Localization of the Slow Conduction Zone During Reentrant
Ventricular Tachycardia
Edward J. Ciaccio, PhD
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Background—Reentrant ventricular tachycardia is sometimes difficult to treat effectively because localizing the slow
conduction zone (SCZ) for catheter ablation may be problematic. It was hypothesized that a linear relationship exists
between activating wave-front acceleration and deceleration in the SCZ and, respectively, contractions and expansions
of the far-field extracellular signal, which could be used for SCZ localization.
Methods and Results—To test the hypothesis, a model was developed to approximate SCZ location on the basis of the time
interval between activation at the recording site and shifts in electrogram far-field deflections. Electrograms were
recorded during reentry from 196 to 312 epicardial sites (canine model, 8 episodes). Activation maps of reentry were
constructed to determine wave-front velocity, and piecewise linear adaptive template matching (PLATM) measured time
shifts in far-field electrogram deflections. Linear trends of cycle length change often occurred during tachycardia (mean
trend, ⫹15 ms/96.8 cardiac cycles; r2⫽0.92). Alteration in the time interval for activation through the SCZ
approximated the change in tachycardia cycle length (mean correspondence, 75.7%). The beginning and end times of
far-field extracellular waveform time shifts measured by PLATM predicted the time from recording site activation to
activation at the SCZ proximal and distal edges, respectively (mean absolute error with respect to activation mapping,
20.3 ms).
Conclusions—During reentry, PLATM estimates the time interval from activation at any recording site near the circuit to
SCZ activation. PLATM time intervals are convertible to arc lengths along the circuit for potentially more rapid and
accurate update of a hand-held probe toward the SCZ for catheter ablation. (Circulation. 2000;102:464-469.)
Key Words: ablation 䡲 reentry 䡲 tachycardia
V
sible, to locate all arrhythmogenic sites.3,7,8 Entrainment with
concealed fusion also occurs by pacing from bystander
pathways.3 At a bystander pathway, activation proceeds from
the main circuit loop but is constrained by block lines having
the shape of a cul-de-sac; ablation there does not terminate
reentry.3 Site-by-site activation mapping also identifies arrhythmogenic sites for ablation, but besides the fact that it is
tedious and time consuming to time synchronize data and
create isochrone maps, this process is subjective when multiple electrogram deflections are present.9 Basket-type catheters in which electrograms are recorded simultaneously from
many sites are also used for mapping; however, good electrode contact at all sites on the endocardium is difficult to
ensure because of irregularities in the ventricular surface, so
areas crucial to reentry may not be recorded.10 Basket
catheters also have limited torque capabilities, which hampers
correct placement, and they may abrade the endocardium.10
Quantitative analysis of dynamic, cycle-by-cycle changes
in electrogram shape is a promising new tool for localizing
reentry features, including arcs of block bounding the isthmus, as has been demonstrated in a canine model of reentrant
VT with a figure-8 pattern of conduction.11 From previous
entricular tachycardia (VT) is an important health concern that can be life threatening. There is abundant
evidence that many VTs occurring in humans are caused by
reentry.1–5 Initiation of a reentrant circuit requires a slow
conduction zone (SCZ) and a zone of unidirectional block. In
large circuits such as those arising from infarct scars, areas of
slow conduction in and around the scar should be targeted for
ablation.2 Clinical studies suggest that targeting this region
will interrupt the circuit and stop tachycardia without recurrence.1,4,5 In a canine study, application of cryothermy terminated reentry only when the circuit was interrupted within the
central isthmus,6 where the SCZ is located.
An effective method to determine arrhythmogenic areas for
ablation is to isolate sites that, when paced during
tachycardia, exhibit entrainment with concealed fusion.3 Such
sites are believed to reside within the reentrant circuit
isthmus, which is bounded by lines of anatomic or functional
block. However, ablation will fail if lesions are too small or
too far away from the reentry pathway to completely interrupt
the circuit.7 Reentrant tract geometry can be complex and
extensive with multiple entrances and exits,8 so it is sometimes difficult and time consuming, and occasionally impos-
Received August 10, 1999; revision received February 25, 2000; accepted February 25, 2000.
From the Departments of Pharmacology and Biomedical Engineering, College of Physicians and Surgeons, Columbia University, New York, NY.
Correspondence to Edward J. Ciaccio, PhD, Department of Pharmacology, PH7W, Columbia University, 630 W 168th St, New York, NY 10032.
