(Circulation. 1997;96:3721-3731.)
© 1997 American Heart Association, Inc.
Articles |
Mechanisms Causing Sustained Ventricular Tachycardia With Multiple QRS Morphologies
Results of Mapping Studies in the Infarcted Canine Heart
From the Departments of Pharmacology and Medicine, College of Physicians and Surgeons, Columbia University, New York, NY.
Correspondence to James Coromilas, MD, Department of Medicine, Columbia University, College of Physicians and Surgeons, 630 W 168 St, New York, NY 10032.
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Abstract |
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Background Sustained reentrant ventricular tachycardias (VTs) with different QRS morphologies have been observed to occur spontaneously and during programmed stimulation in human hearts. We determined mechanisms that can cause tachycardias with multiple morphologies in a canine model of myocardial infarction by mapping reentrant circuits.
Methods and Results Reentrant VT with multiple QRS morphologies was induced in 11 canine hearts with 4-day-old infarcts. Comparison of activation maps of the reentrant circuits in the epicardial border zone associated with each morphology indicated two basic mechanisms. Less frequently, VTs of different morphologies in the same heart were caused by reentrant circuits in different regions of the infarct. Most commonly, the reentrant circuits associated with different morphologies were in the same region. Three different factors caused different exit routes from circuits in the same region, leading to the multiple morphologies. (1) The reentrant wave front for each morphology rotated around the same line of block but in different directions. (2) Reentrant circuits associated with each morphology were similar, but there were small changes in the extent of the central line of block. (3) Reentrant circuits with completely different sizes and shapes caused different morphologies.
Conclusions In this canine model, tachycardias with multiple morphologies most commonly arise from reentrant circuits in the same region of the infarct, suggesting that most often only one area has electrophysiological properties necessary to sustain reentry.
Key Words: tachycardia • reentry • anisotropy • mapping
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Introduction |
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Between 25% and 40% of patients with sustained monomorphic ventricular tachycardia (VT) caused by a reentrant mechanism and associated with ischemic heart disease have been shown to have spontaneous episodes of tachycardia with multiple QRS morphologies.1,2 A larger percentage of patients (25% to 67%) have had tachycardias with multiple morphologies induced by programmed stimulation during electrophysiological studies.1–4 Patients with multiple-tachycardia morphologies are less likely to have successful electrophysiology-guided antiarrhythmic therapy,4 map-guided endocardial resection,5 or catheter ablation.6,7
The mechanisms causing multiple VT morphologies are unclear. On the basis of clinical mapping studies using either single-site, sequential activation mapping or limited simultaneous multielectrode mapping, several possible mechanisms have been proposed. One is that tachycardias with different morphologies arise from different reentrant circuits, located either in widely separated or in closely adjacent areas.1,5,8,9 A second proposed mechanism is that multiple morphologies are caused by different exit routes from the same reentrant circuit.1,9,10
For additional details concerning the mechanisms that might cause tachycardias with multiple QRS morphologies, mapping of the pattern of activity in the reentrant circuit or circuits associated with the different tachycardia morphologies is necessary. At the present time, such detailed mapping is not done routinely in clinical studies, although it has sometimes been done.8,9,11 Reentrant circuits can be mapped, however, during sustained VT in a canine model of myocardial infarction.12,13 As in the clinical cases, multiple tachycardia QRS morphologies occur in the same heart, providing the unique opportunity to determine mechanisms that can cause VTs with multiple morphologies. A preliminary report of our results has been presented in abstract form.14
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Methods |
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Canine Model of Myocardial Infarction
Adult mongrel dogs weighing 30 to 40 kg underwent a two-stage ligation of the left anterior descending coronary artery (LAD)
1 cm from its origin, producing a transmural anterior septal
myocardial infarction.13,15 Four to 5 days later,
electrophysiological studies were performed
on the dogs that survived.
Experimental Preparation
For the electrophysiological study,
the animals were anesthetized with intravenous
pentobarbital sodium (30 mg/kg), intubated, and ventilated. The
heart was exposed via a median sternotomy, and a flexible electrode
array was sutured over the infarcted area,15 with its
margins extending onto noninfarcted myocardium. A heating
lamp was used to maintain the temperature at the surface of the heart
between 37°C and 38°C. Blood pressure recorded with a femoral
artery catheter and two ECG leads (I and II or III) were continuously
displayed on an Electronics for Medicine DR12 oscillographic
recorder.
