(Circulation. 1996;93:1567-1578.)
© 1996 American Heart Association, Inc.
Articles |
Electrophysiological Mechanisms of Spontaneous Termination of Sustained Monomorphic Reentrant Ventricular Tachycardia in the Canine Postinfarction Heart
From the Cardiology Division, Department of Medicine, State University of New York Health Science Center and Veterans Affairs Medical Center, Brooklyn, NY.
Correspondence to Nabil El-Sherif, MD, Cardiology Division, Box 1199, SUNY Health Science Center, 450 Clarkson Ave, Brooklyn, NY 11203. E-mail el-sherif.nabil@brooklyn.va.gov.
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Abstract |
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Background The electrophysiological mechanisms of spontaneous termination of sustained monomorphic ventricular tachycardia (SMVT), in the postinfarction heart, generally considered secondary to a reentrant mechanism, have not been fully investigated.
Method and Results Epicardial activation maps of spontaneous termination of 20 different episodes of SMVT (lasting 30 seconds to 10 minutes) from 8 dogs, 4 to 5 days after one-stage ligation of the left anterior descending coronary artery, were analyzed with the use of 254 bipolar electrode recordings with high density (2.5 to 2.8 mm between bipolar electrodes) in the ischemic zone. All ventricular tachycardias (VTs) were due to circus movement reentry with a characteristic figure-8 configuration. Termination always occurred when the two circulating wave fronts blocked in the central common pathway (CCP). Two basic mechanisms of spontaneous termination were observed: (1) In 15 episodes, acceleration of conduction occurred in parts of the reentrant circuit and was associated with slowing of conduction and finally conduction block in the CCP. Acceleration of conduction occurred in the last few cycles of VT both at the outer border of the arcs of functional conduction block in the "normal" myocardial zone and at the pivot points to the entrance to the CCP. When acceleration of conduction was compensated on a beat-to-beat basis by an equal degree of slowing in the CCP, there was no discernible change in the cycle length of the VT in the ECG. In some episodes, the termination of the original reentrant circuit was followed by the development of a different, slower reentrant pathway that lasted for one or a few cycles prior to termination. (2) In 5 VT episodes, the activation wave front in the CCP abruptly broke across a stable arc of functional conduction block, resulting in premature activation of the CCP and conduction block.
Conclusions Distinct electrophysiological changes always preceded spontaneous termination of stable SMVT. The electrophysiological basis for acceleration of conduction in parts of the reentrant circuit during the last few beats prior to termination and of the abrupt reactivation across a stable arc of block remains to be determined.
Key Words: reentry • arrhythmia • infarction • mapping • tachycardia
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Introduction |
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Sustained monomorphic ventricular tachycardia is not uncommon in patients with previous myocardial infarction and is generally considered to result from circus movement reentry.1 2 The arrhythmia can result in hemodynamic compromise and become life threatening. Spontaneous termination of SMVT is common and can ostensibly prevent potential complications of the arrhythmia. Several clinical studies of ECG changes associated with spontaneous termination of SMVT have been published1 2 but admittedly provide limited insight into the underlying electrophysiological mechanisms. Few studies have investigated the mechanism(s) of spontaneous termination of sustained circus movement reentry in atrial and ventricular models.3 4 The present study is the first to investigate the electrophysiological mechanisms of spontaneous termination of SMVT in a well-documented model of postinfarction circus movement VT in the dog.5 Understanding these mechanisms may help in designing appropriate therapeutic measures.
