(Circulation. 1995;91:2385-2391.)
© 1995 American Heart Association, Inc.
Articles |
Effect of Subendocardial Resection on Sinus Rhythm Endocardial Electrogram Abnormalities
From Temple University Hospital, Philadelphia, Pa.
Correspondence to John M. Miller, MD, Parkinson Pavilion, Temple University Hospital, 3401 N Broad St, Philadelphia, PA 19140.
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Abstract |
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Background Patients with sustained ventricular tachycardia after acute myocardial infarction frequently have characteristic abnormalities of left ventricular endocardial electrical activity, including fractionated (prolonged, multicomponent, low-amplitude), split (having discrete widely separated deflections), and late (extending after the end of the QRS complex) electrograms. The exact cause and source of these electrograms are not clear.
Methods and Results In this study, endocardial electrograms from 18 patients were recorded with a 20-electrode array from the same area immediately before and immediately after resection of subendocardial tissue at the time of surgery for ventricular tachycardia. Electrograms could be compared before and after resection from 298 of 360 (83%) of the electrodes. Before resection, split electrograms were present in 130 (44%) and late components in 81 (27%) of the recordings. Recordings made after resection showed fewer abnormalities, including complete absence of split electrograms as well as all previously recorded late components (P<.02). Mean electrogram amplitude increased from 0.5±0.8 to 1.0±1.6 mV (P<.0001) because of removal of the attenuating effect of endocardial scar; mean duration decreased from 112±38 to 65±27 ms (P<.0001) mainly because of loss of late and split components. Overall electrogram contour was very similar aside from these changes.
Conclusions These data show that (1) some of the signal recorded on the endocardial surface is derived from deeper tissue layers and (2) split and late electrogram components appear to be generated by cells in the superficial endocardial layers, since they are eradicated by removal of this tissue. These findings correspond well with previous histological studies of resection specimens that show bundles of surviving muscle cells separated by layers of dense scar that act as an insulator.
Key Words: tachycardia • electrocardiography • endocardium • mapping
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Introduction |
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TopAbstractIntroductionMethods Results Discussion References |
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In patients with uniform sustained ventricular tachycardia (VT) in the setting of a healed myocardial infarction, abnormal electrical activity can frequently be recorded from the left ventricular endocardium during normal sinus rhythm (NSR).1 2 3 4 5 These abnormal electrograms have been classified in several ways: fractionated (prolonged, multicomponent, low amplitude), late (lasting beyond the end of the surface QRS complex), and split (having two or more discrete electrogram components). There is evidence that these abnormal electrograms account for characteristic abnormalities in the surface signal-averaged ECG (the "late potential").4 6 In many patients undergoing subendocardial resection for VT, the signal-averaged ECG is normalized (loss of a preoperative low-amplitude late potential).7 8 9 We hypothesized that subendocardial resection removed the tissue responsible for the genesis of the surface late potential as well as other endocardial electrogram abnormalities. We investigated this possibility by recording endocardial NSR electrograms from the same location (left ventricular apical septum) before and immediately after subendocardial resection during surgery for sustained VT. We sought to determine whether the abnormal electrograms recorded were intrinsic to the endocardium or represented electrical activity originating in deeper layers.
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Methods |
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TopAbstractIntroductionMethods Results Discussion References |
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Patient Population
The study group in this series consisted of 18 men 55±9 years old (mean±SD; range, 37 to 68 years), all of whom had a history of anteroseptal myocardial infarction from 2 weeks to 24 years previously. Each patient had multiple episodes of sus- tained uniform-morphology VT, and all had undergone electrophysiological studies at which programmed ventricular stimulation yielded an inducible sustained uniform morphology of VT despite the subsequent addition of antiarrhythmic drug ther- apy. In each patient, the decision was made to undergo surgical treatment (map-guided subendocardial resection) for VT.
Intraoperative Study
All patients underwent elective
map-guided subendocardial
resection according to the following protocol: The heart was approached
via median sternotomy in the usual fashion and, after establishment of
normothermic cardiopulmonary bypass, an aneurysmotomy was made at the
left ventricular apex. Right and left ventricular stainless steel
bipolar plunge endocardial electrodes were inserted for recording and
pacing. Throughout the study, recordings were made of surface leads I,
II, III, and V5R, right and left ventricular
endocardial reference electrograms, and the mapping electrodes. VT was
initiated by programmed stimulation and endocardial mapping performed
with a roving bipolar or quadripolar electrode probe. At the conclusion
of VT mapping, a 2x3-cm electrode array (consisting of 20 bipoles with
1-mm interelectrode distance; Fig 1A
) was placed on an
area of the apical septum that was to be resected (Fig 2A).
