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lACC Vol. 4, No.2
August 1934:295-304
EXPERIMENTAL STUDIES
Reentrant Ventricular Arrhythmias in the Late Myocardial
Infarction Period
II. Burst Pacing Versus Multiple Premature Stimulation in the
Induction of Reentry
NABIL EL-SHERIF, MD, FACC, RAHUL MEHRA, PHD, WILLIAM B, GOUGH, PHD,
ROBERT H. ZEILER, PHD
Brooklyn. New York
Isochronal maps of ventricular activation were analyzed
in dogs 1 to 5 days after infarction utilizing a 64 channel
multiplexer. Only dogs in which circus movement reentry could not be induced by a single premature stimulus
were analyzed. Reentrant rhythms could be successfully
induced equally by multiple (double or triple) premature
stimuli and by burst pacing. Successive premature stimuli as well as successive beats during burst pacing resulted in progressively longer arcs of functional conduction block or slower circulating wave fronts, or both,
that succeeded in reexciting myocardial zones on the
proximal side of the arc of block to initiate reentry.
However, for manifest reentry to be induced by burst
pacing, the paced run had to be terminated after the
heat that resulted in a critical degree of conduction delay.
Otherwise, reentrant activation could be confined (con-
Both properly timed premature stimulation and rapid pacing
have been utilized to initiate possible reentrant rhythms in
the experimental (1-3) and clinical (4-6) settings. The postinfarction canine heart is a documented experimental model
for circus movement reentry (7-9). In these hearts, reentry
could be induced by programmed premature stimulation and
by runs of rapid pacing usually referred to as burst pacing
(10), The mechanism of initiation of reentry by more than
one premature stimulus has been described from analysis
of ventricular activation maps (7,8). In an earlier study (3)
that utilized composite electrode recordings, it was shown
that initiation of reentry by burst pacing depends not only
cealed) by the subsequent paced wave front, which could
also arrive earlier to the reentrant circuit zone of slow
conduction resulting in block and interruption of reentry. Termination of a paced run after this beat would
not result in reentry. If the paced run was extended past
this beat, a new sequence of ventricular activation patterns characterized by progressively longer arcs of block
or slower conduction, or both, developed again. The
number of beats in a paced run that could initiate reentry
varied with the cycle length of pacing, as well as in
different experiments, and was difficult to standardize.
It is therefore concluded that random burst pacing as a
technique for induction of reentrant rhythms should
probably be abandoned in favor of multiple premature
stimulation.
on the cycle length of stimulation but also, critically, on
the number of beats in the paced run. Burst pacing has been
applied more frequently during the last several years in the
clinical electrophysiology laboratory for initiation of ventricular arrhythmias (l0,11). The mechanism of initiation
of reentrant rhythms by burst pacing and the relation of this
technique to programmed premature stimulation are not well
understood. Our study was undertaken to investigate this
subject in dogs I to 5 days after infarction by analyzing
ventricular activation maps.
Methods
From the Veterans Administration and State University of New York,
Downstate Medical Center, Brooklyn, New York. This study was supported by the Veterans Administration Medical Research Fund. It was
presented in part at the Annual Meeting of the American College of Cardiology Dallas, Texas, March 1984. Manuscript received November 15,
1983; revised manuscript received January 23, 1984, accepted February
9, 1984.
Address for reprints: Nabil EI-Sherif, MD, Veterans Administration
Medical Center, 800 Poly Place, Brooklyn, New York 11209.
© 1984 r) the American College of Cardiology
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Experimental preparation. In eight mongrel dogs
weighing 15 to 20 kg, the left anterior descending coronary
artery was ligated just distal to the anterior septal branch.
Details of the surgical technique have been described previously (12). The dogs were reanesthetized with sodium
pentobarbital (30 mg/kg intravenously) 1 to 5 days after
coronary artery ligation and received supplemental doses as
0735-1097/84/$3.00
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EL-SHERIF ET AL.