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Methods |
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Surgical Preparation
The studies were approved by the Animal Studies Committee of the local Institutional Review Board. Details of the procedure have been reported previously and will only be described briefly.6 Experiments were performed on 8 male, mongrel dogs weighing 15 to 25 kg that were preanesthetized with sodium thiopental (17.5 mg/kg IV) via the cephalic vein. The dogs were then anesthetized with inhalation anesthesia (1.0% to 2.0% isoflurane vaporized in 100% oxygen) via a positive ventilation anesthesia machine (F500, The Forreger Co). Under sterile conditions, a left thoracotomy was performed at the fourth intercostal space to expose the heart. The LAD coronary artery was dissected free and ligated in one stage, 1 to 2 cm from its origin. Coronary circulation and potential collateral blood flow were assessed. When necessary, large epicardial branches in the anterior left ventricular free wall and apex originating from the left circumflex or posterior descending coronary artery were also ligated. After the ligation, the dog was monitored in the open chest state for 20 minutes. The chest was then closed in layers and the pneumothorax evacuated. The dogs were allowed to recover and received antibiotic (Penicillin-G procaine, 20,000 U/kg IM) and analgesic (buprenorphine, 0.005 to 0.02 mg/kg) as required.
Four to 5 days after ligation, the dog was again preanesthetized with sodium thiopental (17.5 mg/kg IV) via the cephalic vein and anesthetized with inhalation (1.0% to 2.0% isoflurane vaporized in 100% oxygen) via positive ventilation. ECG lead II and aortic blood pressure (Statham, Gould, Inc) were continuously monitored on a VR12 monitor (PPG Industries). The heart was exposed through a left thoracotomy. Core temperature and intrathoracic temperature were monitored with the use of two electronic thermometers (Yellow Springs Instruments). To slow the sinus rate, a Grass S88 stimulator was used to stimulate the right and left vagosympathetic trunks through two pairs of Teflon-insulated silver wires (.010-in diameter) with square-wave pulses of 0.1- to 0.5-ms duration at a frequency of 20 Hz at 1 to 10 V.7
Isochronal Mapping
A sock electrode array was placed on the ventricular
surface for simultaneous recording at 254
epicardial sites. Each bipolar electrode consisted of a pair of silver
wires (125-µm diameter) sutured to the sock with an interpolar
distance of 0.8 to 1.4 mm. The distance between electrodes ranged
between 2.5 and 10 mm. A higher concentration of electrodes covered the
zone of infarction and infarction border and consisted of 184 bipolar
electrodes. These were arranged in 16 parallel rows, and the distance
between rows was 2.5 mm. Each row consisted of alternating sets of 11
or 12 bipolar electrodes in which the distance between electrodes was
2.8 mm (Fig 1
). Additional details of the
recording technique have been reported
previously.8
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Programmed electrical stimulation was provided by a digital stimulator (model DTU-101, Bloom Co) delivering square pulses (2 ms) through a bipolar plunge electrode consisting of two hooked stainless steel wires (enamel-coated, 125-µm diameter) placed in a 23-gauge hypodermic needle (0.64-mm outer diameter). The stimulation site was in the right ventricle, adjacent to the septal border of the infarct or near the right ventricular outflow tract.
After surgical preparation and sock electrode placement, the ribs were
approximated and the chest cavity was closed. Once the core temperature
had stabilized, programmed stimulation was applied to the control site
to induce reentrant rhythms. The control stimulation sequence consisted
of a train of 8 basic driven beats at two cycle lengths
(S1S1, 400 and 300 ms) at twice
diastolic threshold, followed by one or more premature
stimuli that were introduced at decreasing coupling intervals. The end
point of programmed stimulation was the induction of SMVT defined as VT
with uniform QRS morphology lasting 
30 seconds.