Electrode Array and Recording Instrumentation
The electrode array for mapping the epicardial border zone in
the infarcted region13,15 consisted of 292 bipolar
electrodes. Each bipole was formed by two 1-mm-diameter silver disks
2 mm apart. The electrodes were arranged in two overlapping
groups. One group of 192 electrodes was spaced evenly over the entire
9x13-cm array (interelectrode distance of 5 to 10 mm), and the
other group of 192 was concentrated in a 5.5x5.5-cm square at the
center (5 to 7.5 mm between each bipole).15 One of the
two groups could be selected with a switch box for
simultaneous recording. The signals were led to
preamplifiers with automatic gain control and then were multiplexed,
digitized, and stored on wide-band tape (Ampex PCM
System)13 along with the two surface ECGs and blood
pressure. Stimulating electrodes in the electrode array were at the
basal margin, the left lateral margin, and the center as well as on the
right ventricle adjacent to the LAD.15
Electrophysiological Study
VT was initiated by single or double extrastimuli (2 to 4 times
diastolic threshold) during pacing at different basic cycle
lengths or by rapid overdrive pacing from all pacing sites. Sustained
VT was defined as tachycardia originating in the ventricles
lasting longer than 30 seconds, during which blood pressure remained at
a mean value of >50 mm Hg. All VTs were monomorphic.
The QRS morphology of the tachycardias was classified from two orthogonal ECG limb leads as follows: (1) R in which the complex was predominantly an R wave with a small or no Q wave and S wave, (2) QS in which the complex had a small or no R wave, (3) RS in which the complex had an R wave at least 1/4 of the amplitude of the S wave, and (4) QR in which the complex had a Q wave at least 1/4 of the amplitude of the R wave. An experiment was classified as having tachycardias with different QRS morphologies if the morphology was different in at least one of the two leads. This classification is not quantitative and lacks a high degree of sensitivity; it may sometimes have failed to distinguish between different morphologies. However, it does possess a high degree of specificity, ensuring that what we classified as different morphologies always were different morphologies.
Activation Maps
We have previously described our methods for determining local
activation times, drawing isochrones, and designating regions of
conduction block.13,15 We also determined the probable exit
route of the reentrant impulse from the circuit to the ventricles and
correlated the exit route with the QRS morphology. Since the epicardial
border zone lacks, for the most part, intramural
connections,13 the reentrant impulse usually enters the
rest of the ventricle from one of its margins at the edges of the
electrode array.16 Therefore, the region of the electrode
margin that is activated within 20 ms before the onset of the
QRS during tachycardia is designated as the exit
route.16 This was also verified by pacing during sinus
rhythm from the site designated as the exit route to show that the QRS
had a morphology similar to that during tachycardia.
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Results |
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Occurrence of VTs With Multiple Morphologies
In 17 of 42 experiments with sustained VT, tachycardias with more than 1 morphology were induced: 2 morphologies in 14 experiments, 3 morphologies in 2 experiments, and 5 morphologies in 1 experiment. Complete reentrant circuits were mapped in the epicardial border zone for all tachycardia morphologies in 11 of the 17 hearts, 3 of which had more than 2 morphologies, for a total of 27 morphologies. Fourteen of these morphologies were induced a total of 60 times with the same reentrant circuit and exit route associated with the same morphology on more than one induction for 12 of the 14. Two morphologies had both the same and different circuits, but the exit routes were the same for each induction of a given morphology. Thirteen morphologies were induced only once. Mechanisms for multiple morphologies are based on the data obtained from these 11 hearts.
Different Morphologies Due to Reentrant Circuits Around Lines of
Block Located at Different Sites
This group of tachycardias in three experiments is
characterized by reentrant circuits around lines of functional block
(not present during sinus rhythm) at distinctly different sites in
the epicardial border zone (located at least 1 cm apart). Reentrant
circuits at different sites were associated with different exit routes
to the ventricles that caused the different QRS morphologies. In Fig 1A
, recorded during one episode of
tachycardia (cycle length, 204 ms), the QRS complexes are
classified as R waves in both leads I and II. In Fig 1B, recorded
during another episode in the same heart (cycle length, 175 ms), the
QRS complexes are classified as QS in both leads.