BURST PACING VERSUS MULTIPLE PREMATURE STIMULATION
Table 1. Results of Programmed Premature Stimulation and Burst Pacing
Experiment
I
2
3
4
5
6
7
8
Programmed Premature
Stimulation
Burst
Pacing*
Induced
Rhythms
S,S2S3
S,S2S3
S,S2S3
S,S2S3S4
S,S2S 3S4
S,S2S3S4
S,S2S3S4
S,S2S 3S4
4,5, 10
5,9, 10
3,4,8
4, 5, 9, 10
4,8,9
5, 9
5,9, 10
4,5,9
MVT
MVT
PVR
MVT
PVR
PVR, VF
PVR, VF
PVR, VF
*Number of beats in a paced run that resulted in manifest reentry. MVT = monomorphic ventricular
tachycardia (10 or more beats at a cycle length :::;300 ms); PVR = pleomorphic ventricular rhythm (two or
more beats with more than two QRS configurations at a cycle length :::;300 ms); VF = ventricular fibrillation.
required. Each dog was ventilated with room air through an
endotracheal tube with a Harvard positive pressure pump,
and the jugular vein was cannulated for the administration
of fluids. Electrocardiographic lead II and femoral blood
pressure were continuously monitored on an Electronics for
Medicine DRIO electrophysiologic recorder. To slow the
sinus rhythm, stimulation of the right or left vagosympathetic trunk was accomplished by delivery of 0.5 ms square
wave pulses of 1 to 10 V intensity at a frequency of 10 to
20 Hz through two Teflon-insulated silver wires (0.012 inch
[0.03 em] in diameter). The heart was exposed through a
left thoracotomy and cradled in the opened pericardium.
Ventricular pacing was achieved with use of two fine Tefloninsulated stainless steel wires (0.005 inch [0.013 em] in
diameter) inserted by a 21 gauge hypodermic needle into
the right ventricular wall. Both regular pacing and programmed premature stimulation were performed with a programmable digital stimulator (model DTU-lOl MVA, Bloom
Associates, Ltd). The stimulator delivered rectangular pulses
of variable duration (usually 2 to 5 ms) and twice diastolic
threshold with an accuracy of up to alms interval.
Stimulation protocol. Programmed premature stimulation. During regular ventricular pacing (SISI) at cycle
lengths of 350 to 400 ms, single (S2), double (S2S3) or triple
(S2S3S4) premature stimuli were introduced. A single premature stimulus (52) was introduced late in diastole, and
the coupling interval was gradually shortened until a ventricular rhythm was initiated or until the effective refractory
period of the right ventricular myocardium was reached. In
all experiments in the present study, reentry required more
than a single premature beat for initiation. In these experiments, 52 was introduced at an interval 5 ms longer than
the effective refractory period and 53 was introduced at
gradually shorter coupling intervals until S3 either provoked
a response or reached refractoriness. If S3 failed to initiate
reentry, its coupling was fixed at an interval 5 ms longer
than the refractory period and an S4 was introduced at gradually shorter coupling intervals until a ventricular rhythm
was initiated. In all experiments, reentry could be induced
by double or triple premature stimulation.
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Burst pacing, Rapid ventricular pacing was applied during a slower sinus or spontaneous ventricular rhythm in the
form of individual runs of 3 to 12 paced beats at a fixed
cycle length, 5 ms longer than the effective refractory period
of 52 (that is, a cycle length equal to the 5\5 2 coupling
interval during multiple premature stimulation). This assured 1:1 capture during ventricular pacing. All paced runs
were timed manually to start in the late diastolic interval
during the slower spontaneous rhythm; and the cycle length
preceding burst pacing was consistently longer than 350 ms.
The complete burst pacing protocol was applied only at a
single cycle length. In three experiments, activation maps
were also analyzed during regular pacing at different cycle
lengths longer than the one defined in the protocol.
Figure 1. Electrocardiographic recordings from experiment 1 in
which a reentrant tachycardia could be induced by double pre"
mature stimuli (5 15253 , record A) and by burst pacing (BP). Burst
pacing could initiate reentry only after paced runs with a critical
number of beats (records B and D). See text for details.