Electrogram recordings of activation during SMVT were obtained through the multiplexed data acquisition system (INET Corp).8 Each channel was sampled at 1 kHz with 12-bit resolution. To capture the spontaneous termination of SMVT, we used a circular memory buffer with an adjustable pretrigger of 0 to 15 seconds (16 Mbytes). Isochronal maps of epicardial activation were constructed with isochrones delineated by closed contours at 10-ms intervals. Activation times at each recording site were identified with the use of previously published criteria.8 The criteria used for activation detection in bipolar electrograms depend on electrogram configuration.9 In uniphasic and triphasic signals, the peak voltage is a reliable predictor of activation time.9 In biphasic signals, the activation time was selected at the maximum slope. Computer-derived activation times were edited by the operator. Arcs of functional conduction block were defined as an activation time difference between contiguous electrodes of more than 40 ms and by the recording of double potential representing an activation and electrotonic potentials that corresponded, respectively, to electrotonic and activation potentials on the other side of the arc of functional block.8 10
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Results |
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We analyzed epicardial activation patterns of spontaneous termination of 20 different episodes of SMVT from 8 dogs (Table
). SMVTs included in the study lasted from 30
seconds up to 10 minutes (mean±SD, 2.8±1.9 minutes). There were 6
more episodes of SMVT that lasted more than 10 minutes and were
terminated by programmed stimulation or direct current shock (Table)
The VT cycle length of SMVTs that lasted 
10 minutes ranged from 170
to 340 ms (mean±SD, 219±45 ms). This was not significantly different
from SMVTs that lasted >10 minutes (mean±SD, 222±39 ms). There was
no correlation between the cycle length, duration, or
ventricular activation pattern of SMVT and spontaneous
termination at 10 minutes. In all episodes of SMVT, the entire
reentrant circuit could be mapped on the epicardial surface. During
SMVT, the mean arterial blood pressure showed a moderate
decrease from 99±18 to 86±16 mm Hg. All VTs showed a characteristic
figure-8 pattern or a modification thereof.10 The figure-8
pattern consisted of clockwise and counterclockwise activation wave
fronts around two separate arcs of functional conduction block that
joined into a common central wave front. Termination of a figure-8 VT
always occurred when the two circulating wave fronts blocked in the
CCP. Four different patterns of spontaneous VT termination were
observed.
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Pattern 1: Acceleration of conduction in both the normal zone and
the pivot points to the entrance to the CCP. This pattern of
spontaneous termination was observed in 7 different episodes of SMVT
and is shown in Figs 2 and 3. Fig 2
illustrates the epicardial activation maps of the last 4 VT cycles,
while Fig 3 shows the ECG lead and selected electrograms along the
clockwise circulating wave front of the reentrant circuit. Enlarged
sections of the polar map as shown in Fig 1
are illustrated. Activation
isochrones are drawn at 10-ms intervals, and the arcs of functional
conduction block are depicted as heavy solid lines. The activation maps
show a modification of a figure-8 circuit. The cycle length of the SMVT
was 240 ms. There was a stable clockwise wave front around a functional
arc of block close to the anterolateral border of the epicardial
ischemic zone. However, the counterclockwise wave front located
in the lower anteroseptal and apical regions was not stable and varied
from beat to beat as the result of changes in the location and
configuration of the zone of functional conduction block. The two
circulating wave fronts joined into a CCP where conduction was
relatively slow, ie, crowded isochrones, compared with conduction
at the outer borders of the arcs of block.
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Fig 3 illustrates the changes in cycle length of the VT at different
sites along the reentrant circuit. The VT cycle length was stable at
240 ms but showed gradual shortening in the last 4 cycles that was more
marked in the last 2 cycles. The last cycle length of VT at site N was
48 ms shorter compared with the stable VT cycle of 240 ms.
Analysis of the activation maps reveal that approximately 20 ms
of the shortening occurred between sites H and J along the outer border
of the anterolateral arc of block, while the rest of the shortening
occurred between sites J and N spanning the pivot point around the arc
of block. The earlier arrival of the circulating wave front to the CCP
resulted in conduction block and termination of circus movement. The
site of block is represented in Fig 3 between electrograms
Q and A, where site A shows an electrotonic deflection. The last QRS
complex of VT had a shorter duration that could be explained by failure
of activation of a large part of the ventricles during the last cycle
of VT. In summary, the spontaneous termination of the SMVT was due to
acceleration of conduction in the last few cycles with earlier arrival
of the circulating wave front to the CCP where conduction block
occurred. The acceleration of conduction occurred both at the
"normal zone" at the outer border of the arc of block and at the
pivot points to the entrance to the CCP.