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The reentrant circuit that is shown in Fig 2A was associated with the QRS morphology
of the tachycardia in Fig 1A
. A single loop (arrows) occurs
around a long functional line of block located toward the apical area
of the epicardial border zone (longest dark black line); electrograms
in the circuit are displayed to the left. Several other shorter lines
of block are not part of the circuit. To the right are electrograms
from a region that is not part of this reentrant circuit but that were
in the circuit associated with the second tachycardia
morphology (see below).
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During this tachycardia, the junction of the LAD and apical
margins of the electrode array (asterisks in Fig 2A) was designated as
the exit route from the reentrant circuit. Fig 1A shows that
electrograms recorded at these margins of the border zone (37 and
21 enclosed by the diamonds on the map in Fig 2A) occur just before the
onset of the QRS complex. Electrograms recorded from other sites
around the margin occur during or at the end of the QRS. The QRS
complex during pacing from the LAD-stimulating electrodes resembles the
QRS during tachycardia (Fig 1C), although it has a deeper
initial Q wave, probably because it is not at the exact same site
designated as the exit route.
The activation map during the tachycardia with the second
morphology (Fig 1B), shown in Fig 2B, consists of a single reentrant
loop (arrows) around a functional line of block in the center of the
epicardial border zone, 4 cm from the line of block associated with
the first reentrant circuit. The reentrant wave front is moving in the
opposite direction. Several other short lines of block are not
associated with it. The electrograms at the right are from sites around
the circuit, the same sites that were not part of the circuit during
the tachycardia in Fig 2A (at the right). Conversely, the
electrograms shown at the left in Fig 2B are from the sites at which
the first reentrant circuit was located (Fig 2A, left) and are not in
this second circuit.
During this second tachycardia, the LL margin of the
epicardial border zone was designated as the exit route (asterisks on
map in Fig 2B). As shown in Fig 1B, the electrogram (LL) recorded
at this site occurred just before the onset of the QRS, whereas
electrograms recorded at other margins occurred during or just
after the QRS. Pacing from the electrodes on the lateral margin near
the designated exit site resulted in a QRS complex that resembled the
QRS during tachycardia (Fig 1D).
The activation maps described in Fig 2 are
representative of the maps from other experiments in
this group. When reentrant circuits occurred at different sites, at
least one of the circuits consisted of only one wave front circulating
around a single line of block in the mapped region rather than a
figure-eight circuit.12
Different Morphologies Associated With Circuits in the Same Area of
the Epicardial Border Zone
In all 11 experiments, reentrant circuits and their central lines
of functional block associated with different QRS morphologies in each
heart were located in the same region of the epicardial border
zone, including the three experiments that had circuits at distinctly
different locations, because each had several different morphologies at
one of the different sites. Despite the similar location of circuits
associated with different morphologies in this group, each morphology
was associated with a distinctly different exit route from the
circuit.
Propagation of Wave Fronts in Opposite Directions Around Similar
Reentrant Circuits
In eight hearts, different QRS morphologies were associated with
reentrant wave fronts moving in opposite directions around the same
line of block. Fig 3A and 3B shows ECGs
of two tachycardias in one of these hearts. The QRS in
panel A (cycle length, 227 ms) is classified as QS in both leads, and
the QRS in panel B (cycle length, 240 ms) is classified as QR in lead I
and R in lead II. The activation map of the VT in Fig 3A is shown in
Fig 4A. One reentrant wave front moves in
a counterclockwise direction (arrows) around a long line of functional
block toward the LL margin. Electrograms in the circuit are below.
Another long line of functional block formed parallel and to the left
of the first one. Activation moves clockwise around the upper end of
this line from the 20-ms isochrone to the 90-ms isochrone.
(This wave front may have conducted slowly across the line of apparent
block, because the 20-ms isochrone is parallel to the
line.13) This clockwise wave front lags behind the
counterclockwise wave front, which is already halfway through the
central common pathway (between the two lines of block) by 90 ms and
does not finish a complete revolution. The exit site is designated
between the apex and the lateral margin (asterisks).
