From the Division of Cardiothoracic Surgery, Washington University School
of Medicine, St Louis, Mo.
Correspondence to Richard B. Schuessler, PhD, Division of Cardiothoracic Surgery, Box 8234–3308 CSRB, Washington University School of Medicine, 660 S Euclid Ave, St Louis, MO 63110. E-mail rick{at}cts7.wustl.edu
Methods and Results—Epicardial mapping was performed with 253
unipolar electrodes during and after entrainment of 13 morphologies of
ventricular tachycardia that were induced in
dogs 4 days after infarction. The return cycle was calculated by
subtracting the first activation time from the second activation time
after the last stimulus and the return cycle distribution map was
constructed for each stimulation site. The return cycle isochrones
equal to the ventricular tachycardia cycle
length converged on the lines of conduction block irrespective of the
stimulation site, and the central common pathway was localized at the
region between the intersections of the return cycle isochrones
after entrainment from different stimulation sites. The potentials from
the central common pathway were not required to localize the pathway,
and the mapping accuracy did not change with or without
analysis of the potentials from the pathway. According to the
correlation between the electrode resolution and the mapping accuracy,
an interelectrode distance of 8.5 mm was estimated as sufficient
resolution for successful tachycardia termination during
radiofrequency ablation guided by return cycle mapping.
Conclusions—Return cycle mapping after entrainment localizes the
central common pathway without pacing at the pathway or
recording the potentials from the pathway. This new mapping
technique could improve the success rate of the ablative procedures.
The return cycle after entrainment, which is the time interval between
the first and second activation times after cessation of pacing, is
specific to the recording site in the reentrant
circuit.13 14 We have previously demonstrated
that return cycle mapping after entrainment demonstrates a
characteristic pattern that depends on the pacing rate and the spatial
correlation between the stimulation site and the reentrant circuit and
that the return cycle isochrones equal to the VT cycle length
converge on the lines of conduction block of the reentrant circuit
irrespective of the stimulation site.15 16 The
hypothesis of this study is that the return cycle isochrones equal
to the VT cycle length localize the lines of block. The objective of
this study was to demonstrate that return cycle mapping after
entrainment localizes the CCP without pacing at the pathway or
recording potentials from the pathway. Specifically, the goals
of this study were (1) to determine if the potential from the CCP was
essential in localizing the lines of block by return cycle mapping and
(2) to determine the required electrode resolution to localize the
pathway by this mapping technique.
Four days after the surgery, the animals were
reanesthetized with intravenous sodium
pentobarbital (30 mg/kg). Supplemental doses of thiopental (10 mg/kg)
were given as needed to maintain the surgical plane of
anesthesia. The animals were intubated and ventilated as
described above. A femoral arterial line was inserted to
monitor systemic arterial pressure continuously.
Arterial blood samples were drawn every 30 minutes to
determine PAO2, acid-base balance,
and electrolyte levels. Ringer's lactate solution was continuously
infused, and sodium bicarbonate, potassium chloride, and calcium
chloride were supplemented as indicated to maintain pH and electrolyte
within normal values. The heart was exposed through a median sternotomy
and was suspended in a pericardial cradle. After systemic
heparinization (3 mg/kg), the right atrium and femoral artery were
cannulated, and normothermic cardiopulmonary bypass
was instituted to maintain stable hemodynamics during
sustained VT.
An electrode patch containing 253 unipolar electrodes and 16 bipolar
pacing electrodes was sutured on the epicardium of the left ventricle
to cover the infarct and surrounding area. The electrode patch was made
of a silicon sheet molded to fit the convexity of the left
ventricular free wall. Both unipolar and bipolar electrodes
were constructed from silver balls (diameter, 1 mm) and from
Teflon-insulated silver wires (diameter, 125 µm). The
interelectrode distance between the unipolar electrodes was 3 to 5
mm, with higher resolution over the infarcted area and lower resolution
over the remaining areas. The intraelectrode distance of the bipolar
electrodes was 1 mm. The location of each unipolar and bipolar
electrode is shown in the left panel of Fig 1
Programmed electrical stimulation (DTU-101, Bloom Associates Ltd) was
performed to induce VT. Each stimulation was performed through the
bipolar pacing electrodes mounted on the electrode patch. A pacing
threshold was determined, and all stimulation was performed at a pulse
width of 2 ms and at twice the diastolic threshold. After a
train of eight paced beats (S1) at a paced cycle length of 300 ms,
single or double extrastimuli (S2 and S3) were delivered at varying
coupling intervals until VT was induced. Once a stable sustained VT was
induced, continuous pacing was performed to entrain the VT from various
epicardial sites through the bipolar electrodes. The pacing cycle
length was set 5 to 10 ms less than the VT cycle length. Surface ECGs,
pacing artifacts, and reference electrograms from the unipolar
electrodes were continuously monitored, and the VT cycle length was
displayed digitally in a beat-by-beat fashion. After constant fusion
beats in the surface ECG and constant capture of the reference
electrogram at the pacing rate were demonstrated, the pacing was
abruptly terminated. Several attempts to entrain the VT were repeated
from different bipolar electrode locations. Entrainment of the
tachycardia was directly verified by the activation maps
during pacing.