Pattern 2: Acceleration of conduction in parts of the reentrant
circuit with compensatory slowing in the CCP prior to block. In 5
different episodes of SMVT, spontaneous termination was associated with
gradual acceleration of conduction in parts of the reentrant circuit
associated with a compensatory beat-to-beat slowing of
conduction and eventual block in the CCP. In one episode, there was
lengthening of the last VT cycle length. However, in 4 of the 5
episodes, no significant change in the cycle length of the VT was
apparent in the surface ECG. This is illustrated in Figs 4 and 5. The bottom of Fig 4 shows the
surface ECG and selected electrograms of spontaneous termination of an
episode of SMVT. The top of Fig 4 illustrates the epicardial activation
map of the last stable reentrant cycle
(VT-5) and the next-to-last
reentrant cycle (VT-1). During the
stable figure-8 reentrant circuit, significant slowing of conduction
occurred both at the pivot points to the entrance to the CCP and in the
CCP itself. This is illustrated by the conduction delay between sites I
and J and between sites K and A, respectively. During the last 5
reentrant cycles, there was a gradual acceleration of conduction around
the pivot points of the entrance to the CCP associated with
compensatory gradual slowing of conduction in the CCP. Finally,
conduction block developed between sites K and A in the CCP, resulting
in termination of reentry.
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Fig 5 illustrates the gradual acceleration of conduction between sites
I and J associated with gradual slowing of conduction between sites K
and A. Note the gradual shortening of the interval between the
electrotonic and activation potentials in electrogram J. Also note the
gradual widening of the duration of electrogram K associated with
gradual increase of the conduction time between K and A and the
shortening of the duration of the last K potential associated with the
development of conduction block between K and A. The conduction time
between sites I and A showed minor oscillations; however,
the duration between surface QRS complexes was almost constant. The
changes of conduction in the central part of the reentrant circuit
could not have been detected by analysis of the intervals
between electrograms outside this zone.
Pattern 3: Acceleration of conduction of the last one or few cycles
with termination of the original VT and initiation of a different
short-lived slower circuit. This pattern of spontaneous
termination was observed in 3 different episodes of VT and is
illustrated in Figs 6 through 10. Fig 6 illustrates the
isochronal activation map of the original stable VT circuit. The
circuit consisted of a counterclockwise wave front around an arc of
functional conduction block at the anterolateral border of the
epicardial ischemic zone and a clockwise wave front around a
separate arc of block at the apical region of the ischemic
zone. The two wave fronts joined into a broad, common wave front. Note
that the arcs of functional conduction block are long and that most of
the slowed conduction took place at the pivot points around the end of
the arcs of block rather than in the broad CCP.
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Fig 7 shows the surface ECG lead and selected
electrograms of the counterclockwise wave front of the last 6 VT cycles
prior to termination. The stable VT cycle length of 185 ms is
represented by VT-5.
There was a 10-ms progressive shortening of the cycle lengths of
VT-3 and
VT-2 (see electrogram Q) that
resulted in termination of the original reentrant circuit (see block
between electrograms R and S). This was followed by the development of
different slower reentrant wave fronts that lasted for two complete
cycles (VT-2 and
VT-1) before it terminated
(VT).
Fig 8 illustrates the epicardial activation maps of the
last 6 reentrant cycles (VT-5 to
VT). The VT-5 map
represents the last stable VT cycle. The maps of
VT-3 and
VT-2 illustrate the acceleration of
conduction of the circulating wave fronts, with an earlier arrival of
the wave front to the entrance of the CCP resulting in conduction block
and termination of the original reentrant circuit as shown in
VT-2. However, reentrant excitation
continued in the form of a very slow and circuitous wave front at the
apical region that circulated for two cycles before it blocked with
termination of VT.
