista
terminalis and interatrial septum, respectively; AN1, N2 and NH3 are microelectroderecordings from cells in the atrionodal,
nodal and nodal-His regions, respectively, of the atrioventricular node. Subscripts 1-3 refer to sites identified in the
schematic diagrams. H = bipolar His bundle recordings. SCtand S,, indicate the timing of stimuli introduced at the
indicated intervals (in milliseconds) at each of these input regions. In the accompanying schematic diagrams of the
atrioventricular junction, the relative positions of the bipolar recording electrodes
I., stimulating electrodes (00)and
microelectrode impalements 1-3 (*) are indicated. Subsequent figures (2-5)are organized and labelled similarly.
A V atrial reentry
In Figure lA, AV junctional conduction utilizing the perinodal atrial fibers is demonstrated. Basic stimulation of the crista terminalis (CT) produced activation of the atrio-nodal
(ANl), nodal (N2) and nodal-His (NH3) fibers,
with subsequent activation of the His bundle.
Premature stimulation of the CT 120 msec after the basic drive engendered conduction to
the level of the AN1 fiber, and only a local
response (arrow) was seen at the level of the
N2 fiber. Subsequent but delayed activation
from the septum activated fiber N2 with retrograde activation of fiber AN1 and CT (Fig.
1, triangle). Activation after the extrastimulus
via IAS (multiple arrowheads) to N2, fiber
NH3 and then to the His bundle was noted.
Alternatively, fiber N2 could have been activated by a slowly conducting wavefront in a
contiguous pathway but manifest intranodal
reentry was never observed in this preparation. Furthermore, local responses or hump
formation were not observed in AN and NH
regions to indicate fractionation or continguous pathways in this instance. Subsequent
IAS activation occurred via the perinodal fibers. In Figure l B , recorded from different AN
fibers, as indicated in the schematic, there was
a similar activation pattern from the CT. The
premature stimulus altered the morphology of
the action potential in fibers AN1 and AN2
and only concealed retrograde conduction to
these fibers (arrows) without manifest retro-
Fig. 2.A. Both concealed and manifest reentry is seen following premature stimulation a t the IAS. Multiple reentries,
probably within the N region, are apparent (small arrows). B. An additional stimulus a t the crista terminalis (CT) prevented
perinodal reentry.
grade activation of the CT or subsequent perinodal activation of the IAS, as seen in Figure
Mechanism of initiation and termination of
the reentry mechanism
In Figure 2A, following the last basic stimulus from the CT, a pair of stimuli was given
to the CT and IAS (at 200 and 220 msec, respectively), and the septum was then stimulated 130 msec later. Notably, the CT was not
activated via the perinodal fibers after the last
stimulation of IAS. Activation of the IAS, N2
and AN1 proceeded in that order, with retrograde conduction to the CT (triangle) and presumably subsequent conduction to the IAS via
perinodal atrial fibers. It is possible that local
reentries in the region of the N2 fiber could
have emerged to depolarize the IAS. These analog records present presumptive evidence
that reentry via the perinodal tissue activated
the IAS, N2 and AN1 but failed to exit at the
CT. Multiple AN1 and N2 activations presumably resulted from fragmentation or local reentries (small arrows) within this area. In contrast, when the identical stimulation sequence
was repeated (Fig. 2B) but a n additional premature stimulation a t the CT input (curved
arrow) was introduced, earlier activation of
fiber AN1 occurred than was seen in Figure
1A. Presumably, Figure lB, retrograde activation of AN1 did not occur because of the earlier stimulation of the CT region. This prevented the retrograde wavefront from exiting
at the CT atrio-nodaI region and thereby prevented perinodal activation and AV junctional
An example of the initiation of another pattern of AV junctional reentry is shown in Figure 3A. After the last basic drive from CT, a
220 j
Fig. 3.A. In this case, repetitive reentry was produced by stimulation a t the crista and interatrial septum. The IAS was
stimulated 220 msec after the last basic drive at the CT. The conditioning stimuli 5 msec apart engenedered the reentry
movement with activation sequences indicated by the arrows. B. The strength of the stimulus was increased a t the CT
(2 x to 2.5 x 1, which produced depolarization in this region. Earlier activation of the area of the crista prevented repetitive
reentries, and the mechanism terminated. C. The crista terminalis was depolarized 200 msec after the last basic stimulus,
and because of the altered refractoriness, reentry could not be produced.