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The activation map of the VT in Fig 3B is shown in Fig 4B. The line of
block toward the lower right and lateral margin is in exactly the same
location as it was during the first tachycardia in Fig 4A.
However, the reentrant wave front moves around this line in the
opposite (clockwise) direction (see electrograms in the circuit below
the map recorded from the same sites as in A). The midportion of
the second line of block at the upper left is also unchanged, but the
ends are slightly altered. Arrival of the wave front that moves
counterclockwise around this line of block, at the apical entrance to
the central common pathway, also lags behind arrival of the wave front
from the opposite line of block, and it may not complete a reentrant
cycle. The exit site occurred between the LAD margin and the base
(asterisks).
In other experiments in this group, reversal of the reentrant wave front around the same line of block also resulted in switching of the exit route from one margin of the array to the opposite margin.
Propagation of Wave Fronts in the Same Direction Around Similar
Reentrant Circuits
In three hearts, different QRS morphologies were
associated with reentrant wave fronts moving in the same direction
around the same line of block. Fig 3C and 3D shows ECG tracings from
one of these hearts. In 3C, the morphology is classified as QR in lead
I and as R in lead II (cycle length, 220 ms). In 3D, the QRS is
narrower and is classified as QS in lead I and R in lead II (cycle
length, 278 ms).
In Fig 5A (the circuit associated with
the QRS in Fig 3C), two wave fronts (arrows) rotate around nearly
parallel lines of functional block in a figure-eight
pattern.12 The counterclockwise wave front entered the
central common pathway 50 ms after the clockwise wave front and
therefore did not complete the circuit. Activation also may occur
slowly and simultaneously across the lower line of block
between circled activation times 48 and 98 (small straight arrows),
because the isochrones on the distal side of this line are parallel
to it.13 The fractionated electrogram
recorded at site 48 (see electrograms below) is also
consistent with this interpretation. This is characteristic of
anisotropic reentry.13 The LAD margin was designated as the
exit route (asterisks).
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The reentrant circuit shown in Fig 5B was associated with the second
QRS morphology (Fig 3D). The wave front in the central common pathway
between the lines of block moves toward the LAD margin as before.
However, the clockwise wave front turns to the right earlier than in
Fig 5A and moves more rapidly through the region (circled electrograms
with activation times 51, 63, and 92) in which there was a line of
apparent block during the reentry that was described in Fig 5A.
Activation time is 29 ms between circled electrode sites 63 and 92,
whereas in the map in Fig 5A, the time was 50 ms (between circled sites
48 and 98, which are the same sites as in B). Therefore, the right line
of block is shortened. The counterclockwise wave front still trails the
clockwise wave front as it enters the apical end of the central common
pathway. Activation of the LAD margin (asterisks) and the left lateral
margin (asterisks) occur nearly simultaneously and are both
designated as the exit routes. The earlier activation at the LL margin
(compared with Fig 5A) resulting in its becoming an exit route was a
consequence of the change in the right line of block. This example
shows that only small changes in the reentrant circuit can result in
alteration of the QRS morphology.
Different Reentrant Circuits and Lines of Block in the Same
Region
In three hearts, different QRS morphologies were associated with
different reentrant circuits at the same site. Fig 6 shows ECGs of two different
tachycardias in one of these hearts. The morphology in
panel A (cycle length, 165 ms) is classified as RS. The morphology in
panel B (cycle length, 156 ms) is classified as QS. The activation map
during the tachycardia in Fig 6A shows a double loop
(figure-eight) reentrant circuit (Fig 7A, center panel), with rotation of two wave fronts (arrows) around two
lines of functional block. Electrograms around the right circuit are
shown at the left. The LAD margin (asterisks) is the exit route. An
electrogram from this margin activated at 48 ms (enclosed in
the diamond on the map) is shown below the ECG in Fig 6A. Also shown in
Fig 6A are electrograms recorded from other margins of the
electrode array that were activated after the onset of the
QRS.
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The map during the VT with the second morphology (Fig 6B) is shown in
Fig 7B. It shows a single circuit (arrows) (electrograms at the right)
around a small unexcited area (cross-hatches) that showed occasional
activation, indicating a high degree of conduction block. The apical
margin represents the exit route (asterisks). An electrogram
recorded from the apical margin activated at 65 ms
(enclosed within the diamond on the map) occurred just before the onset
of the QRS and is shown below the ECG in Fig 6B, along with
electrograms recorded from the other margins of the electrode
array. Note that the LAD margin is now activated late.