Fig 9 illustrates in more detail the acceleration of
conduction of the counterclockwise wave front during
VT-3 and
VT-2. The acceleration of
conduction occurred primarily in the "normal zone" along the
outer border of the arc of block between electrode sites K and g. Fig 10 illustrates in more detail the complex activation
pattern of the last 3 reentrant cycles,
VT-2,
VT-1, and
VT, as well as selected electrograms along the
reentrant pathway. The electrograms show bridging of the
diastolic intervals. However, the resolution of
recording sites was inadequate to accurately map the details of
the slow and circuitous reentrant pathway.
Pattern 4: Breakthrough of the reentrant wave front across a stable
arc of functional conduction block resulting in premature activation
and conduction block in the CCP. This mechanism of spontaneous
termination of SMVT was observed in 5 different episodes and is
illustrated in Figs 11 through 13. Fig 11 illustrates
the activation map of the stable VT represented by
VT-2. The circuit had a figure-8
pattern in the form of clockwise and counterclockwise wave fronts that
joined into a long CCP. The CCP narrowed significantly in the middle
portion as the result of extension of the arcs of functional conduction
block. Fig 12 shows the surface ECG lead and selected
electrograms of spontaneous termination of the SMVT. The last QRS of
the VT is inscribed prematurely and has a different configuration.
Electrogram X represents a site in the middle of the CCP very
close to the lateral arc of functional block, while electrogram C
represents a contiguous site on the other side of the arc of
block. Electrogram X has two deflections, one of which is marked by an
asterisk and represents activation, while the second deflection
represents the electrotonus of the activation potential at the
contiguous site C across the arc. Also note the presence of a
low-amplitude electrotonic potential in electrogram C corresponding
to the activation potential of X. Fig 13 illustrates
the activation maps of the last two VT cycles. During the
VT-1 cycle, the activation wave
front at site X suddenly reactivated site C across the arc
of functional block. This is represented in electrogram C
in Fig 12 by a series of slow deflections that started at the
electrotonic potential and ended by a sharper activation potential. The
slow conduction between sites X and C was approximately 40 ms (see the
enlarged section in Fig 13). Once site C was reactivated,
the wave front circulated in both clockwise and counterclockwise
directions around the lateral arc of block. The clockwise wave front
then prematurely conducted to the narrow isthmus of the CCP, resulting
in conduction block and termination of reentry (the VT
map). Fig 12 shows the site of block between electrograms M and N.
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Comparison of SMVT that spontaneously terminated within 10 minutes
with SMVT that lasted >10 minutes. The Table shows that the cycle
length of the 6 episodes of SMVT that lasted >10 minutes was not
significantly different from SMVT that spontaneously terminated within
10 minutes. The cycle length of the nonterminating SMVT remained
constant until the arrhythmia was terminated by programmed
stimulation or direct current shock. In one experiment (No. 3), an SMVT
with a similar activation pattern was induced twice, and both times it
terminated spontaneously as the result of acceleration of conduction in
the last few cycles. In two other experiments (Nos. 1 and 6), an SMVT
with similar activation pattern was induced twice in the same
experiment, and only one of the episodes terminated spontaneously. The
spontaneous termination was due to abrupt acceleration of conduction in
the last few cycles. By contrast, the similar episode that failed to
terminate within 10 minutes maintained a constant cycle length.