conditioning premature stimulus was given at
the IAS (220 msec). Late activation of CT from
the IAS via perinodal fibers was seen (arrow),
although slow intranodal conduction not involving fiber AN1 could have activated the CT
in this instance. In Figure 3A, 175 msec after
the last IAS conditioning stimulation, the IAS
and CT were stimulated within 5 msec. An
electrogram was seen a t the IAS, but only a
stimulus artifact was observed at CT due to
refractoriness in this region. The activation
sequence following IAS stimulation was antegrade through the AV node to His. Fiber AN1
and CT were subsequently to be activated.
Activation of the IAS was via the perinodal
fibers, with subsequent reentry movements,
for a total of 10 cycles. Finally, progressive
delay and block occurred between AN1 and CT,
and the reentry was terminated (not shown).
In Figure 3B, a stimulation pattern similar to
A was used, but the stimulation strength was
increased from twice to two and one-half times
threshold. The IAS conditioning stimulus was
conducted via perinodal fibers to the CT somewhat earlier (Fig. 3B, arrow and dotted line).
The last stimulation of the CT then elicited a
local response but was not sufficient to prevent
retrograde reentrant activation of AN1 and
N2. However, this local response at CT was
sufficient to delay the subsequent echo activation of CT (triangle), but it failed to activate
the IAS, and the reentry loop was terminated.
In Figure 3A and B, the premature activation of CT was via perinodal conduction. In
Figure 3C, CT depolarization was earlier due
to active stimulation (curved arrow) at the CT
site in addition to the conditioning activiation
at the IAS (straight arrow). A more uniform
engagegment of AN1 and N2 with conduction
to H was seen. Thus, retrograde conduction to
the CT, as shown in Figure 3A and B, could
not occur to initiate the reentry movement. In
Figure 3C, the earlier activation of CT (curved
arrow) permitted depolarization of the CT during the last set of stimuli, and thus reentry did
not occur. The earlier stimulation of the CT
altered refractoriness such that the second extrastimulus was successful and subsequent
reentry could not emerge. The last activation
of IAS and CT within 5 msec resulted i n antegrade AV conduction to His.
Further variations in the patterns of reentry, dependent on the time relationship of the
CT and IAS activation, are shown in Figure
4. In Figure 4A the time differential between
the two last stimuli was 20 msec. Initial activation occurred a t the IAS input, with subsequent activation of fiber N2 and retrograde
activation of fiber N1 and CT (triangle). Since
there was no further activation of the IAS, the
second depolarization of fiber N2 (arrow) occurred from a local reentry, but subsequent
conduction to His was absent. Alternatively,
the activation of N1 could also be explained by
collision of the antegrade impulse from the CT
depolarization, with the retrograde waveform
from N2 producing slow conduction and a reentry from N1 back to the CT. If this were the
case then the second N2 depolarization would
occur in a n antegrade fashion but block to His.
In Figure 4B, the reentry was somewhat sim-
ilar to that shown in Figure 4A, but in this
instance the IAS was activated 11msec earlier
(i.e., 31 msec before CT, vs. 20 msec) and the
following pattern of activation resulted. Fiber
N2 was initially activated from the IAS. Fiber
N1 activation followed either from continuation of the wavefront from N2 in a retrograde
manner or from reentry above fiber N1 and
subsequent retrograde activation of the CT
(Fig. 4B, triangle). The second hump (curved
arrow) at fiber N2 probably was a result of
antegrade conduction from the reentry loop
with subsequent conduction to the His. The
last group of complexes most likely occcurred
from a spontaneous antegrade conduction sequence from CT, but the reentry movement
terminated. In Figure 4C, stimulation of IAS
13 msec earlier than that shown in Figure 4B
produced a pattern of reentry movement similar to the one in Figure 4B. Reentry to the CT
(Fig. 4C, triangle) allowed perinodal conduction to occur and enter the AV node via the
IAS (circle). However, in this case a second
reentry loop also occurred via fibers N1 and
N2 (star) and may have influenced CT activation before the reentry terminated.