Therefore, the two tachycardias described are located in
the same area with overlapping reentrant circuits. Each circuit has a
different size and shape and exit route.
Mode of Onset of VTs With Multiple Morphologies
Initiation by Programmed Stimulation of Tachycardias
With Different Morphologies
In five experiments, sustained VTs with different QRS morphologies
were associated with different sites of stimulation. The initial lines
of block that formed during conduction of the premature impulses from
different sites were in distinctly different regions. This in turn
influenced either where the stable line(s) of block formed in the
reentrant circuit, the direction in which the reentrant wave front
circled around the stable line of block, or both. Fig 8A is initiation of
tachycardia by a premature stimulus delivered through the
lateral electrodes (coupling interval, 135 ms at a basic drive cycle of
280 ms), and Fig 8B shows initiation with the premature stimulus
through the LAD electrodes in the same heart (coupling interval, 150
ms; basic drive cycle, 280 ms). The maps in Fig 9A through D are from the initiation at
the lateral margin (ECG in Fig 8A). Activation of the border zone
(arrows) during the basic drive did not show any evidence of conduction
block (Fig 9A). The premature impulse, however, blocked (small arrows
and horizontal heavy black line) (Fig 9B), with propagation around both
ends of this line to the opposite side (large curved solid and open
arrows). The wave fronts then conducted retrogradely through this line
of block (Fig 9C, isochrones 10 to 40) to form the reentrant
circuit shown in Fig 9D. In this case, the line of block at the center
of the single reentrant circuit is part of the same line of block that
occurred during block of the initiating premature impulse. Exit from
the epicardial border zone occurred at the LL margin (asterisks). The
activation maps of initiation of the second morphology in this heart
from the LAD margin (Fig 8B) are shown in Fig 10. Fig 10A shows activation by the
basic drive. Conduction block of the premature impulse (Fig 10B)
occurred toward the LAD margin (heavy black line) at a different site
from the block caused by lateral stimulation (compare with Fig 9B).
Conduction of the premature impulse occurred around both ends of the
line of block to the opposite side (curved solid arrows). Reemergence
of the premature impulse retrogradely through the line of block (shaded
region) is shown in Fig 10C. This resulted in the formation of two
widely separated smaller lines of block, perpendicular to the first
one, around which two wave fronts rotated during sustained
tachycardia (Fig 10D). The exit route from this circuit was
at the LAD margin (asterisks). In this example, the initial line of
block did not become part of the line of block in the stable reentrant
circuit, which is a much more common occurrence than the pattern shown
in Fig 9. One of the reentrant wave fronts in Fig 10D moved in the
opposite direction to the reentrant wave front in Fig 9D because of the
different site of initiation. In other experiments (not shown), lines
of block occurred in the same place despite the different sites of
stimulation, but the reentrant wave fronts rotated in opposite
directions because of the different initiation sites.
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Sustained tachycardias with different QRS morphologies were
initiated in five hearts by stimulation at the same site with the same
(four experiments) or different (one experiment) stimulation patterns
(Fig 8C and 8D). Like the activation maps shown in Figs 9 and 10, when
stimulation at the same site resulted in different QRS morphologies,
the lines of block caused by premature activation occurred in different
regions, causing different reentrant circuits, although the direction
of activation was usually the same.
Spontaneous Change in Tachycardia Morphology
In one experiment (described in Figs 3C and 3D and 5), the
morphology of a monomorphic tachycardia that was stable
changed spontaneously (Fig 11).
Spontaneous shortening of one of the lines of block (Fig 5) resulted in
a change in the exit route from the LAD margin (LAD electrograms
indicated by asterisk, which precede onset of QRS during the first two
beats in Fig 11) to simultaneous exits from the border zone
at both the LAD and lateral (LL) margins (LAD and LL electrograms
indicated by asterisks, which precede QRS during the last two beats).
The reason for the change in the line of block is not apparent.
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Discussion |
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In this canine model of healing myocardial infarction, sustained VTs with different QRS morphologies can be induced in the same heart by programmed stimulation, similar to observations in some patients with sustained tachycardia.1–4 Detailed mapping allowed us to determine the mechanisms for the different QRS morphologies.