E-mail [email protected]
© 2000 American Heart Association, Inc.
Circulation is available at http://www.circulationaha.org
464
Ciaccio
Figure 1. Model of SCZ conduction velocity changes and effect
on electrogram deflections. A and B, Hypothetical circuit and
relationship of activation at SCZ proximal and distal edges to
arbitrary site (F) when conduction velocity changes. C, Effect of
varying SCZ conduction velocity on extracellular waveform
deflections.
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observations of changing conduction in the SCZ,11 it was
hypothesized that a linear relationship exists between activating wave-front acceleration and deceleration in the SCZ and,
respectively, contractions and expansions of the far-field
extracellular signal, which could be used for SCZ localization. Because similar trends in cycle length change have also
been observed in human VT,12 an approach based on this
hypothesis, described herein, is of potential relevance to
clinical ablation therapy.
Methods
Data Collection and Activation Mapping
A canine model of VT caused by reentrant excitation that has been
described elsewhere13 was used for creation of activation maps and
measurement of cycle length. Bipolar electrograms from 196 to 312
sites on the epicardial border zone in the anterior left ventricle of the
heart are digitized at 1 to 2 kHz and recorded simultaneously.11,13 For
each of 8 reentry episodes (7 experiments), cycle length was
computed from onset to termination on the basis of the ECG R-R
interval and plotted with respect to cycle number. When a trend in
cycle length, defined as a general tendency for linear cycle length
increase or general tendency for linear decrease, occurred over ⱖ50
cycles, 2 of the cycles 25 and 50 cycles apart were selected for
further analysis. Activation maps of these cycles were constructed to
determine the time interval for the activating wave front to propagate
from the proximal to the distal edge of the SCZ and the temporal
relationship between activation at each recording site and SCZ
activation for comparison with electrogram shape analysis measurements described below.
Time-to-Distance Model
A simple model was used to approximate electrogram deflection
alterations occurring when conduction velocity changes over an arc
of the circuit (Figure 1A). Let the SCZ, denoted by the shaded region
in the isthmus, cover a 30-mm arc. The remaining arc, shown for the
right-hand loop, is 150 mm in length (180-mm total length of the
loop). Let conduction velocity be 0.5 mm/ms in the SCZ and
1.0 mm/ms elsewhere during cycle k of tachycardia. The time for the
activating wave front to propagate from the SCZ proximal to distal
edge is 30 mm/(0.5 mm/ms)⫽60 ms and from the distal to proximal
edge is 150 mm/(1.0 mm/ms)⫽150 ms. The tachycardia cycle length
is therefore 60⫹150 ms⫽210 ms. For an arbitrary site three fourths
of the way along the arc of the SCZ referenced at 0 ms (solid black
circle in Figure 1A), the time between activation at the site and
activation at the SCZ proximal edge is ⫺45 ms and to activation at
Localization of Slow Conduction Zone
465
the distal edge is ⫹15 ms. Now suppose that conduction velocity
decreases to 0.3 mm/ms in the SCZ and remains at 1.0 mm/ms
elsewhere during cycle k⫹n of tachycardia (Figure 1B). Then the
new time for the wave front to traverse the SCZ is 30 mm/(0.3 mm/
ms)⫽100 ms, and the cycle length is 100⫹150 ms⫽250 ms. For the
arbitrary site referenced at 0 ms (solid black circle in Figure 1B), the
time between activation at the site and activation at the SCZ
proximal and distal edges is now ⫺75 and ⫹25 ms, respectively.
As a first approximation, the only change at the source that
generates the electrogram deflections during SCZ activation, from
cycle k to k⫹n, can be considered to be a deceleration of the process
by 100 ms/60 ms⫽1.67. Then the electrogram deflections caused by
SCZ activation during cycle k⫹n will appear exactly the same as
during cycle k, except that they will be expanded by 1.67 along the
time axis. This is illustrated in Figure 1C for the arbitrary site in
Figure 1A and 1B. The 2 electrograms (cycle k, thick trace, and cycle
k⫹n, thin trace) are time aligned at the point of activation at the
recording site, which is taken as the extremum point (negative
electrogram peak at time 0 ms denoted by solid vertical line). The
time interval for activation of the SCZ is shown by thick vertical
dotted lines (cycle k) and by thin vertical dotted lines (cycle k⫹n).