An additional reentry mechanism dependent upon the interrelationship of both CT and
IAS inputs is shown in Figure 5. In Figure 5A,
premature activation of the CT 155 msec after
the last basic CT depolarization produced activation of fiber AN1, but only a small hump
at the level of fiber N1 (curved arrow). Subsequent activation of Fiber N2, indicated by
a larger and fuller action potential, probably
resulted from a second input from the region
of the IAS. This second impulse presumably
resulted from perinodal conduction of the initial stimulus from the CT. Reentry did not occur, but subsequent His bundle activation was
seen. As shown in Figure 5B, when the IAS
was additionally activated 10 msec earlier
than the CT, several graded responses or
humps were seen in fiber N2 (small arrows).
Subsequently, reentry to the IAS and CT was
seen. Antegrade conduction then penetrated
as far as fiber AN1 without subsequent conduction, and the reentry loop was terminated.
As shown in Figure 5C, a similar sequence of
reentry movement was reproduced merely by
moving the stimulation time at the CT 10 msec
earlier (i.e., 145 msec) than in Figure 5A. Activation of fiber AN1 occurred with a small
hump formation at the level of fiber N2. Septa1
activation probably occurred via the perinodal
tissue and was responsible for activation of fiber N2 (larger hump, curved arrow), with reen-
Figure 4.A. Initial activation a t the IAS input by the conditioning stimuli which were 20 msec apart with subsequent
antegrade activation of fiber N2 antegrade and retrograde activation of fiber N1 and CT (triangle).The second depolarization
following this pair of stimuli a t N2 (arrow) resulted from retrograde activation from local reentry without conduction to
His. B. The IAS was activated 31 msec before the CT, which resulted in sustained reentry movements with subsequent
activation of His. C. Stimulation of IAS 13 msec earlier than in B produced a pattern of reentry movement; however, in
this instance perinodal conduction occurred and activated the IAS (circle).
try to the IAS and CT, and with subsequent
activation of fiber AN1. The reentry mechanism then terminated spontaneously.
to be operative in the presence of reentry tachycardias associated with the Wolff-ParkinsonWhite syndrome, the mechanism of reentry
within the AV nodal junction is less obvious.
Janse et al. ('76) clearly demonstrated that
While two anatomically distinct atrioventri- during a regular sinus rhythm the AV node
cular conducting pathways have been shown receives dual input from the CT and IAS. How-
Fig. 5. A. Premature activation of the CT 155 msec after the last basic CT depolarization produced activation of fiber
ANI, with only a small hump at the level of fiber AN2. The second input from the region of the IAS produced a larger
fuller action potential a t fiber N2. B. When the IAS was activated in addition, 10 msec earlier than in A, several graded
responses were seen (small arrows) a t fiber N2, with subsequent reentry to the CT and IAS. C. A similar sequence of
reentry movement was reproduced merely by moving the stimulation time a t the CT alone 10 msec earlier.
ever, premature stimulation of the atria resulted in block of the impulse to the posterior
input, with the AV node then exclusively activated via the interatrial septum. Then, after
a considerable interatrial conduction delay,
the wavefront reached the AV node and was
able to reexcite the posterior input travelling
along the CT in a retrograde direction. Al-
in Janse's ('76) experiments, the exact course
of the circuit with respect t o the perinodal
atrial tissue remained somewhat unclear.
Janse et al. ('76) further demonstrated that
both summation and fragmentation of impulses affected AV transmission and the ability
to produce echo beats.