Multiple Morphologies Caused by Reentrant Circuits in
Different Regions
There is a relatively low incidence of reentrant circuits at
separate sites causing sustained tachycardias with multiple
morphologies both in this laboratory model (18% of multiple
morphologies) and in infarcted human hearts (11% to
47%).1,5 In the canine model, in which functional
anisotropic reentry is an important cause of
tachycardia,13 it appears that only limited
regions of the epicardial border zone are capable of forming stable
lines of functional block and have anisotropic conduction properties
suitable for maintaining sustained reentry after programmed
stimulation. The appropriate characteristics of block and conduction
probably depend on how the infarction process has shaped the
microanatomy of the epicardial border zone, which influences
its electrophysiological properties. The
functional lines of block of stable reentrant circuits form in the
thinnest regions, in which there are boundaries between
myocardium with normal gap junctional distribution and gap
junctional disarray.17 The cause of the disarray and how it
predisposes a region to conduction block are not known. It is possible
that in hearts with reentrant circuits in different regions, such
boundaries occur at several different locations while occurring in only
one region in hearts that do not have stable circuits at different
sites. The occurrence of multiple regions with appropriate properties
for lines of block and anisotropic conduction would seem to be more
likely in hearts with larger infarcts or several discrete infarcted
regions, but we did not quantify infarct size in this study. Patients
with multiple infarcts, in whom total infarct size might also be
larger, are more likely to have more than one tachycardia
morphology occurring spontaneously, arising at sites that are
designated as being different by clinical
criteria.1,2,5
The cause of reentry in human hearts with healing or healed infarction may sometimes be functional11,18 and other times have an anatomic basis.19 Nevertheless, it is still necessary that different regions have appropriate anatomic and electrophysiological properties to support different stable reentrant circuits if multiple morphologies are to result from circuits at different sites. The likelihood of this occurring may be related to the extent of ischemic damage.
Multiple Morphologies Associated With Reentrant Circuits Located in
the Same Region
We found that different QRS morphologies are most commonly
associated with reentrant circuits in the same region of the infarcted
ventricles, as have clinical studies based on activation mapping, often
with less spatial resolution.1,6,8–11,20–23 Our results
provide new information on possible mechanisms whereby functional
reentrant circuits in the same region can lead to different QRS
morphologies.
In anatomic reentrant circuits, exit routes to the ventricles are most
likely through anatomically distinct pathways. The number and location
of these pathways may determine whether multiple-morphology
tachycardias occur. Conversely, functional anisotropic
reentrant circuits in the canine model are connected to the ventricles
around their entire circumference at the margins of the epicardial
border zone. The exit route is most often at either the LAD or lateral
apical margins; the wave front conducts most rapidly along the
longitudinal axis of the muscle fiber bundles toward these margins,
whereas conduction toward the base or apical margins is in the slow
transverse direction, leading to delayed activation at these
margins.13,16 Usually the exit route is only at one margin
(LAD or lateral-apical) instead of both. This is the margin that is
reached when the ventricles have recovered excitability. Activation of
both margins usually occurs within half a reentrant cycle; one margin
is usually activated during diastole and the other
during the QRS or T wave, while the ventricles are refractory.
Illustration of this point is the pattern of activation in Fig 5A. The
LAD margin is activated at 105 to 110 ms (asterisks), just
before the onset of the QRS, while the lateral margin is
activated nearly half a reentrant cycle later during the end of
the QRS (Fig 11). In general, when the LAD region is activated
first, the QRS complex is predominantly positive in both leads (Figs 1A, 3B, and 3C), whereas it exhibits a QS pattern when the lateral
region is activated first (Figs 1B and 3A). In our series of
experiments, the most common cause for tachycardias with
different morphologies was rotation of the reentrant wave front in
opposite directions around the same line of functional block. Because
of the different direction of rotation, the wave front exited the
central common pathway in a different direction and a different margin
of the border zone was activated during diastole
for each morphology (see Fig 4). Rotation of a reentrant wave front in
opposite directions has previously been described for experimental
anatomic circuits.24,25 It has also been postulated to
occur in humans in cases in which complete circuits could not be
mapped.20–23
Based on clinical mapping studies, it has also been proposed that a
common mechanism for multiple-morphology tachycardias is
reentrant wave fronts rotating in the same direction in the same
reentrant circuit but with different exit routes.9,10,22 In
our series of experiments, we rarely found the exact same circuit to be
associated with different tachycardia morphologies, as
might occur in anatomic circuits in which the reentrant pathway is
fixed; there was often a slight change in the circuit. Because of the
delicate balance between margins of the border zone that are
activated when the ventricles are excitable and borders
activated when they are not, a very small change in a reentrant
circuit caused by a change in the length of one of the functional lines
of block, for example, can lead to a change in the exit route and a
change in QRS morphology (Fig 5). In other instances, although located
in the same region, reentrant circuits associated with different
tachycardia morphologies were markedly different (Fig 7).