The decreased conduction velocity in the SCZ, which increases the
time for the activating impulse to traverse the region by 40 ms,
causes the electrogram of cycle k⫹n (thin trace) to expand by 40 ms
with respect to the electrogram of cycle k (thick trace). The phase lag
or shift resulting from expansion, defined as the relative position in
time of corresponding electrogram deflections of cycle k versus
k⫹n, changes by ⫺30 ms from activation at the recording site (solid
vertical line; Figure 1C) to activation at the SCZ proximal edge (left
dotted lines) and changes by ⫹10 ms from activation at the recording
site to activation at the SCZ distal edge (right dotted lines; Figure
1C). Outside the SCZ activation interval, no further change in phase
lag occurs; it remains ⫺30 ms at times before SCZ activation and
⫹10 ms at times after SCZ activation (see also phase lag trace in
Figure 1C, top). At any recording site in the circuit, electrogram
far-field deflections occurring during the SCZ activation interval are
affected in the same way as the arbitrary site of Figure 1. However,
the time interval from activation at the recording site to the point
where phase lag changes will differ at each site, depending on its
distance along the loop of the circuit with respect to the SCZ.
PLATM Quantification of Electrogram Deflections
A modified form of adaptive template matching11 called piecewise
linear adaptive template matching (PLATM) was used to quantify
phase shifts in electrogram far-field deflections caused by changes in
SCZ conduction velocity. In this procedure, a 40-ms sliding window
is used to match short segments of 2 electrograms from the same
recording site, that are extracted from cardiac cycles with disparate
cycle lengths. During matching, weight parameters of 2-dimensional
scale (amplitude and time base or duration) and shift (phase lag and
average baseline) are used to adjust one (input) electrogram to best
overlap the other (template) electrogram. The weights at convergence to best overlap are a measure of shape difference between
template and input before weighting. After convergence, the window
is shifted by 5 ms, and the new template/input electrogram segments
are matched. This procedure is repeated until the weights are
computed at 5-ms incremental shifts of the window over an entire
cardiac cycle. For any given site, when phase lag weight at
convergence is plotted versus time in the cardiac cycle, the resulting
graph will look much like Figure 1C (top). However, the position of
phase lag change will depend on the recording site location in the
circuit with respect to the SCZ, and the magnitude of the phase lag
change will approximate cycle length disparity between template and
input cycles.
Following the model of Figure 1, for the template/input electrogram pair of any recording site, the starting and ending times of the
largest contiguous phase lag change measured by PLATM were
taken as the estimated time intervals from activation at the site to
activation of the SCZ proximal and distal edges, respectively. Maps
were constructed of the data with the use of 2-dimensional computerized grids to denote recording site position, as in activation
466
Circulation
July 25, 2000
Figure 2. Cycle length changes, 2 reentry episodes (EP). Vertical dashed lines denote end points for measurement (see text).
mapping. However, the number printed at each recording site was
not the activation time but rather the PLATM-estimated time interval
from activation at the site to activation at the SCZ. Separate maps
were created to show activation time intervals from recording sites to
the SCZ proximal edge and to the distal edge. Also, in separate tests,
electrograms from template/input cardiac cycles separated by 25 and
50 cycles were used for PLATM analysis. The mean error of
PLATM estimates with respect to activation mapping was tabulated.
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Results
Relationship of Tachycardia Cycle Length to
the SCZ
In Figure 2, cycle length change with respect to cycle number
is given for 2 monomorphic VT episodes. In each episode,
there was an approximately linear trend in cycle length over
many cardiac cycles. In episode 1A (pace termination), there
were alternating upward and downward trends in cycle length
(labeled i through iv), whereas in episode 2 (spontaneous
termination), the only trend in cycle length was upward.
During a given trend, 1- to 5-ms oscillations occurred. These
examples were typical of trends of cycle length change in the
other reentry episodes; cycle length tended to prolong (mean
trend, ⫹15 ms/96.8 cardiac cycles; r2⫽0.92). Cycle length
change was caused mostly by alterations in SCZ conduction
velocity as is shown in Figure 3 for reentry episode 1A. In
Figure 3A, the activation map is shown for cycle 61. The
isthmus is located near the map center, and arrows denote
Figure 4. Overlapped electrograms from successive cycles of
sites 55 and 74, episode 1A. One complete cycle occurs from
approximately ⫺110 ms to 110 ms. Red bar denotes SCZ activation interval.
wave-front direction. In Figure 3B through 3D, electrograms
from selected sites in the isthmus, circled in Figure 3A, are
shown for cycles 11 and 12, 61 and 62, and 111 and 112,
respectively. The SCZ is considered to extend between sites
58 and 54, where slow conduction occurs. There is an
approximate correspondence of cycle length disparity between cycles 11 and 61 (20 ms, Figure 3B and 3C) and
between cycles 61 and 111 (⫺12 ms, Figure 3C and 3D), with
the change in activation time through the SCZ and, more
precisely, through isthmus sites 58 to 52 (104⫺82⫽22 ms
and 87⫺104⫽⫺17 ms, respectively). During all trends, an
approximate correspondence existed between cycle length
disparity and alteration in SCZ activation interval.