This was in all cases on or near a septal
endocardial site from which earliest electrical activity during at
least one VT could be recorded. The array was oriented in such a
fashion that one edge of the array was aligned with the ventriculotomy
incision to facilitate reproducibility of placement of the array after
resection. In the first several cases, a marking suture was affixed to
the endocardium at one corner of the array; this proved unnecessary for
accurate placement and was not continued during the remainder of the
study. Recordings were made with the electrode array during sinus
rhythm, after which the electrode array was removed and subendocardial
resection was performed on the normothermic heart (Fig 2B).
Immediately
after resection, the electrode array was placed back in the same
location as before resection, aligning with previously determined
landmarks (Fig 2D). Recordings were then repeated during sinus
rhythm.
In three cases, the resected specimen was fit back in situ, the
electrode array was placed over the specimen, and recordings were
repeated during sinus rhythm. After these recordings, the remainder of
the surgical procedure was performed, which included endocardial
cryoablation in 10 patients and instillation of cardioplegia into the
aortic root and coronary artery bypass graft surgery in 8 patients.
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Data Analysis
Electrograms recorded with the electrode array
were written on
paper at a speed of 200 mm/s, and measurements were made of amplitude
(peak to peak) and electrogram duration (onset to offset);
reproducibility and accuracy of measurements were consistently ±0.1 mV
in amplitude and ±5 ms in duration. Electrograms were classified
according to the following criteria (see Fig 1B
): normal,
amplitude
>0.6 mV and duration <70 ms (all other electrograms were classified
as abnormal); fractionated, abnormal electrogram with amplitude <0.3
mV and duration >90 ms; split, abnormal electrogram with two or more
discrete components separated by at least 30 ms of electrical
quiescence; and late, an abnormal electrogram, a portion of which
extended beyond the end of the surface QRS complex. Electrograms could
be classified in more than one way (eg, fractionated and late).
Statistical analysis was performed with the paired
t test (comparing electrogram parameters before and
after resection), and qualitative abnormalities were compared by
2 analysis; statistical significance was
ascribed to differences with P<.05.
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Results |
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Electrograms could be analyzed from 301 of 360 (84%) of the electrodes before resection and from 311 of 360 (86%) after resection (the difference is accounted for by extremely low-amplitude signals before resection having increased in amplitude after resection). Before resection, 15 electrograms (5%) were normal, 63 (21%) fractionated, and 223 (74%) abnormal but not fractionated, compared with 161 (52%) normal, 24 (8%) fractionated, and 126 (40%) abnormal/nonfractionated after resection (P<.001). Split potentials were present in 130 recordings (44%) before resection but in none after resection; late electrogram components were present in 81 recordings (27%) before and 5 (2%) after resection. All of the latter 5 electrograms were from a single patient and were recorded at sites lacking late components before resection.
Among 298 electrograms that could be compared before and after
resection (ie, recorded from the same electrode), the mean amplitude
increased from 0.5±0.8 to 1.0±1.6 mV (P<.0001) and
the
mean duration decreased from 112±38 to 65±27 ms
(P<.0001). Increases in amplitude of >0.2 mV were
present in 146 recordings (49%), a similar decrease in amplitude
was present in 37 (12%), and 115 electrograms (39%) changed by
0.2 mV after resection. Among the same electrograms, 242 (81%)
decreased by >5 ms in duration, 43 (14%) increased in duration by the
same amount, and 13 (5%) showed 5 ms change in duration. Examples of
changes in electrograms after resection are shown in Figs 3 and
4. A summary of how each type of
electrogram was affected by resection is shown in Fig 5.
In general, signals recorded from each electrode were less abnormal
after resection than before resection because of the combination of
increased amplitude and decreased duration as noted above. Among these
298 paired recordings, the proportion of normal electrograms increased
from 5% to 52% (15 to 154) of the total, abnormal electrograms
decreased in prevalence from 74% to 40% (220 to 120), and
fractionated electrograms decreased from 21% to 8% (63 to 24); this
shift was significant at the P<.03 level. Similarly, the
marked changes in the prevalence of split and late electrograms
after resection was significant (P<.02).
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In the 3 patients who had the resected specimen replaced in situ and
recordings repeated with the array, a total of 50 recordings could be
compared (before resection versus after replacement of specimen). Among
these, the mean amplitude decreased from 1.0±1.5 to 0.7±1.0 mV
(P<.002), and the mean duration decreased from 118±50 to
66±21 ms (P<.0001). In each case, the morphology of the
electrograms after specimen replacement was very similar to that
recorded before resection, except for the absence of late and split
potentials (Fig 4).