B
__LW
c
-.l.!L_ _
BP
BP
D
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August 1%4:295-304
Epicardial isochronal maps. These were constructed from
62 simultaneous bipolar electrode recordings obtained with
a sock electrode. A higher density of electrodes (approximately I) to 10 mm between pairs) covered the area of the
infarction and the border zones, and a lower density (approximately 15 mm) covered the remaining surface of the
heart. In some experiments, a patch electrode was also used
to obtain epicardial recordings at a closer interelectrode
distance (4 mm). Intramural recordings were obtained with
specially designed 21 gauge needles. Details of the recording techniques, the mapping system and the methods for
construction of epicardial isochronal maps were reported
previously (7,8). After termination of the electrophysiologic
study, the anatomic location of the infarction was determined and correlated with epicardial and intramural
recordings.
Results
In three of the eight experiments, reentrant rhythms could
be induced by S1S2S3 premature stimulation. In the remaining five experiments, S1S2S3S4 stimulation was required. In all experiments, reentrant rhythms could also be
induced by burst pacing. However, manifest reentry was
dependent on the number of beats in a paced run. The latter
varied with the cycle length of pacing as well as from one
experiment to the other. The cycle length of burst pacing
ranged from 180 to 225 ms. Each programmed stimulation
protocol was repeated twice and, with few exceptions, the
results were reproducible. Reentrant beats with different
QRS morphologic features (that is, pleomorphic) were induced in four of five experiments in which three premature
stimuli as well as burst pacing were used and in one of the
three experiments in which reentry was initiated by two
premature stimuli. The pleomorphic configuration was due
to varying sites of early reexcitation resulting in different
ventricular activation patterns. In the remaining three experiments, a monomorphic rhythm was induced by both
premature stimulation and burst pacing. In three experiments, a pleomorphic rhythm induced by burst pacing degenerated into ventricular fibrillation. In two of these experiments, ventricular fibrillation could also be induced by
SIS2S3S4 stimulation. Results from all experiments are summarized in Table 1.
Monomorphic ventricular tachycardia. Electrocardiogram. Figure 1 illustrates electrocardiographic recordings
from experiment 1, in which a monomorphic reentrant
tachycardia could be induced by both S1S2S3 premature
stimulation and burst pacing. Record l A shows that during
SIS1 stimulation at a cycle length of 350 ms, S2 and S3
stimuli were introduced at coupling intervals of 220 and
185 ms, respectively, and initiated a monomorphic ventric-
ECG
Figure 2. Epicardial isochronal maps
during SlSZS3 premature stimulation and
the first reentrant beat (V I) from the same
experiment shown in Figure I (see text
for details), In this and subsequent maps,
the epicardial surface is depicted as if the
ventricles were folded out after a cut was
made from the crux to the apex. The top
left and right borders represent the right
and left atrioventricularjunctions. The two
curvilinear surfaces on the right and left
are contiguous and extend from the posterior base to the apex of the heart. The
arcs of functional conduction block are
represented by heavy solid lines and are
depicted to separate contiguous areas that
are activated at least 40 ms apart. The
epicardial border of the infarction is delineated by the interrupted line on the
S1 map. The isochronal maps are drawn
at 20 ms intervals. ECG = electrocardiogram.
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297
SOOMS
298
EL-SHERIF ET AL.
BURST PACING VERSUS MULTIPLE PREMATURE STIMULATION
ular tachycardia at a cycle length of 220 to 230 ms. Burst
pacing at a cycle length of 220 ms could initiate the ventricular rhythm only after paced runs of 4 (record IB), 5 or
10 beats (record ID) , but not with paced runs of 6, 7, 8
(record ici, 9, II or 12 beats.
Epicardial isochronal maps . Figures 2 to 4 illustrate epicardial isochronal maps from the same experiment shown
in Figure I . Figure 2 illustrates the epicardial maps during
SlS2S3 premature stimulation and the first reentrant beat
(VI) . The isochronal maps were drawn at 20 ms intervals.