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Discussion |
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The present study illustrates some of the topological variations of the classic figure-8 reentrant circuit. Although the typical topology is in the form of two circulating wave fronts that join into a CCP, in some instances a single, stable, circulating wave front could sustain the reentrant process as shown in Fig 2
. We have
shown previously that a single reentrant loop also could develop in a
syncytium if the functional block extends to an anatomic barrier, as in
the case of circus movement atrial flutter.11 The topology
and degree of slow conduction in the CCP can also vary. A relatively
short and narrow CCP is usually associated with markedly slow
conduction, as shown in Fig 4, while conduction velocity may or may not
be significantly slowed in a circuit with a long and broad CCP as shown
in Figs 2 and 6. In both types of figure-8 circuits, however, a major
component of conduction delay takes place at the pivot points around
the two arcs of functional conduction block and especially at the
entrance to the CCP. The slowing of conduction at the pivot points of
the reentrant circuit could be related primarily to alterations in
current loading resulting from the pivoting process that depresses
excitability and slows local conduction.12 13 Although
there was no attempt in the present study to correlate precisely
the location of the arcs of functional conduction block in relation to
epicardial fiber orientation, in many instances the arcs appeared to
occur both along and across fiber orientation.8
The present study showed essentially two basic mechanisms for
spontaneous termination of SMVT. The first mechanism is an acceleration
of conduction in some parts of the reentrant circuit leading to
premature activation and block in the CCP. The acceleration of
conduction could be associated with slowing of conduction prior to
conduction block in the CCP. The acceleration of conduction occurred in
the last few cycles of VT and was either gradual in nature (Figs 5 and 9) or irregular (Figs 2 and 3). The acceleration of conduction occurred
both at the outer border of the arcs of functional conduction block,
ostensibly in "normal" myocardial zones, and at the pivot points
to the entrance to the CCP where conduction is usually slowed. The
acceleration of conduction around the pivot points was not associated
with any discernible shortening of the length of the arc. Although in
most instances the acceleration of conduction represented
the primary event that was followed by slowing of conduction in the
CCP, in one instance it was difficult to exclude as a primary event the
slowing of conduction in the CCP with compensatory acceleration in
other parts of the reentrant circuit. When the acceleration of
conduction was compensated on a beat-to-beat basis by an equal
degree of slowing in the CCP, there was no discernible change in the
cycle length of VT prior to termination, as seen in the surface ECG or
in electrograms outside the reentrant circuit (Figs 4 and 5). In three
different episodes of SMVT, the termination of the original reentrant
circuit was followed by the development of different slower circulating
wave fronts that lasted for one or few cycles prior to termination
(Figs 6, 8, and 10). In these episodes, marked variations in the last
few VT cycle lengths in the surface ECG were observed in the form of
shortening, followed by lengthening of one or more cycles.
The second mechanism of spontaneous termination of SMVT was more
intriguing. During SMVT, the activation wave front in the CCP abruptly
broke across a stable arc of functional conduction block, resulting in
premature activation of the CCP leading to conduction block. This
process was associated with slowed conduction at the site of
reactivation across the arc (see Figs 12 and 13). Premature activation
across the arc suggests that the intensity of the local electrotonic
current provided to that site by the activating current on the other
side of the arc has reached the threshold voltage for a propagated
activation. This could be due to changes of passive or active membrane
properties at the current source, ie, the activating wave front or the
current sink, ie, the reactivated site. These changes are
usually rate dependent.14 However, we were not able to
discern any changes in the cycle length of VT, the amplitude, or the
configuration of the local electrograms prior to the abrupt
reactivation across the arc.
The episodes of SMVT that failed to terminate within 10 minutes maintained a constant cycle length. The number of observations was too small to answer the question of whether acceleration of conduction in parts of the circuit can occur without spontaneous termination. However, in the two experiments in which an SMVT with a similar activation pattern was induced twice, the one episode that terminated spontaneously showed acceleration of conduction in the last few cycles as contrasted with the constant cycle length of the nonterminating episode.
Several clinical studies analyzed the ECG correlates of spontaneous termination of SMVT in patients with coronary artery disease. Some studies showed no specific patterns of cycle length variability characteristic of VT termination, although cycle length variability increased immediately before spontaneous termination.1 A change in QRS morphology occurred before termination in only a small percentage of VT episodes.1 Transient shortening of QRS just before termination and paradoxical prolongation of the QRS to the peak of T-wave interval after abrupt shortening of VT cycle length were also described.2 It is difficult to relate any of these ECG changes to a particular electrophysiological mechanism.