One patient died of low cardiac output in the perioperative period. The remaining patients underwent postoperative electrophysiological stimulation to assess the efficacy of surgery in preventing inducibility of VT. The stimulation protocol included delivery of one, two, and three ventricular extrastimuli after at least two drive cycle lengths from two right ventricular sites and burst pacing at cycle lengths from 350 to 250 ms except for 1 patient who suffered a perioperative pulmonary embolus; stimulation was performed with epicardial pacing wires (one site) and included quadruple extrastimuli after four drive cycle lengths. Among these 17 patients, 1 had inducible sustained monomorphic VT.
Preoperative and postoperative signal-averaged ECGs were comparable in 10 of the patients (in the remainder, either one of the studies had not been performed or a new bundle branch block or complete heart block was present after surgery, precluding direct comparison). Among these patients, 7 had a positive study (a low-amplitude late potential) before surgery. In 4 of these patients, the low-amplitude late potential was absent after surgery, whereas the study became positive in 2 additional patients who had negative studies before surgery. One patient had negative studies before and after surgery. The 1 patient with persistence of inducible VT after surgery had a normal study before surgery that became abnormal after surgery; the patient in whom endocardial late electrograms were first recorded after resection had abnormal signal-averaged ECGs before and after surgery.
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Discussion |
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TopAbstractIntroductionMethods Results Discussion References |
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This is the first study to directly compare characteristics of endocardial electrograms recorded before and immediately after resection of arrhythmogenic ventricular tissue. In this study, there was an overall tendency for electrograms to change to less abnormal types after resection; that is, fractionated electrograms generally became either abnormal or even normal, and abnormal electrograms tended to become normal. Of greater interest, late and split components were uniformly eliminated by resection.
The observed increase in electrogram amplitude after resection appears
to be due to removal of scar tissue that had attenuated the signal from
deeper layers. This is evidenced by both the similarity in basic
electrogram morphology before and after resection (except for the
tendency toward an increase in signal amplitude after resection) and
the striking similarity in electrogram morphology when the preresection
recordings were compared with those made after replacement of the
specimen (Fig 4). The decrease in overall electrogram duration
after
resection was primarily due to removal of late electrogram components;
in all sites from which either late or split components were recorded
before resection, these components were absent in the postresection
recordings. This indicates that these electrogram components were
generated by cells in the more superficial layers of endocardium that
had been removed with the resection. The absence of these components in
recordings made after replacement of the specimen is further evidence
of their endocardial origin.
Low-amplitude late components were first observed after resection in five recordings (not present in preresection recordings). This is probably explained by the signal-attenuating effect of the overlying scar tissue, the removal of which allowed the late components to be observed. This also suggests that although late components are almost always recorded from the superficial endocardial layers, this is not uniformly the case.
Split and Late Electrograms
A large proportion of recordings
made during NSR in this study
showed split electrograms: two activations recorded from the same area
but at different times. These activations clearly do not derive from
the same cells, since the interval between discrete activations is far
less than a ventricular or Purkinje effective refractory period.
Rather, the two or more discrete spikes in these electrograms appear to
represent activations of bundles of cells anatomically near
those giving rise to the other discrete activations recorded in the
same electrode but insulated from the effects of depolarization of
these cells by interposed scar tissue.10 11 Similar
split
potentials can be observed during VT (Fig 3). Previous models
of VT
have generally been two-dimensional and have depicted the cells
responsible for split potentials as separated in the same (horizontal)
plane.12 13 The present study suggests that the cells
responsible for the discrete components of a split electrogram are
separated in the vertical plane: the later-occurring component is
recorded from the endocardial surface and the earlier component from
subjacent myocardial layers, since the later components of these
electrograms are uniformly eradicated by subendocardial resection.
The discrete endocardial late and split potentials resemble His-Purkinje potentials. The subendocardial Purkinje network remains relatively intact after acute infarction10 and thus would be expected to produce recordable depolarizations. Although many patients in this study had normal QRS durations in NSR and no evidence of His-Purkinje dysfunction to account for the delayed activation of portions of the Purkinje network, these remain a possible cause of portions of late and split electrograms. This study did not specifically address the potential role of the Purkinje network in the genesis of these electrograms.
The proportions of endocardial split (44%) and late (28%) electrograms in this study were larger than in prior studies1 2 3 5 9 14 ; this is probably a result of differences in mapping techniques. Previous studies have sampled the entire left ventricular endocardium, much of which had relatively normal electrogram characteristics; in this study, electrograms were sampled only in abnormal areas with a much higher likelihood of recording these potentials.