In the present study, AV junctional reentry
demonstrated (Fig. 1).Premature stimulation
a t the area of the CT resulted in antegrade
block in the region of the N fibers. An impulse
could travel through the perinodal fibers and
enter the interatrial septum, and it could conduct retrogradely t o the CT and atrium, and
antegradely to the ventricles.
To verify that the echo actually used a perinodal pathway, programmed stimulation was
applied first to initiate the reentry mechanism.
This was done by introducing a properly timed
premature stimulus in the region of the interatrial septum (Fig. 2A). This impulse travelled
retrogradely through the AV node and returned via the perinodal atrial fibers to the
interatrial septa1 input and then to the His,
with multiple fragmentary waves within the
N region. However, an additional stimulus
placed at the CT could block the retrograde
impulse to the atria and thus interrupt the
perinodal reentry pathway (Fig. 2B). In Figure
3 premature stimulation in the region of the
CT input either aborted the reentry mechanism or prevented it entirely. This was dependent on the ability of the premature stimulation to depolarize the CT and prevent the
retrograde reentry mechanism to the atria,
thereby blocking the perinodal input to the
The patterns of AV junctional reentry varied
in any given preparation dependent on the
time relationship of activation of CT versus
IAS. Further evidence for the role of appropriately timed stimuli a t the CT and IAS in
the initiation of reentry is shown in Figure 4.
Here both concealed local reentry, as well as
manifest reentry utilizing the perinodal fibers
of the atria, were apparently operative.
A reentry mechanism dependent upon the
interrelationship of the inputs to both the CT
and IAS was also demonstrated (Fig. 5). This
occurred as a result of fragmentation of wavefronts in an antegrade fashion. When there
was sufficient conduction delay the impulse
could then converge to activate the perinodal
fibers of the atria. Such impulses could then
reenter the AV node. In Figure 5A, the initial
hump in fiber N1 (arrow) may have resulted
from electrotonic spread in an antegrade direction. The fuller action potential a t N2 could
then have resulted from a subsequent antegrade wavefront via the CT, but more likely
entered via the IAS input since the CT electrogram was inscribed prior to fiber N2. When
the premature stimulus was further conditioned by a 10 msec earlier stimulation a t the
IAS (Fig. 5B) multiple humps (small arrows)
appeared at N2, the wavefront exited via N2,
and the IAS and returned via the CT and AN1.
A reentry activation sequence was also produced merely by delivering a n earlier premature stimulus to the CT (e.g., 145 msec rather
than 155 msec) as shown in Figure 5C. In this
instance fragmentation of the antegrade wave
produced an initial hump a t N2, followed by
a large action potential. Perinodal conduction
then occurred to both the CT and the IAS with
subsequent activation of AN1 before the reentry terminated.
Thus, the present study has demonstrated
that dual input to the AV node from the CT
and IAS could result in either fragmentation,
cancellation, or, alternatively, summation of
wavefronts. Hence, there was evidence of an
interaction between the two inputs of the AV
node shown clearly by varying the timing of
stimulation of the CT and IAS. Mapping of
activation patterns suggested that delayed
conduction within the AV node itself allowed
an impulse to enter one atrio-nodal input region, emerge from the other atrio-nodal “input” region and conduct via the perinodal fibers to reenter the AV node from the initial
input area. The use of programmed stimulation to induce block in one or the other of the
atrio-nodal input regions could then interrupt
the reentry mechanism, proving that the perinodal atrial tissue was a necessary link in the
reentry circuit. Finally, although concealed
intranodal reentry was identified by intranodal mapping techniques, manifest reentry confined strictly to within the AV node and not
using the perinodal atrial tissues as a necessary link €or the reentry mechanism was not
This work was done during Dr. Mazgalev’s
tenure as a Visiting Scientist from BAN Institute of Physiology in Sofia, Bulgaria under
the sponsorship of the Bulgarian Academy of
Sciences and the National Academy of Sciences, Washington, D.C.
Dr. Michelson is the recipient of Clinical Investigatorship Award 1KO8 HL00709-01 from
the National Heart, Lung and Blood Institute,
National Institutes of Health, Bethesda, Maryland.
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