Changes in Electrogram Deflections
In Figure 2A (episode 1A), cycle length increases gradually
over ⬇50 cardiac cycles and then decreases gradually over
⬇50 cycles. Changes in electrogram deflections occurring
Figure 3. Activation map and electrograms for
selected cycles, episode 1A. A, Activation
map. B through D, Selected electrograms and
activation times. Activation marks are denoted
by thin vertical lines; numbers between cycles
are activation intervals between adjacent sites
and, parenthetically, cycle length at recording
site. Thick vertical bars mark SCZ/RCZ boundaries (described in text); numbers there are
activation intervals. Channel numbers are
shown in left of B. LAD indicates left anterior
descending coronary artery; LL, left lateral
margin.
Ciaccio
Localization of Slow Conduction Zone
467
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Figure 5. PLATM maps (episode 2) of time
interval from activation at each of 196 recording sites to activation of SCZ. Top, Zero line is
SCZ proximal edge; Bottom, zero line is SCZ
distal edge. LAD indicates left anterior
descending coronary artery; LL, left lateral
margin.
during these gradual trends in cycle length are shown in
Figure 4 for 2 representative electrograms (site 55 in Figure
4A and 4C and site 74 in Figure 4B and 4D). Site 55 was
located in the SCZ, and site 74 was near the isthmus entrance
(Figure 3A). Figure 4A shows overlapped electrograms
extracted from 50 cardiac cycles of the site 55 recording,
aligned with respect to the extremum point (cycles 11 to 60
when cycle length prolonged; see Figure 2A). The electrograms of the first 12 cardiac cycles are red; the next 12 to 13
are yellow and then green and blue. The electrograms of
Figure 4A expand over 50 cycles in approximately the same
way as in the model (Figure 1C). The 50 electrograms
extracted from cycles 11 to 60 of site 74 (Figure 4B) show
similar electrogram expansions; however, expansions begin
about 20 ms after activation at the recording site, in accordance with the position in the circuit of site 74 with respect to
the SCZ. In Figure 4A and 4B, the total change in phase lag
between the deflections is ⬇20 ms, in conformity with cycle
length change over the interval. Figure 4C and 4D shows 50
electrograms of sites 55 and 74, respectively, extracted from
cycles 61 to 110 of episode 1A (Figure 2A). The time
intervals and extent of phase lag changes between deflections
are similar to those in Figure 4A and 4B but are reversed in
direction because cycle length decreased by ⬇12 ms from
cycle 61 to 110 and therefore SCZ conduction velocity
increased in approximate proportion. These gradual cycle-tocycle changes in far-field electrogram deflections, of approximately linear proportion to the change in SCZ conduction
velocity and change in tachycardia cycle length, were typical
of those at all other sites in the same and in other episodes of
tachycardia.