A 256-channel computerized data acquisition and analysis system
was used to collect, process, and display data. The mapping system was
based on a VaxStation II/GPX graphics workstation connected to two
128-channel PDP 11/23+ based data acquisition subsystems. Unipolar
electrograms were recorded at a gain of 250, with a frequency
response of 0.05 to 500 Hz. Each channel was digitized at 1000 Hz with
a 12-bit resolution. Two-hundred fifty-three unipolar electrograms, as
well as surface ECGs, pacing artifacts, and reference electrograms,
were recorded during and after entrainment of each VT. The data
were stored on the hard disk of the VaxStation and on an optical disk.
The optical disks from each experiment were replayed afterward for
off-line data analysis. Local activation times were determined
at the time of the maximum negative derivative in each unipolar
electrogram. All electrograms were edited visually to verify accuracy
of the computer-picked activation times. Activation maps of the first
and second cardiac cycle after entrainment were constructed. A site of
conduction block was defined as the site between any two adjacent
electrodes having an activation time gradient of >10 ms/mm, associated
with a different activation sequence on opposite sites of the putative
block and a different morphology of the electrograms. The return cycle
after entrainment was calculated by subtracting the first activation
time from the second activation time after the last stimulus at each
unipolar electrode location. The return cycle map was constructed as an
isotemporal map for each stimulation site. The region where the
isochrones equal to the VT cycle length converged and intersected
was identified from the return cycle maps in each VT.
To determine if analysis of the potentials from the CCP is
essential for localizing the pathway by return cycle mapping after
entrainment, the potentials from the electrodes located adjacent to the
lines of block and the electrodes located between the lines were not
analyzed (Fig 6
All animals received humane care in compliance with the "Principles
of Laboratory Animal Care" formulated by the National Society of
Medical Research and the "Guide for the Care and Use of Laboratory
Animals" prepared by the National Academy of Science and published by
the National Institutes of Health (NIH publication No. 86–23, revised
1985). In addition, the study protocol was approved by the Washington
University Animal Studies Committee.
Return Cycle Distribution
Potentials From the CCP and the Accuracy of Mapping
The number of electrodes not analyzed was 56±24 (22±9.5% of
253 electrodes), and the corresponding area was 7.0±3.5
cm2 (19±9.5% of the total mapped area). The
accuracy of mapping with and without analysis of the potentials
from the CCP was evaluated by the distance between the intersection of
the return cycle isochrones equal to the VT cycle length and the
line of block localized by the activation map during VT. The distance
was 1.0±1.4 mm with analysis of the potentials from the
CCP and 1.5±1.3 mm without analysis of the potentials. No
statistical differences were found between the two analyses
with or without analysis of the potentials from the CCP.
Mapping Resolution and Accuracy of Localizing the CCP
The effect of the interelectrode distance on the mapping accuracy of
this technique is shown in Fig 8
Return Cycle After Entrainment
The primary mechanism for localizing the CCP by return cycle mapping is
in that the return cycle isochrones equal to the VT cycle length
converge on the lines of conduction block of the reentrant circuit.
This is because the revolution time around the line of block after
cessation of pacing is the cycle length of the tachycardia
as long as an excitable gap exists along the lines of block. The
present study also showed that the potentials from the CCP were not
necessarily required to have the return cycle isochrones converge
on the lines of block, and that the mapping accuracy did not change
with or without analysis of the potentials from the CCP. The
reason for this is that the return cycle isochrones equal to the VT
cycle length radiate from the CCP. In addition, as shown in Figs 5 to 7
Limitations
In the present study, the reentrant circuit of the induced VT was
located in the thin epicardial tissue overlying a subendocardial
infarct, so that it was only necessary to map the epicardium. However,
intramural reentry may be the mechanism of the VT in
patients.23 24 Although this mapping technique
does not require the potentials from the CCP to localize the pathway
and could be easily extended for three-dimensional return cycle
mapping, further studies are necessary to determine whether a CCP
located intramurally can be also localized by interpreting return
cycles mapped endocardially or epicardially.
Clinical Implications
Application of this mapping technique for catheter mapping requires
simultaneous recording of multipoint potentials.
Recently, a basket-shaped mapping catheter carrying 64 electrodes was
developed, tested, and applied in patients with recurrent sustained
VT.26 27 There is a limit to the number of
electrodes that a catheter can carry. In the present study, we
estimated the sufficient interelectrode distance for catheter ablation
guided by this mapping method. The size of the lesion created by
radiofrequency energy is determined by the power and exposure duration
of the energy and can be large as 8 mm in
diameter.18 If mapping error is less than half of
the diameter of the ablation lesion, the delivered energy can terminate
the tachycardia. According to the correlation between the
interelectrode distance and the mapping accuracy shown in Fig 8
Received July 14, 1997;
revision received October 9, 1997;
accepted October 21, 1997.