During SJ, the entire epicardial surface was activated within
80 ms, with the last isochrone located in the central part of
the epicardial surface of the infarct (the latter is marked by
the dotted line). During S2, an arc of functional conduction
block (represented by the heavy solid line) developed inside
~t
l
'50DMS
I
lACC Vol. 4. No.2
August 1984:295- 304
the septal border of the infraction . The activation wave front
circulated around the upper and lower ends of the arc of
block . The central and apical parts of the epicardial surface
of the infarct were the last to be activated at 120 ms. The
second premature stimulus (S3) resulted in a much longer
arc of conduction block inside the upper, septal, apical and
lower lateral borders of the infarction. The activation wave
front circulated around both ends of the arc of block, coalesced and then advanced slowly in a direction from the
lateral to the septal border of the infarction. The slow wave
front reached the distal side of the arc of block 200 rns from
the onset of right ventricular activation before reactivating
an area on the proximal side of the arc to initiate the first
reentrant beat (V d. Epicardial activation during V 1 continued in the form of two circulating wave fronts around two
_
5,5 25354 V, V2
Figure 3. Epicardial isochronal maps
during a four beat run of burst pacing
that induced a reentrant tachycardia
from the same experiment shown in
Figures I and 2. See text for details.
ECG = electrocardiogram.
JDD
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JACC Vol -i, No.2
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299
ECG'--'I--..rI
500 MS
oLLUWJJJ----------.
Figure 4. Epicardial isochronal maps of S,
to S10 during a 10 beat run of burst pacing
that induced a reentrant rhythm from the same
experiment shown in Figures I to 3. The S I
to S4 maps were similar to those in Figure
3. Reentrant activation initiated by S4 continued during S, with limited contribution
from the paced wave front. S6 interrupted
reentrant activation, while S7 to SIO resulted
in a new sequence of ventricular activation
patternsof paced beats characterized by progressively longer arcs of conduction block
and slower wave fronts with StO initiating
reentrant activation (represented by the dotted line). See text for details.
/
arcs of block that coalesced into a single wave front. This
single wave front conducted slowly over a circuitous pathway before reactivating myocardial sites on the septal border
of the infarct to initiate the second reentrant beat.
Figure 3 illustrates epicardial isochronal maps during a
four beat run of burst pacing that induced a reentrant tachycardia. The activation maps of Stand S2 were similar to
those shown in Figure 2. In this and all other experiments,
the activation map of S I did not vary in relation to the
preceding cycle (::=: 350 ms) or the origin of the preceding
beat (supraventricular or ventricular). The second premature
stimulus (53) during burst pacing has a coupling interval of
220 ms compared with a 185 ms coupling interval during
premature stimulation. It resulted in a shorter arc of conduction block and less conduction delay of the common
reentrant wave front. The latter reached the distal side of
the arc of block 180 ms from the onset of right ventricular
activation compared with 200 ms during the second premature stimulus (S3) in Figure 2. This probably did not
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provide sufficient time for refractoriness of myocardial zones
on the proximal side of the arc of block to expire and
explains why a three beat run of burst pacing failed to initiate
reentry. In contrast, S4 resulted in more extensive conduction block and a slower wave front that succeeded in reexciting myocardium on the proximal side of the arc of block
thus initiating the first reentrant beat (V I). The activation
maps of V I and V2 were approximately similar to the V I
map shown in Figure 2. Specifically, the upper circulating
wave front advanced around a circular zone of functional
block that changed its position from beat to beat during the
reentrant tachycardia.
Figure 4 illustrates the epicardial maps of55to 5 10 during
a 10 beat paced run that induced a reentrant rhythm. The
S I to S4 maps were similar to the ones shown in Figure 3.
The 55 map was remarkably similar to that of V I in Figure
3. This, in addition to the fact that a five beat paced run
could also induce a reentrant rhythm, strongly suggests
that circus movement reentry continued during S5' How-
300
EL-SHERIF ET AL.