PLATM Maps of SCZ Boundaries
PLATM maps of time intervals from activation at each of 196
recording sites to SCZ activation are shown in Figure 5 for
episode 2 (n⫽25), which had the most accurate results
compared with activation mapping (see the Table described
below). Cycles 11 and 36 (Figure 2B) were used to construct
the map. The small numbers in the top panel of Figure 5 are
the PLATM-estimated time intervals from activation at the
468
Circulation
July 25, 2000
Error Between PLATM and Activation Mapping
SCZp⫾SE
(n⫽50), ms
SCZd⫾SE
(n⫽50), ms
SCZp⫾SE
(n⫽25), ms
SCZd⫾SE
(n⫽25), ms
1A,i
23.7⫾3.1
24.2⫾3.2
26.6⫾3.1
26.8⫾3.1
1A,ii
30.3⫾3.1
30.9⫾3.1
32.4⫾3.0
31.7⫾3.0
1A,iii
22.2⫾3.1
23.0⫾3.2
26.4⫾3.0
27.2⫾3.0
1B
14.7⫾0.9
15.1⫾0.9
17.5⫾1.0
16.9⫾1.0
2
9.7⫾0.6
10.7⫾0.7
6.7⫾0.4
8.4⫾0.5
3
19.8⫾0.9
20.7⫾0.9
14.9⫾0.9
16.3⫾1.0
4
21.4⫾1.2
21.7⫾1.2
16.8⫾1.0
16.2⫾1.1
5
20.9⫾1.1
21.7⫾1.1
12.3⫾0.9
15.9⫾0.9
6
16.1⫾1.0
9.2⫾0.6
17.8⫾0.9
17.8⫾0.9
7
20.1⫾1.0
27.2⫾1.4
27.6⫾1.4
33.6⫾1.6
Mean
19.9⫾1.6
20.4⫾1.6
19.9⫾1.6
21.1⫾1.6
Episode,
Trend
n indicates number of cardiac cycles that separate template/input cycles;
SCZp, SCZ proximal border; and SCZd, SCZ distal border.
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recording sites to the SCZ proximal edge. These intervals
were not error corrected. Thick curved lines denoting block
are drawn between adjacent sites where PLATM time intervals are disparate by ⬎40 ms, and isochrones are drawn at
20-ms intervals. Sites where intervals appeared to be erroneous on the basis of context with neighboring sites were
ignored when block lines and isochrones were drawn. The
block lines determined by PLATM followed those determined by activation mapping except where shown by thick
dashed lines (no block lines occurred in activation maps at
these areas). The zero line on the map (Figure 5, top) is the
estimated SCZ proximal edge position based on PLATM
measurements at all sites. As the wave front propagates out of
the isthmus, PLATM time intervals become more negative
because estimated SCZ proximal edge activation time precedes activation at the recording sites by a longer time
interval. Similarly, retrograde to the isthmus in the circuit,
PLATM intervals become more positive because SCZ proximal edge activation time follows activation at the recording
sites by a longer interval. The bottom panel of Figure 5 is
similar to the top panel except that the zero line is the
estimated position of the SCZ distal edge and the small
numbers are PLATM-estimated time intervals from recording
site activation to activation at the distal SCZ border.
The Table shows how PLATM measurements compare
with activation mapping measurements. The mean absolute
differences in PLATM versus activation mapping measurements of time intervals from recording site activation to SCZ
activation are given (SCZp, SCZd). There was no significant
correlation between cycle length or rate of change of cycle
length with method accuracy. There was also little difference
in accuracy whether or not the input electrogram used for
matching followed the template by 50 or 25 cycles. The
lowest PLATM error occurred for the single trend of episode
2, 25 cycles (6.7- and 8.4-ms difference to proximal and distal
edges, respectively). The largest error (32.4 ms) occurred for
estimation of the SCZ proximal edge for the second trend of
episode 1A, 25 cycles, when conduction accelerated in the
SCZ and caused cycle length shortening. The mean absolute
difference between PLATM time intervals and corresponding
activation map intervals was 20.3⫾1.6 ms over all sites for
the 10 trends. PLATM measurements were not manually
corrected for errors.
Discussion
Possible Clinical Method to Determine Optimal
Ablation Sites
Limitations in existing clinical methods to determine
optimal ablation sites led us to consider the potential of
beat-to-beat electrogram measurements for identifying reentrant circuit features because circuits are often dynamic,
not static, entities, with variation in the reentrant path and
conduction velocity,11 both of which cause alterations in
electrogram shape. Unlike activation mapping, PLATM
measurement of electrograms at a single recording site
suffices to determine the time interval from activation at
that site to activation of the SCZ. Unlike entrainment
methods, bystander areas are unlikely to significantly
affect isthmus and SCZ localization because they did not
show dramatic conduction velocity changes in these experiments and therefore would not be expected to significantly influence changes in far-field deflections. Furthermore, no complex instrumentation is needed to adapt
clinical mapping systems to include PLATM analysis.
PLATM might therefore be useful as an adjunct to existing
clinical entrainment and mapping procedures to more
rapidly and accurately “home in” on the best site to ablate.
Model of Conduction Velocity Change
The model described in Figure 1 was used to estimate
alterations in electrogram deflections caused by SCZ conduction velocity changes. Although conduction velocity changes
during reentry in the same canine model have been reported
to occur in other areas of the circuit such as at wave-front
pivot points,13 our observations suggest that the bulk of the
alteration in conduction velocity occurs within the SCZ.