2.
Josephson ME, Harken AH, Horowitz LN. Endocardial
excision: a new surgical technique for the treatment of recurrent
ventricular tachycardia.
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Trappe HJ, Klein H, Auricchio A, Wenzlaff P, Lichtlen
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7.
Downar E, Saito J, Doig JC, Chen TC, Sevaptsidis E,
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8.
Kaltenbrunner W, Cardinal R, Dubuc M, Shenasa M,
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endocardial mapping of ventricular tachycardia
in patients with myocardial infarction: is the origin of the
tachycardia always subendocardially localized?
Circulation. 1991;84:1058–1071.
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Waldo AL, Henthorn RW. Use of transient entrainment
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10.
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deBuitleir M, Sousa J. Concealed entrainment as a guide for catheter
ablation of ventricular tachycardia in patients
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11.
Stevenson WG, Khan H, Sager P, Saxon LA, Middlekauff
HR, Natterson PD, Wiener I. Identification of reentry circuit sites
during catheter mapping and radiofrequency ablation of
ventricular tachycardia late after myocardial
infarction. Circulation. 1993;88:1647–1670.
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Bogun F, Bahu M, Knight BP, Weiss R, Paladino W, Harvey
M, Goyal R, Daoud E, Man KC, Strickberger SA, Morady F. Comparison of
effective and ineffective target sites that demonstrate concealed
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radiofrequency ablation of ventricular
tachycardia. Circulation. 1997;95:183–190.
13.
Waldecker B, Coromilas J, Saltman AE, Dillon SM, Wit
AL. Overdrive stimulation of functional reentrant circuits causing
ventricular tachycardia in the infarcted canine
heart: resetting and entrainment. Circulation. 1993;87:1286–1305.
14.
Mann DE, Lawrie GM, Luck JC, Griffin JC, Magro SA,
Wyndham RC. Importance of pacing site in entrainment of
ventricular tachycardia. J Am Coll
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Nitta T, Mitsuno M, Rokkas CK, Isobe F, Cronin CS,
Schuessler RB, Boineau JP, Cox JL. Distribution mapping of the time
intervals after entrainment of ventricular
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16.
Nitta T, Mitsuno M, Cronin CS, Isobe F, Rokkas CK,
Schuessler RB, Boineau JP, Cox JL. Distribution mapping of the time
intervals after entrainment of ventricular
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© 1998 American Heart Association, Inc.
Basic Science Reports
Return Cycle Mapping After Entrainment of Ventricular Tachycardia
Abstract
Top
Abstract
Introduction
Methods
Results
Discussion
References
Background—The central common
pathway, which is the target for ablation in reentrant
ventricular tachycardia, can be localized by
entrainment mapping techniques. However, localization of the pathway is
not always possible because of the elevated pacing threshold and the
low voltage and fractionated potentials at the pathway. We examined
whether return cycle mapping after entrainment localizes the pathway
without pacing at the pathway or recording the potentials from
the pathway and determined the required electrode resolution to
localize the pathway.
Key Words: tachycardia • reentry • entrainment • mapping • ventricles
Introduction
Top
Abstract
Introduction
Methods
Results
Discussion
References
Ablation or
resection of tissue by the catheter technique or surgery can abolish
ventricular tachycardia
(VT).1 2 Successful elimination of VT by these
techniques largely depends on localizing the critical region of the VT
reentrant circuit. Clinical and experimental studies have revealed that
the critical region for the sustenance of VT is the central common
pathway (CCP) or the slow conduction zone of the reentrant
circuit,3 4 because the CCP is the region where
the activation wave fronts are confined to a narrow isthmus and it is
only necessary to ablate a small amount of myocardium at
the CCP to eliminate VT. During surgery, high-resolution mapping with
hundreds of electrodes can record potentials from the CCP and
localize the pathway.5 6 7 8 However, the potentials
at the CCP are frequently low voltage and fractionated; thus
construction of activation maps of the reentrant circuit requires
careful analysis and extensive editing. The entrainment mapping
technique has been widely used in localizing the CCP during catheter
ablation.9 10 11 12 Demonstration of concealed
entrainment combined with other criteria has been shown to
predict VT termination during radiofrequency
application.11 12 However, concealed entrainment
is not always demonstrable in patients with sustained VT, and the
success rate for VT ablation is low in cases in which concealed
entrainment or other criteria are not demonstrable. This is because
that the present technique is basically a site-by-site mapping
method and requires pacing at the CCP and recording potentials
from the pathway to demonstrate that the electrode is located at the
pathway. The pacing threshold is frequently elevated and the potentials
are complex and fractionated at the pathway. Therefore if one cannot
demonstrate the above criteria, the pathway is never localized even if
the electrode is positioned at the pathway. A new mapping technique is
required in catheter ablation or surgery for reentrant VT, a technique
capable of localizing the CCP without placing electrodes at the
pathway. Such a technique would provide rapid and accurate mapping of
the critical region of VT, consequently improving the success rate of
the ablative procedures.