BURST PACING VERSUS MULTIPLE PREMATURE STIMULATION
ever, the pacing stimulus did result in activation of part of
the right ventricular epicardium, although the line of fusion
between the paced and reentrant wave fronts could not be
determined precisely. On the other hand, the epicardial map
of S6 shows that the activation wave front advanced rapidly
from the site of right ventricular stimulation to the narrow
isthmus of slow conduction on the lateral border of the
infarction. During S6, conduction from the site of right
ventricular stimulation to the narrow isthmus of slow conduction was 40 to 60 ms compared with 120 to 140 ms
between the two sites during reentrant activation. The fast
arrival of the paced wave front before expiration of refractoriness of the myocardium at this critical site of the reentrant circuit probably explains conduction block of the wave
front at this site. The S6 map also shows that the circulating
wave front during S5 succeeded in reexciting a localized
myocardial zone at the septal border of infarction. Thus,
the most plausible explanation of the S6 map is that the
paced wave front resulted in containment of reentrant activation into a small part of the paraseptal myocardium while
at the same time it advanced rapidly to the area of previous
slow conduction resulting in conduction block and termination of reentrant activation. The relatively fast arrival of
the paced wave front could be explained by conduction in
myocardial zones that were enclosed within the upper island
of functional conduction block and, therefore, were not
activated during S5'
The S7 map showed an activation pattern very similar to
that of SI in Figure 3 (that is, fast conduction with the entire
epicardial surface being activated within 80 ms). The S8,
S9 and SIO maps were also, respectively, similar to the S2,
S3 and S4 maps in Figure 3. Thus, termination of a 10 beat
Figure S. Electrocardiographic recordings from experiment 5 in
which three premature stimuli (S,S2S3S4) were required to initiate
a reentrant rhythm. See text for details.
lACC Vol. 4, No.2
August 1984:295-304
paced run resulted in a reentrant rhythm, as did termination
of a 4 beat paced run. The S 11 and S'2 maps were to some
extent similar to the S6 and S7 maps in Figure 4, and II or
12 beat paced runs did not initiate a reentrant rhythm.
Pleomorphic ventricular rhythms. Electrocardiograms.
Figure 5 illustrates electrocardiographic recordings from
experiment 5 in which three premature stimuli were required
to initiate reentry. SISt cycle length was 400 ms and S2,
53 and S4premature stimuli were introduced at cycle lengths
of 200, 180 and 165 ms, respectively. SIS2S354 stimulation
resulted in three reentrant beats with a negative QRS configuration in lead II. Figure 6 shows electrocardiographic
recordings obtained from the same experiment and illustrates the results of burst pacing at a cycle length of 200
ms. Only four, eight and nine beat paced runs could initiate
a reentrant rhythm. A four beat paced run induced four
reentrant beats with pleomorphic configuration. The first
reentrant beat had a narrow predominantly positive QRS
configuration, while the remaining three beats had a negative
QRS configuration. An eight beat paced run only intermittently resulted in a single reentrant beat with a negative QRS
configuration. Similarly, a nine beat paced run could oc-
Figure 6. Electrocardiographic recordings from the same experiment shown in Figure 5, illustrating the results of 3 to 12 beat
runs of burst pacing (BP). Only four, eight and nine beat paced
runs could initiate one or more reentrant beats (the first reentrant
beat is marked by an asterisk). The tracing on the bottom of each
electrocardiographic recording denotes the timing of stimulation.
See text for details.
BP
BP
3~8~
~
~
4~9~
4-L9~
~
~
5
~
~
6~10~
~
~
7~11.J8Wv
~
~
8
I
1SEC
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~ 12~AMMij\~
EL-SHERIF ET AL.
BURST PACING VERSUS MULTIPLE PREMATURE STIMULATION
JACC Vol 4, No, 2
August 19~4:295-304
casionally result in a single reentrant beat with prolonged
coupling and a positive QR5 configuration.
Epicardial isochronal maps. Figure 7 illustrates the epicardial maps during a four beat paced run that initiated a
pleomorphic reentrant rhythm. The entire epicardial surface
was activated within 80 ms during S I, with the central part
of the epicardial surface of the infarction being the last to
be activated; 52 resulted in a relatively short arc offunctional
conduction block and a limited degree of slow conduction
(last isochrone at 120 ms). 53 and 54 resulted in progressively longer arcs of conduction block and slower conduction, During S4, the slow common reentrant wave front
reached a site on the distal border of the septal arc of block
at the 200 ms isochrone and succeeded in reexciting myo-
cardial zones on the septal border of the infarction to initiate
reentry. The septal breakthrough resulted in a predominantly
basal to apical activation of the left ventricle during V I and
may explain the narrow positive QR5 configuration in lead
II. Ventricular activation continued during VI in the form
of two circulating wave fronts that coalesced and conducted
slowly toward the apex before reexciting apical zones to
initiate the second reentrant beat (V 2). The predominantly
apical to basal ventricular activation during V2 explains the
negative QR5 complex in lead II.