Conduction velocity and changes in conduction velocity were
approximated as being uniform throughout the SCZ. However, real conduction velocity varies, as in Figure 3B through
3D, in which the activation time intervals between sites in the
SCZ are not uniform although the sites are approximately
equidistant (5-mm spacing). The lowest conduction velocity
and the largest conduction velocity change over many cycles
occur toward the SCZ center between sites 55 and 56.
Increased conduction velocity and smaller changes between
cycles occur toward the SCZ proximal and distal edges. This
pattern, observed in all tachycardia episodes of this study,
may be related to isthmus width and shape as suggested by a
theoretical model14 and an experimental study.15 An improved model of SCZ conduction velocity change would
include these factors.
When SCZ conduction velocity decreased, a concomitant increase in conduction velocity was often observed in
the region just distal to its distal edge toward the exit of the
isthmus; note the decrease in the activation interval between sites 54 and 52 from 16 ms (Figure 3B) to 8 ms
(Figure 3C). This region can be considered a rapid conduction zone (RCZ) with properties opposite to the SCZ.
Ciaccio
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Acceleration of the wave front in the RCZ when cycle
length prolongs, which may be due to increased time for
recovery there, results in advance rather than delay of
phase lag between electrogram deflections. This can be
observed during time 60 to 120 ms, just after activation of
the SCZ distal edge, for the electrograms of site 55,
episode 1A (Figure 4A). The electrogram deflections on
successive cardiac cycles advance (shift to the left) rather
than delay during time 60 to 120 ms. There is deceleration
of the wave front in the RCZ when cycle length shortens,
and electrogram deflections on successive cardiac cycles
delay slightly (shift subtly to the right) during time 60 to
120 ms (Figure 4C). For simplicity, the RCZ was not
modeled in this study, but it accounts for much of the
discrepancy between cycle length disparity and change in
SCZ activation interval. The relationships between conduction velocity and changes in amplitude and baseline
level of the extracellular signal, which require further
elaboration, also were not modeled.
PLATM and the conduction velocity model of Figure 1 might be
useful for determining the arc length along the circuit from recording site to the proximal and distal SCZ edges. If, for example, the
PLATM interval from recording site to SCZ proximal edge activation is 20 ms, as at site 74 (Figure 4B and 4D), then arc length to the
edge would be estimated as 20 ms⫻1 mm/ms⫽20 mm (approximately correct for site 74 based on 5-mm electrode spacing; see
Figure 3A). If a quadripolar catheter with specialized electrode
configuration were available, wave-front velocity (speed and direction) could be automatically calculated with the Sobel operator.16
The catheter line could then be dragged along the endocardium
toward the SCZ, using the angle of the propagating wave front with
respect to the recording site as a guide while taking PLATM
measurements at regular intervals to gauge SCZ distance. When
PLATM measurements showed the probe to reside within the SCZ,
then the heart would be ablated.
Influence of Far-Field Potential on the
Extracellular Waveform
It was considered that the extracellular signal during 1 cardiac
cycle represented primarily events occurring at the activating
wave-front leading edge. Large directional changes in the
leading edge as it pivoted around obstacles to conduction were
observed to correspond in time to peaks in far-field electrogram
deflections. Therefore, areas along the circuit loop at which
peaks in far-field deflections will be generated include the ends
of arcs of block around which the wave front pivots to enter or
exit the isthmus, as well as other obstacles to conduction such as
spurs protruding from arcs of block, isolated block lines, and the
characteristic curvature of the isthmus itself. Bipolar electrodes,
used in these recordings and often used clinically to record from
the ablation catheter tip, sense far-field activity differently from
unipolar electrodes (decreased amplitudes and slopes in bipolar
recordings).17 However, this factor would not be expected to
significantly influence PLATM measurements, which are relative, not absolute, and therefore independent of slope and peak
absolute magnitudes.
Study Limitations and Future Directions
Erroneous PLATM measurements can result from flawed
weight initialization and from noise effects on weight
Localization of Slow Conduction Zone
469
convergence, which are subjects of further research. Because there is an inverse relationship between field
strength of the extracellular potential and distance to site
of origin,18 increased voltage resolution and higher signalto-noise ratio systems may also increase accuracy. Occasional presence of T waves might be distinguished in part
from far-field activation by use of the timing constraint
imposed by the repolarization process.