Methods
Top
Abstract
Introduction
Methods
Results
Discussion
References
In 18 adult mongrel dogs of either sex, weighing 23 to 37 kg,
anesthesia was induced with intravenous sodium
thiopental (20 mg/kg) and was maintained with inhaled halothane (1% to
3%). The animals were intubated and ventilated with the use of a
volume-limited ventilator (Harvard Apparatus Co). The heart
was exposed through a left thoracotomy at the fourth intercostal space
with sterile surgical technique and was suspended in a pericardial
cradle. The left anterior descending coronary artery (LAD) was
carefully dissected at the portion proximal to the branching of the
first diagonal artery and was occluded for 2 hours. A bolus injection
of intravenous lidocaine (2 mg/kg) was given 5 minutes
before the coronary occlusion, and a continuous infusion of
lidocaine (1 mg/kg per hour) was administered for 5 hours after the
coronary occlusion. Another bolus injection of lidocaine (1
mg/kg) was given 5 minutes before the reperfusion. The chest was closed
in layers, and the animals were allowed recover. 
.
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Figure 1. Activation maps during pacing and sustained
ventricular tachycardia (VT). Left, ECG and
activation map during continuous pacing at a paced cycle length of 300
ms from the bipolar electrodes located at the anterior free wall of the
left ventricle in a dog 4 days after infarction. The boxed area on the
ECG is the data window analyzed to construct the activation
map. The electrode patch covered the anterior free wall of the left
ventricle from the basal left ventricle 1 to 2 cm away from the left
atrioventricular groove to the inferior
apex of the left ventricle. The left margin of the electrode array was
adjacent to the left anterior descending coronary artery (LAD).
A total of 253 unipolar electrodes were distributed over the infarcted
anterior left ventricle. Interelectrode distance of the electrodes was
3 to 5 mm, with higher resolution over the infarcted area and
lower resolution over the remaining areas. The stimulation site in this
map is denoted as a rectangle. The locations of the other 15 bipolar
electrodes used for stimulation are shown as asterisks. Numbers in the
map represent the activation times in milliseconds at each
electrode location. Isochrones are drawn in 10-ms increments. The
location of each electrode in the following figures is the same as in
this figure. Right, the ECG and the activation map during sustained VT
induced in the same infarcted heart as shown on the left. The VT was
induced by double extrastimuli from a pair of the bipolar electrodes.
The cycle length of the VT was 147 ms. The activation wave fronts are
denoted as arrows and lines of block of the reentrant circuit are
denoted as bold lines. RV indicates right ventricle; LAA, left atrial
appendage. ). In addition, to determine the required
electrode resolution for the mapping technique, the number of the
recording electrodes was decreased from 253 to 127, 64, and 32
(Fig 7). Analysis of the potentials from every other electrode
provided 127-electrode analysis. Analysis of the
potentials from every fourth and every eighth electrode provided 64 and
32-electrode analyses, respectively. The accuracy of the
mapping technique with and without analyzing the potentials from the
CCP and with various electrode resolutions was evaluated by the
distance between the mapped site demonstrated by the return cycle
mapping with each technique and the lines of block during VT defined by
the activation maps with 253 electrodes. The distances were measured on
the electrode patch and were expressed as mean±1 SD. The accuracy of
the mapping technique with and without analyzing the potentials from
the CCP was compared by Student's paired t test.
Mapping accuracy with various electrode resolutions was compared with
mapping accuracy using 253 electrodes by Student's paired t
test. In addition, the effect of average interelectrode distance on the
mapping accuracy was examined by linear regression analysis and
analysis of variance. A value of P<.05 was
considered statistically significant.
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Figure 6. The effect of analyzing the potentials from the
CCP on localizing the line of block during VT by return cycle mapping.
ECG during VT induced in an infarcted heart is shown. The VT cycle
length is 153 ms. The activation map during VT is shown on the middle
left. The boxed area on the ECG represents the data window
analyzed to construct the activation map. Entrainment of the VT
was performed from three epicardial sites (A, B, and C in the lower
right) at the same paced cycle length of 140 ms. The return cycle map
after entrainment from the anterior left ventricular free
wall (denoted as a rectangle, site A) is shown on the middle right. On
the lower left, the activation map when the potentials from the CCP and
the adjacent region (shaded area) were not analyzed. The
asterisk shows the earliest activation site. The activation was
discontinuous from 120 ms to the earliest activation. On the lower
right, the return cycle isochrones equal to the VT cycle length
(153 ms), corresponding to each stimulation site are illustrated. The
return cycle isochrones, corresponding to each stimulation site (A,
B, and C), are illustrated as broken, dotted, and solid lines,
respectively. The shaded area indicates the region where the potentials
were not analyzed and the bold lines denote the lines of block
of the reentrant circuit. Even without the analysis of the
potentials from the CCP, the return cycle isochrones equal to the
VT cycle length converged on the lines of block. Also see abbreviations
in Figs 1 
and 2.