On the other hand, there are few basic studies of the mechanism of spontaneous termination of sustained reentry. Simson et al15 demonstrated in a computer model of atrioventricular reentrant tachycardia that for a reentrant circuit to continue, it must be able to dampen spontaneous oscillations in conduction and refractoriness. Frame and Simson3 later investigated the mechanism of cycle length oscillation and its role in spontaneous termination of reentry in an in vitro preparation of canine atrial tissue surrounding the tricuspid orifice. Oscillations caused most spontaneous terminations in this model. Two dynamic tissue properties, interval-dependent conduction and interval-dependent changes in action potential duration, ie, electrical restitution, were sufficient to explain the local changes in conduction that contribute to the oscillations and the mechanism by which oscillations caused termination. Cycle length oscillations were not observed in the present study and were not reported in clinical ECG studies of spontaneous VT termination.1 2
Brugada et al4 have shown in a reentry model in rings of anisotropic left ventricular epicardium of the rabbit that termination of VT could occur by collision of the circulating impulse with a spontaneous antidromic wave front reflected within the circuit. This phenomenon occurred when the circulating impulse encountered an arc of functional conduction block that did not extend along the whole width of the ring. As a result, the impulse dissociated into a continuing orthodromic circulating wave and a returning antidromic echo wave caused by microreentry within the ring. Such a mechanism was not observed in the present study.
In a preliminary report by Waldecker et al,16 the mechanisms of spontaneous termination of SMVT in the canine postinfarction heart were investigated. Conduction slowing in the CCP prior to block and abrupt activation across the arc of block were observed. However, acceleration of conduction in parts of the reentrant circuit as a primary event prior to slowing of conduction in the CCP was not observed. Further, in 9 of 21 episodes of VT, no changes in conduction or cycle length were observed, and the mechanism of termination was not discernible. This is in sharp contrast to the present study, in which distinct electrophysiological changes always preceded spontaneous termination of SMVT.
Limitations of the Study
As in many studies on mapping of cardiac activation, the
resolution of the activation map is directly related to the number and
density of recording sites. Although the present study used
relatively high-resolution recordings in the
ischemic zone, some fine details of activation could not be
analyzed adequately. These include but are not limited to
details of the changes of conduction at the pivot points to the CCP
prior to block (Fig 3), the circuitous conduction in some of the
reentrant circuits (Fig 10), and the nature of the very slowed
conduction in some CCP, as in Fig 4 (possibly a markedly circuitous
wave front).
The most significant limitation of the present study, however, is that it provides no explanation of the apparently sudden acceleration of conduction in parts of the reentrant circuit prior to termination. We can only speculate that this may be related to a local change in the autonomic tone and/or circulating catecholamines. In a previous study we have shown differential effects of these changes on refractoriness and conduction of the normal and ischemic zones of the postinfarction canine heart.17 The trigger for such changes, however, remains unclear. In this regard we were not able to discern any changes in the arterial blood pressure immediately prior to termination. An alternative mechanism for acceleration of conduction is suggested by the work of Davidenko et al,18 who showed that the excitability of normal myocardium may increase during activity, ie, active facilitation. Primary slowing of conduction in the CCP, possibly a "fatigue" phenomenon, with secondary acceleration of conduction in other parts of the circuit may be operational in some episodes of VT termination but was not observed in the present study. More intriguing is the mechanism by which a passive electrotonus can suddenly reach threshold and trigger active propagation. These basic hypotheses require further investigation.
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Selected Abbreviations and Acronyms |
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Acknowledgments |
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This work was supported by Veterans Administration Medical Research Funds (Merit Grants) to Dr El-Sherif and Dr Restivo. The authors would like to thank Antoinette Wells and her staff in the animal facility, Mohammed Piracha, and Richard Levin for their technical assistance and Valerie Sussman for typing the manuscript.
Received August 23, 1995; revision received October 18, 1995; accepted October 20, 1995.
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