Acknowledgments
This work was supported by an Established Investigator Award from
the American Heart Association, a Whitaker Foundation Research
Grant, and grants R37 HL-31393 and HL-30557 from the Heart,
Lung and Blood Institute, National Institutes of Health.
References
1. Morady F, Frank R, Kou WH, et al. Identification and catheter ablation of
a zone of slow conduction in the reentrant circuit of ventricular
tachycardia in humans. J Am Coll Cardiol. 1988;11:775–782.
2. Stevenson WG, Sager P, Nademanee K, et al. Identifying sites for catheter
ablation of ventricular tachycardia. Herz. 1992;17:158–170.
3. Stevenson WG, Sager PT, Natterson PD, et al. Relation of pace mapping
QRS configuration and conduction delay to ventricular tachycardia reentry
circuits in human infarct scars. J Am Coll Cardiol. 1995;26:481–488.
4. Wilber DJ, Kopp DE, Glascock DN, et al. Catheter ablation of the mitral
isthmus for ventricular tachycardia associated with inferior infarction. Circulation. 1995;92:3481–3489.
5. Sato M, Sakurai M, Yotsukura A, et al. The efficacy of radiofrequency
catheter ablation for the treatment of ventricular tachycardia associated with
cardiomyopathy. Jpn Circ J. 1997;61:55–63.
6. El-Sherif N, Mehra R, Gough WB, et al. Reentrant ventricular tachycardias
in the late myocardial infarction period: interruption of reentrant circuits by
cryothermal techniques. Circulation. 1983;68:644–656.
7. Blanchard SM, Walcott GP, Wharton JM, et al. Why is catheter ablation less
successful than surgery for treating ventricular tachycardia that results from
coronary artery disease? Pacing Clin Electrophysiol. 1994;17:2315–2335.
8. Downar E, Saito J, Doig JC, et al. Endocardial mapping of ventricular
tachycardia in the intact human ventricle, III: evidence of multiuse reentry
with spontaneous and induced block in portions of the reentrant path
complex. J Am Coll Cardiol. 1995;25:1591–1600.
9. Bollacker KD, Simpson EV, Hillsley RE, et al. An automated technique for
identification and analysis of activation fronts in a two-dimensional electrogram array. Comput Biomed Res. 1994;27:229–244.
10. Schalij MJ, van Rugge FP, Siezenga M, et al. Endocardial activation mapping
of ventricular tachycardia in patients: first application of a 32-site bipolar
mapping electrode catheter. Circulation. 1998;98:2168–2179.
11. Ciaccio EJ, Scheinman MM, Fridman V, et al. A new approach to the
analysis of electrogram features for the localization of reentrant circuits.
J Cardiovasc Electrophysiol. 1999;10:194–213.
12. Geibel A, Zehender M, Brugada P. Changes in cycle length at the onset of
sustained tachycardias: importance for antitachycardia pacing. Am Heart J.
1988;115:588–592.
13. Dillon SM, Allessie MA, Ursell PC, et al. Influence of anisotropic tissue
structure on reentrant circuits in the epicardial border zone of subacute canine
infarcts. Circ Res. 1988;63:182–206.
14. Kogan BY, Karplus WJ, Billett BS, et al. Excitation wave propagation within
narrow pathways: geometric configurations facilitating unidirectional block
and reentry. Physica D. 1992;59:275–296.
15. Rohr S, Salzberg RM. Characterization of impulse propagation at the microscopic level across geometrically defined expansions of excitable tissues:
multiple site optical recording of transmembrane voltage (MSORTV) in
patterned growth heart cell cultures. J Gen Physiol. 1994;104:287–309.
16. Russ JC. The Image Processing Handbook. Boca Raton, Fla: CRC Press;
1995:240.
17. Nayak HM, Tsao L, Santoni-Rugiu F, et al. A pitfall in using far-field bipolar
electrograms in arrhythmia discrimination in a patient with an implantable
cardioverter defibrillator. Pacing Clin Electrophysiol. 1997;20:2864–2866.
18. Spach MS, Miller WT III, Miller-Jones E, et al. Extracellular potentials
related to intracellular action potentials during impulse conduction in anisotropic canine cardiac muscle. Circ Res. 1979;45:188–204.
Localization of the Slow Conduction Zone During Reentrant Ventricular Tachycardia
Edward J. Ciaccio
Circulation. 2000;102:464-469
doi: 10.1161/01.CIR.102.4.464
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