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Figure 7. Effects of the mapping resolution on the
activation maps and on the localization of the lines of block by return
cycle mapping. The activation times during a ventricular
tachycardia (VT) were analyzed with four degrees of
mapping resolution. The VT cycle length was 140 ms. The VT was
entrained from three different epicardial sites (A, B, and C) at a
paced cycle length of 130 ms. Each stimulation site is denoted as a
rectangle. The activation map in each mapping resolution is illustrated
in the left maps and the return cycle isochrones equal to the VT
cycle length (140 ms) are illustrated on the right. The numbers of
channels analyzed were 253, 127, 64, and 32 for the maps in
each row of A through D. The numbers in the activation maps denote the
activation times during VT at each electrode location. The bold lines
show the lines of block and the isochrones are drawn in 10-ms
increments. On the right maps, the return cycle isochrones equal to
the VT cycle length (140 ms), corresponding to each stimulation site
(A, B, and C), are illustrated as broken, dotted, and solid lines,
respectively. Overlap of more than two lines is expressed as a solid
line.
Results
Top
Abstract
Introduction
Methods
Results
Discussion
References
VT Characteristics
A total of 41 morphologies of sustained monomorphic VT were
induced in 18 animals. In 7 animals, the reentrant circuit was mapped
on the epicardial surface in 13 morphologies of VT, and the return
cycle distribution after entrainment was examined. The VT cycle lengths
ranged from 127 to 241 ms (170±37 ms). The reentrant circuits
demonstrated a double loop circuit with lines of conduction block and a
CCP between the lines. The lines of block were perpendicular to the LAD
in 11 of 13 morphologies of VT and parallel to the LAD in 2
morphologies. The lines of block were longer and the CCP was narrower
in the VTs in which the lines were perpendicular to the LAD, compared
with the VTs in which the lines were parallel to the LAD. The width of
the CCP ranged from 6 to 30 mm and the length of the line of block
ranged from 9 to 44 mm. To evaluate conduction over the infarct,
activation maps were constructed during continuous pacing from the
bipolar electrode located at the anterior left ventricle, before the
induction of VT in all animals. An example is shown in Fig 1. The lines
of conduction block seen during VT were not evident during pacing,
suggesting that the conduction block during VT was functional. These
characteristics of the reentrant circuit were present also in the
other VTs in this study. In the histological
examination of the excised heart, extensive infarction of the anterior
left ventricle was seen. The number of surviving subepicardial muscle
layers varied from one third of the total ventricular wall
thickness to very thin layers of muscle. A transmural extent of
infarction was also found.
The VTs were entrained from three to five different epicardial
sites and the effects of the stimulation site on the return cycle
distribution were studied. Sample data are illustrated in Figs 2, 3, and 4. The return cycle
distribution was divided into two regions: longer than the pacing cycle
length and equal to the pacing cycle length. In the region where the
last stimulus caused the first activation after the cessation of
pacing, the return cycle was greater than the pacing cycle length. In
the region where the second to last stimulus caused the first
activation after the cessation of pacing, the return cycle equaled the
pacing cycle length. These return cycle distributions shifted and
rotated around the lines of block as the spatial correlation between
the stimulation site and CCP changed. Two different patterns of
transition were observed between these return cycle distributions. The
transition was precipitous at the region where the orthodromic
activation was transposed from the last stimulated activation to the
activation of the preceding stimulation (sites E and F in Fig 2, sites
E and F in Fig 3, and sites G and H in
Fig 4), while it was gradual at the
collision region of the antidromic and orthodromic wave fronts (sites G
and H in Fig 2, sites G and H in Fig 3, and sites C through J in Fig 4). Adjacent to the collision region, there was a return cycle
isochrone equal to the VT cycle length, and this isochrone
represented a unique spatial correlation with the lines of
conduction block. An example is shown in Fig 5. Although the isochrone shifted and
changed the shape as the stimulation site changed, the isochrone
always converged on the lines of block irrespective of the stimulation
site. As a result, the intersections of the return cycle isochrones
equal to the VT cycle length after entrainment from different pacing
sites coincided with the lines of conduction block in the reentrant
circuit during VT. Therefore, the CCP was localized at the region
between the intersections of the return cycle isochrones equal to
the VT cycle length.
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Figure 2. Activation sequence and return cycle after
entrainment from a site proximal to the central common pathway (CCP).
The VT shown in Fig 1 was entrained at a paced cycle length of 140 ms.
ECG is shown, with pacing artifacts and electrograms from selected
sites (A-J) in the maps. The vertical line indicates the time of the
last paced stimulation. After cessation of pacing, the
tachycardia resumed at a cycle length of 143 to 144 ms. The
time intervals between each activation are shown as numbers in
milliseconds. Arrows indicate the activation sequence. The activation
map of the last stimulation is shown on the lower left and the return
cycle map is shown on the lower right. The stimulation site is denoted
by a rectangle in both maps. In the activation map, time zero indicates
the time of the last stimulation. Closed arrows indicate the stimulated
wave fronts; open arrows indicate the wave fronts of the preceding
stimulation. The return cycle isochrones are constructed at 10-ms
increments from the pacing cycle length plus 5 ms. Broken bold lines
denote the lines of conduction block during VT. Note that the return
cycle isochrone of 145 ms coincides with the lines of block. The
configuration of the figure and the map symbols in the following
figures are the same as those used in this figure. Also see
abbreviations in Fig 1.