Figure 8 illustrates the epicardial maps of S4 to Sg during
an eight beat paced run that initiated a single reentrant
beat (VI) with a negative QRS complex. Similar to what
was described in Figure 4, 55 initiated an activation wave
20
60
Figure 7. Epicardial isochronal maps
during a four beat burst pacing run that
initiated a pleomorphic reentrant rhythm
from the same experiment shown in Figures 5 and 6. See text for details. ECG
= electrocardiogram.
240
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302
EL-SHERIF ET AL.
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lACC Vol. 4, No.2
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ECG~
-------,
Figure 8. Epicardial isochronal maps of
S4 to S8 during an eight beat burst pacing
run that initiated a single reentrant beat
(VI) from the same experimentshown in
Figures 5 to 7. The SI to S4 maps were
similarto thosein Figure7. S5 interrupted
the reentrant activation that was initiated
by S4. Subsequently, S6 to S8 showedprogressively longerarcsof conduction block
and slowerwave fronts, with S8 initiating
a single reentrant beat. See text for details. ECG = electrocardiogram,
Sa
front that advanced rapidly through myocardial zones that
were not excited during 54' As a consequence, the wave
front reached the areas of slow conduction at the apex and
the central part of the infarct before expiration of their refractoriness, resulting in conduction block and the termination of the reentrant process. The paced activation front
also resulted in containment of the reentrant wave front
induced by 54 into a small localized zone on the septal border
of the infarction. 56, S7 and S8 initiated a new series of
sequential activation patterns showing progressively longer
arcs of conduction block and slower conduction. During S8,
the last isochrone at 200 ms could intermittently succeed in
reexciting apical myocardium to initiate a single reentrant
beat with a negative QRS configuration (VI)' During Vb
the two circulating wave fronts failed to conduct in the
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central part of the epicardial surface of the infarct, resulting
in termination of the reentrant process.
Ventricular activation during rapid ventricular pacing
at long cycle lengths. Patterns of ventricular activation
during rapid ventricular pacing at cycle lengths longer than
the SISz coupling interval were analyzed in three experiments. In each experiment, sequential paced beats showed
similar ventricular activation patterns with relatively rapid
conduction and no arcs of functional conduction block up
to a critical short pacing cycle length. At shorter cycle
lengths, sequential beats showed progressively longer arcs
of functional block and slower conduction. For example, in
the experiment in Figures I to 4, sequential ventricular paced
beats at cycle lengths longer than 240 ms showed similar
ventricular activation patterns with relatively fast conduction
EL-SHERIF ET AL.
BURST PACING VERSUS MULTIPLE PREMATURE STIMULATION
lACC Vol. 4, No.2
August 1 9 ~4 : 295-304
and no arcs of conduction block . However , during pacing
at a cycle length of 240 ms, functional conduction block
and slow conduction began to develop and increased in
magnitude in sequential beats . A five beat paced run was
required before sufficient conduction delay developed so
that the slow wave front could reexcite myocardial zones
on the proximal side of the arc to block and initiate reentrant
activation. In contrast, a four beat paced run was only required when pacing was applied at 220 ms. The range of
cycle lengths during which paced runs could initiate reentry
in the same experiment varied from 10 to 30 ms.
Discussion
Our report includes only experiments in which reentry
was induced by more than one premature stimulus. In experiments in which a reentrant rhythm could be induced by
a single premature stimulus, burst pacing could also initiate
reentry and the e1ectrophysiologic mechanism is essentially
similar to the one described in this study. Those experiments
were not included , however , because of their limited clinical
relevance . Usually in a clinical setting, burst pacing is not
utilized when arrhythmias can be induced by a single premature stimulus .