Initiation of Tachycardias With Multiple QRS
Morphologies
The reason why different morphologies occurred in our series of
experiments was mostly related to the activation pattern during
initiation with programmed stimulation (although in one example shown
in Fig 11, the QRS morphology changed spontaneously during
tachycardia). In clinical evaluation of patients with
sustained VT, programmed stimulation has resulted in initiation of
tachycardias with multiple morphologies, some of which were
not observed to occur spontaneously, and the likelihood of multiple
morphologies is increased with more aggressive stimulation
protocols.1–4 Spontaneously occurring
tachycardias were not documented in our experiments, and
the stimulation protocols that initiated multiple morphologies were not
more aggressive than in experiments in which only a single morphology
was induced. Seventy-five percent of the morphologies were induced by
single premature stimuli, and the remainder were initiated by doubles
or overdrive. However, more aggressive protocols might have induced
additional morphologies. The different sites or patterns of programmed
stimulation resulted in different lines of block of the premature
impulses. This in turn influenced the location of the reentrant
circuit. Also, the site of stimulation influenced the direction that
the reentrant wave front propagated around the line of block (Figs 9 and 10).
Limitations and Conclusions
We recorded only two surface ECG leads and, therefore, may
have underestimated the number of different tachycardia
morphologies. A quantitative approach involving determination of the
frontal axis or recording additional leads would have been more
sensitive. It is possible that sometimes, when the QRS morphology in
the two recorded leads appeared identical, differences might have
been evident in other leads. However, the purpose of the study was not
to document the incidence of multiple morphologies in this animal model
but rather the mechanism for multiple morphologies. Therefore, the
limited sensitivity of our method does not affect the results. Our
criteria for designating that morphologies were different was highly
specific and to a large extent eliminated the possibility that
different morphologies were actually the same. The accuracy of pacing
at the margins of the electrode array during sinus rhythm to confirm
exit routes is also limited by the availability of only two ECG leads
and by the fixed locations of the stimulating electrodes, which did not
allow stimulation at the exact sites designated as exit routes. Also,
there is the question of the clinical relevance of this animal model,
in which reentry occurs in the epicardial border zone. Clinically
occurring reentrant VT often involves
subendocardial1,5,8–11 reentrant circuits, although
circuits have been found to occur in
epimyocardium.26 The role of anisotropy in
causing reentry in human hearts is also unknown. Nevertheless,
experimental studies on animal models are useful for suggesting
possible mechanisms of clinical events. Our study shows how changes in
the direction of wave front rotation or length of lines of block in
functional reentrant circuits localized in the same region of the
ventricle have profound effects on exit routes and QRS morphologies.
The results also emphasize the possibility that despite large
differences in early sites of activation, which may represent
exit routes, tachycardias with different morphologies may
have similar sites of origin. In clinical studies with limited mapping
sites, many of these tachycardias could be misclassified as
having different sites of origin despite circuits in the same region,
because the exit sites were separated by 4 to 5 cm. Our results suggest
that multiple VT morphologies may be eliminated by ablating one
discrete area that may serve as the central common pathway for two
circuits moving in opposite directions or different circuits in the
same region with different exit routes.
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Acknowledgments |
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This study was supported by grant R32HL-31393 from the National Heart, Lung, and Blood Institute, National Institutes of Health.
Received May 5, 1997; revision received July 24, 1997; accepted August 2, 1997.
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References |
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