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Figure 3. Activation sequence and return cycle after
entrainment from the site in the CCP. The VT is the same VT as shown in
Fig 1 . The pacing cycle length was 140 ms, and the return
tachycardia cycle length ranged from 146 to 148 ms. The ECG
and electrograms from selected sites (A-J) are shown. The activation
map of the last stimulation and the return cycle map are shown on the
lower left and right. Note that the antidromic activation is confined
to a limited region within the CCP and that the activation sequence
outside the CCP is similar to the sequence during VT (Fig 1). Also see
Fig 2.
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Figure 4. Activation sequence and return cycle after
entrainment from a site distal to the CCP. The VT is the same VT as
shown in Fig 1 . The pacing cycle length was 140 ms, and the return
tachycardia cycle length was 145 to 146 ms. The ECG and
electrograms from selected sites (A-J) are shown. The activation map of
the last stimulation and the return cycle map are shown on the lower
left and right. Also see Figs 1 and 2.
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Figure 5. The spatial correlation of the return cycle
isochrones equal to the ventricular
tachycardia (VT) cycle length and the lines of conduction
block during VT. ECG during VT is shown. The VT cycle length was 136
ms. The activation map during VT is shown on the lower left. The boxed
area on the ECG represents the data window analyzed to
construct the activation map. The VT was entrained from three different
epicardial sites (A, B, and C on lower right) at the same paced cycle
length of 130 ms. The return cycle map after entrainment from site A is
shown in the lower middle. The stimulation site is denoted as a
rectangle. The lines of conduction block during VT are shown as bold
lines. The right lower panel demonstrates the spatial correlation of
the return cycle isochrones equal to the VT cycle length and the
lines of block during VT. The sites of stimulation (A, B, and C) are
shown as rectangles. The return cycle isochrones equal to the VT
cycle length (136 ms), corresponding to each stimulation site (A, B,
and C), are illustrated as broken, dotted, and solid lines,
respectively. The return cycle isochrones equal to the VT cycle
length converge on the lines of block irrespective of the stimulation
site.
The effect of recording the CCP potentials on localizing
the pathway by return cycle mapping was examined. An example is shown
in Fig 6. In the activation map during VT
with analysis of all the potentials recorded, two lines of
block and a CCP between them are evident. The return cycle map
demonstrated the characteristic pattern as described above and the
return cycle isochrone equal to the VT cycle length (153 ms)
converged on the line of conduction block during VT. In the activation
map in which the potentials from the CCP were not analyzed, a
time gap of approximately 30 ms was seen between the latest activation
and the earliest activation, and the lines of block and the CCP were
not localized. However, the return cycle isochrones converged on a
region that coincided with the line of block nearest the entrance of
the CCP even when the potentials from the CCP were not
analyzed.
The effect of electrode resolution on return cycle mapping
was examined. Fig 7 illustrates how the
mapping resolution affected the activation maps during VT and the
localization of the lines of block by return cycle mapping. In the
activation map with 253 electrodes (left map of panel A), almost all of
the entire sequence of activation during VT was elucidated. As the
number of electrodes decreased, the isochrones of activation became
smooth and simple, and the location, shape, and length of the lines of
block changed. As a result, the location and extent of the CCP became
ambiguous with fewer electrodes (left maps of panels B, C, and D). In
the right map of panel A, the return cycle isochrones equal to the
VT cycle length converged on the lines of block. As the number of
electrodes decreased, the return cycle isochrones became smooth and
simple. However, the region where the return cycle isochrones
intersected remained nearby (right maps of panels B, C, and D). . The
mapping accuracy was evaluated by the distance between the lines of
block localized by the activation maps with 253 electrodes and the
intersections of the return cycle isochrones equal to the VT cycle
length in each mapping resolution. The distance was 1.0±1.4, 1.9±1.5,
4.0±2.6, and 6.8±3.0 mm for each analysis group of 253,
127, 64, and 32 electrodes, respectively. The average interelectrode
distance was 4.3, 6.0, 8.5, and 12.0 mm for each analysis
group of 253, 127, 64, and 32 electrodes. As the interelectrode
distance increased, the mapping accuracy decreased. However, there was
no statistical difference in the mapping accuracy between the 127- or
64-electrode analysis groups and the baseline analysis
(253-electrode analysis). The mapping accuracy with 32
electrodes was significantly lower than the mapping accuracy with 253
electrodes. There was a significant linear correlation between the
average interelectrode distance and the mapping accuracy
(r=.72, P<.001).