Mechanism of induction of reentrant rhythms byburst
pacing. The mechanism by which burst pacing could initiate reentry was suggested from earlier studies (3) that
utilized composite electrode recordings. However , detailed
analysis of ventricular activation pattems of successive paced
beats was necessary for a more thorough elucidation of the
mechanism. In the present study , successive paced beats
applied at a critically short cycle length resulted in progressively longer arcs of functional conduction block or
slower circulating wave fronts, or both. The slow wave front
reaching the distal side of the arc of block after a critical
degree of conduction delay could reexcite myocardial zones
on the proximal side of the arc after expiration of their
refractoriness to initiate circus movement reentry. However.
for manifest reentry to take place , the paced run should be
terminated after the beat that resulted in a critical degree of
conduction delay. If rapid pacing was extended past this
beat , reentrant activation could be confined (concealed) to
a zone of early reexcitation or a varying degree of fusion
between the reentrant and paced wave fronts, or both, could
occur . Furthermore , a paced wave front could advance rapidly to the critical zone of slow conduction of the reentrant
circuit before expiration of its refractoriness. This would
result in conduction block and interruption of circulating
excitation. Termination of a paced run after this beat would
not result in reentrant activation . In our study . the earlier
arriva l of the paced wave front could be attributed, at least
in part. to activation of myocardial zones that were not
stimulated during the preceding beat and thereby had recovered full excitability. However , because this was asso-
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303
ciated with a change of the pathway of the paced wave front
the role of a " faster" rate of conduction of the wave front
in certain myocardial zones could not be precisely determined . When the paced run was continued past the beat that
interrupted reentry , a new sequence of ventricular activation
patterns of paced beats characterized by progressively longer
arcs of conduction block or slower wave fronts, or both,
developed . Once again , manifest reentry could only develop
if the paced run was terminated after the beat that resulted
in a critical degree of conduction delay. It should be emphasized that the rules for initiation of reentrant rhythms by
burst pacing are the same whether the resulting rhythm is
a monomorphic tachycardia or a nonsustained pleomorphic
rhythm.
Our study has shown that the mechanism of induction of
reentry by a series of paced beats at a critically short cycle
length is essentially similar to that of multiple premature
stimulation. A minor difference was that multiple premature
stimuli were introduced at gradually shorter cycle lengths
compared with the constant cycle length during burst pacing.
This resulted in a more prompt development of the necessary
prerequisites of reentry in terms of zones of functional conduction block and slow circulating wave fronts . Thus, in
the experiments shown in Figures I to 4, two premature
stimuli at a cycle length of 220 and 185 ms, respectivel y,
could initiate reentry , while a series of three short cycles at
220 ms during a four beat paced run was required to do the
same.
Clinical implications. The present study was only designed to analyze the mechanism of induction of reentry by
burst pacing and to compare this with multiple premature
stimulation. It does not address other issues that may be
relevant in the clinical setting . One such issue is the clinical
significance of reentrant rhythms induced by more aggressive stimulation protocols, such as triple premature stimuli
and burst pacing particularly in the absence of a spontaneous
clinical arrhythmia. However, this study may provide useful
guideline s regarding the use of burst pacing to initiate reentrant rhythms in the clinical laboratory . In our experiments,
multiple premature stimuli and burst pacing were equally
successful in inducing reentry . However, because burst pacing was critically dependent on the number of beats in the
paced run , the majority of paced runs applied in a single
experiment failed to initiate reentry and only a few did. The
critical number of beats in runs of burst pacing that can
initiate reentry is difficult to standardize and varies in different experiments as well as with the cycle length of pacing
in the same experiment. This is not the case with programmed multiple premature stimulation . Therefore, within
accepted limits of extrapolating experimental observations
to the clinical setting, our study suggests that random burst
pacing as a technique of induction of reentrant rhythms
should be abandoned in favor of multiple premature
stimulation.
304
EL-SHERIF ET AL.
BURST PACING VERSUS MULTIPLE PREMATURE STlMULATIO/\
We thank Gerald Cohen and his staff for technical assistance, Ann Basile
aIId Barbara Grebin for the preparation of the manuscript and Mike Yu
for the art work.
lACC Vol. 4. No.2
August 1984:295· 304
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