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Figure 8. The effect of the interelectrode distance on the
accuracy of the return cycle mapping. The mapping accuracy was
evaluated as the distance between the intersection of the return cycle
isochrones equal to the ventricular
tachycardia (VT) cycle length and the lines of block during
VT defined by the activation maps with 253 electrodes. Mapping accuracy
using various electrode resolutions was compared with mapping accuracy
using 253 electrodes. There was a significant linear correlation
between the average interelectrode distance and the mapping accuracy
(r=.72, P<.001). A regression line is
shown.
Discussion
Top
Abstract
Introduction
Methods
Results
Discussion
References
Mapping During VT Ablation
The most important finding in the present study is that return
cycle mapping localizes the CCP without pacing at the pathway or
recording potentials from the pathway. The CCP is the region
where the activation wave fronts are confined to a narrow
isthmus.13 17 This causes the
diastolic phase in the tachycardia cycle,
because of the small volume of tissue that is activated as the
wave front traverses the CCP. Therefore ablation of a small amount of
myocardium at the CCP is necessary to eradicate reentry and
successful elimination of the VT largely depends on mapping the
pathway. Unfortunately, mapping the CCP is not always feasible during
surgery or catheter ablation. Therefore this new mapping technique
would help in localizing the CCP and improve the success rate of the
ablative procedures. During surgery for VT, high-resolution mapping
with hundreds of electrodes can exhibit the entire reentrant circuit
and localize the CCP. Although computers are used to process multiple
simultaneous recordings, determination of the
activation times at the CCP frequently requires careful
analysis and extensive manual editing of the complex and
fractionated electrograms. This process significantly lengthens the
duration of mapping. During catheter ablation of VT, precise
localization of the CCP is essential because the ablation lesion
created by the delivered energy through a catheter is
small.18 The entrainment mapping technique is
helpful for localizing the CCP with fewer electrodes. As demonstrated
in Fig 3, during entrainment from a site in the CCP, the antidromic
activation is confined to a limited area and the activation sequence
outside the CCP is similar to the sequence during VT. As a result, the
QRS morphology during entrainment is identical to the QRS morphology
during VT (concealed entrainment). Unfortunately, the predictive value
of concealed entrainment alone for localizing the successful ablation
site is 
50%,10 because the concealed
entrainment can be demonstrable during pacing from a bystander pathway
or inner loop of the reentrant circuit. The other criteria, such as the
presence of isolated mid-diastolic potentials or
electrogram-QRS interval=stimulus-QRS interval, have been shown to
enhance the predictive value of the concealed entrainment for
successful ablation.12 The postpacing interval
(the time interval from the last stimulus to the return cycle
potential) has also been shown to predict VT termination during
radiofrequency current application.11 Combining
these criteria with the demonstration of concealed entrainment has been
shown to correlate with a high likelihood of VT termination by
radiofrequency energy.11 12 On the other hand, in
the case in which concealed entrainment or other criteria are not
demonstrated, the success rate for VT ablation is low. The present
technique is a site-by-site mapping method, yet requires pacing at the
CCP or recording potentials from the pathway to demonstrate
that the electrode is positioned at the pathway. The pacing
threshold is frequently elevated and the potentials are complex and
fractionated at the CCP because the pathway usually consists of islets
of surviving myocardium in the scar tissue. Return cycle
mapping localizes the CCP by intersecting the return cycle
isochrones equal to the VT cycle length after entrainment from the
sites outside the CCP. Moreover, this technique does not necessarily
require the potentials from the CCP to localize the pathway. Therefore
return cycle mapping after entrainment localizes the CCP even when no
electrodes are positioned at the pathway.
The return cycle was defined in the present study as the time
interval between the first and second activation times after cessation
of pacing. As shown in Figs 2 to 4, the return cycle equals the pacing
cycle length at the region activated by the preceding
stimulation orthodromically, because the return cycle is the time
interval between the last two stimulated activation times in this
region. In the rest of the region, the return cycle is the time
interval between the last stimulated activation and the first
tachycardia activation. This definition of the return cycle
helps the distribution map of the return cycle to localize the lines of
conduction block, because the computer can automatically measure and
calculate the return cycle, which is merely the first time interval
after the last pacing artifact. In contrast, determination of the time
interval between the last stimulated activation and the first
tachycardia activation after entrainment can be ambiguous
at the region where the antidromic and orthodromic wave fronts collide
(site H in Fig 2, site G in Fig 3, and site J in Fig 4). This is
because the first tachycardia activation after entrainment
is the continuation of the last paced stimulation, and it is extremely
difficult to determine by the potential morphology whether the
activation is caused by the last paced stimulation or the preceding
stimulation at the region. , the return cycle isochrone was inclined to converge at the line
of block nearest the entrance of the CCP. The mechanism for this is
illustrated in Fig 9. As the stimulation
site shifts from site A to site B, the collision region of the
antidromic and orthodromic wave fronts shifts, the return cycle
isochrone equal to the VT cycle length also shifts. The degree of
shift of the return cycle isochrones depends on the conduction time
difference from each stimulation site to the reentry circuit and to the
collision region. The presence of slow conduction at the edge of the
lines of block and in the CCP allows the collision region to rotate
slowly at the region around the end of the lines as the stimulation
site shifts. As a result, the degree of shift of the return cycle
isochrone is more gradual at the region close to the reentrant
circuit than at the region distant from the reentrant circuit. This
allows the return cycle isochrones converge at the lines of block
nearest the entrance of the CCP even without the potentials from the
pathway.
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Figure 9. Mechanism for converging the return cycle
isochrones equal to the ventricular
tachycardia (VT) cycle length on the lines of functional
block. Schematic illustrates the shift of the return cycle
isochrones equal to the VT cycle length corresponding to each
stimulation site (A and B). Each arrow indicates the shift of the
isochrone for each stimulation site. CCP indicates central common
pathway; N, the region activated by the last stimulus; and N-1,
the region activated by the preceding stimulus.
Localization of the CCP by entrainment mapping is based on the
assumption that the reentrant circuit has a fully excitable gap that
allows a pacing impulse to reset the tachycardia without
decremental conduction in the circuit.19 20 Almendral and
colleagues21 and Gottlieb et
al22 demonstrated, in human ischemic VT
using the resetting response pattern, that there were some patients
whose VT showed an increasing pattern in the resetting response that
suggested decremental conduction in the reentrant circuit or in the
region between the stimulation site and the reentrant circuit.
Decremental conduction in the reentrant circuit as a response to rapid
pacing may impair the accuracy of the entrainment mapping technique.
The return cycle mapping shares the same limitation. In this study, we
examined the return cycle distribution after entrainment at a paced
cycle length close to the VT cycle length, therefore the decremental
conduction was not significant. Entrainment at a shorter pacing cycle
length can cause a change in the location and shape of functional block
or result in its acceleration or termination. Therefore pacing should
be performed with a cycle length long enough to capture all the
myocardium and avoid decremental conduction in the
reentrant circuit in this mapping technique.
This new mapping technique can be easily applied intraoperatively
during surgery for VT.25 Determination of the
activation times and calculation of the return cycle can be performed
using currently available mapping systems. Our mapping system takes <3
minutes to display the return cycle map for 253 electrode locations. To
obtain the intersections of the return cycle isochrones equal to
the VT cycle length, VT should be entrained from more than two
different ventricular sites. As shown in the present
study, the pattern of the return cycle distribution depended on the
spatial correlation between the stimulation site and the CCP.
Entrainment from sites outside and distant from the CCP may demonstrate
an expedient distribution of the return cycle to localize the CCP,
because the antidromic and orthodromic wave fronts collide outside the
CCP. In consequence, the return cycle isochrones equal to the VT
cycle length also distribute outside the CCP. When the
diastolic potentials are recorded from the CCP, the
return cycle isochrones equal to the VT cycle length intersect at
two regions that coincide with the ends of the lines of block nearest
the entrance of the CCP. The distance between the two intersections
gives the width of the pathway; thus ablation of the tissue between the
intersections would interrupt the CCP completely. When no potentials
are recorded from the CCP, the return cycle isochrones equal to
the VT cycle length intersect at a single region at the entrance of the
CCP. Ablation between the earliest activation site and the intersection
of the return cycle isochrones would interrupt the CCP.
Demonstration of a return cycle equal or close to the VT cycle length
at most areas except for the region around the stimulation site
suggests that the VT is entrained from inside or close to the CCP. The
location of the return cycle isochrone equal to the VT cycle length
can be ambiguous, because the isochrone forms a small circle in the
CCP and the difference in return cycles between the neighboring
electrode positions is small. The stimulation site should be changed
until the return cycle map demonstrates the proper distribution pattern
as described above. , the
required interelectrode distance is estimated to be 8.5 mm for the
radiofrequency energy to terminate VT guided by return cycle mapping.
The basket-shaped catheter described above provides enough mapping
resolution. Specifically, the whole endocardial surface of right and
left ventricles will be mapped with the basket-shaped catheters, and
the CCP will be localized by return cycle mapping. A radiofrequency
catheter then will be directed to the mapped site to ablate the VT, or
the mapping electrodes will be replaced with a different type of
multielectrode catheter to localize the CCP more precisely. Combining
the multichannel catheter mapping technique with return cycle mapping
would provide a rapid and systematic means of localizing the CCP during
catheter ablation of VT.
Acknowledgments
This study was supported in part by National Institutes of
Health Grant R01-HL-32257. The authors would like to acknowledge the
excellent technical assistance of Donna Hand, Steven Labarbera, Timothy
Morris, Duane Probst, and Dennis Gordon. We also thank Barry Branham
and John Platt for computer programming and Dawn Schuessler for
preparation of the manuscript.
References
Top
Abstract
Introduction
Methods
Results
Discussion
References
1.
Morady F, Scheinman MM, Di Carlo LA Jr, Davis JC,
Herre JM, Griffin JC, Winston SA, de Buitleir M, Hantler CB, Wahr JA,
Kou WH, Nelson SD. Catheter ablation of ventricular
tachycardia with intracardiac shocks: results in 33
patients. Circulation. 1987;75:1037–1049.
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