Implications for VT Mapping
El Sherif et al15
have shown that the wave front in
canine infarction models of VT circulates in a figure-eight manner
incorporating a central zone of slow conduction. There is some evidence
of this type of reentry pattern in humans, demonstrated with multipolar
electrode balloon arrays13 16 during intraoperative
mapping. However, not all activation patterns during VT are compatible
with a figure-eight model, at least at the resolution of the recording
techniques.13 17 Many VTs appear to have a
"focal"
origin (that is, an effective point source for the onset of endocardial
activation) without any clear reentrant loop on the endocardium. These
tachycardias could still be based on a figure-eight pattern of reentry,
but a portion of the reentrant loop may be intramural rather than
entirely within the superficial endocardial layers.
Previous studies
have shown a poor correlation between sites from which
late or split electrograms were recorded in NSR and sites from which
the earliest diastolic activity during VT was
recorded,5 18 19 whereas other studies
have shown a
relation between NSR late/split electrograms and middiastolic
potentials recorded at the same sites during VT.20 Such a
relation is demonstrated in Fig 3. The present study does not
resolve this issue, although it shows that the pathophysiology
underlying late and split electrograms—spatial separation of surviving
muscle bundles—is the same as that in current models of VT. In cases
in which the earliest diastolic activity in VT is recorded from sites
that show these delayed electrogram components in NSR, the evidence
that they appear to derive from the superficial (endocardial) layers
serves as an explanation for both the capacity of subendocardial
resection to cure VT and why catheter ablation techniques that target
middiastolic potentials21 22 can be successful in
eliminating VT. Although prior investigations suggested that late and
split electrograms recorded in NSR represent slow conduction
along the endocardial surface, the present study suggests that they
are instead the result of depolarization of different layers of cells
not necessarily activated in sequence.
Signal-Averaged ECG
Previous studies have correlated
resection of endocardial areas
from which late electrograms were recorded at the time of surgery with
changes in the signal-averaged ECG.7 8 9
These studies
showed that when surgery is successful in eliminating inducible VT
after surgery, the signal-averaged ECG is frequently normalized; when
VT is still inducible, the signal-averaged ECG generally remains
abnormal. However, some patients with persistence of inducible VT had
no postoperative late potential, whereas others with a persistent late
potential had a successful surgical outcome. The results of
signal-averaged ECGs in the present study are similar to what has
been reported previously, although only a small sample could be
analyzed.
There are at least three possible explanations for the persistence of an abnormal signal-averaged ECG after even successful subendocardial resection: First, some of the late electrogram components responsible for the surface late potential could derive from residual endocardial scar tissue that was not resected. Second, some of the late electrogram components may originate in deeper (nonresected) layers, as was the case in one of our patients. Last, the surface ECG may be altered by resection (development of bundle branch block or complete heart block requiring ventricular pacing), making comparison of preoperative and postoperative signal-averaged ECGs impossible.
Limitations
The most important potential limitation in this
study is the
ability to replace the recording array after resection precisely over
the area from which recordings were made before resection. As noted
above, marking sutures were initially used to facilitate identical
electrode positioning, but further experience showed this to be
unnecessary. The similarity of electrogram morphologies recorded from
the same electrode before and after resection suggests good
reproducibility in positioning of the array. In addition, the large
proportion of late and split potentials observed in this study were
recorded from several different electrodes on the array; a shift of a
few millimeters in the placement of the array after resection would not
be expected to result in failure to record any of these potentials. It
is possible that tissue trauma incurred during resection could
transiently depolarize some cells, causing their component of the
electrogram to not be recorded after resection. Although this
possibility cannot be excluded, the effect would have to be very
selective (affecting only late and split components), since other parts
of the signal from the same electrodes generally increased in
amplitude.
Finally, this series of patients was relatively homogeneous: all were men with anterior wall myocardial infarctions. The same results may not necessarily apply to patients with VT in the setting of inferior wall infarctions.
Conclusions
This study provides new insight into the nature
of some of the
abnormal endocardial electrogram types observed in patients with VT.
Specifically, our data show that "endocardial" recordings may
actually be generated by cells in multiple tissue layers, since removal
of the superficial endocardial tissue eradicates both the
latest-occurring portion of a split electrogram as well as true late
components (ie, extending beyond the end of the surface QRS complex).
These findings correspond with the known histological abnormalities in
resection specimens, which have shown strata of surviving muscle
bundles separated by layers of dense collagenous scar.
In cases in which split and late electrograms are recorded in sinus rhythm from sites showing middiastolic activity during VT, the VT circuit may traverse a course incorporating some of the deeper layers rather than being exclusively endocardial. Removal or ablation of these sites can still cure VT by eliminating a critical component of the circuit, rather than the entire circuit. Use of advanced mapping tools, such as multipolar electrode arrays,13 16 should allow more precise characterization of the relation between endocardial sinus rhythm electrogram abnormalities and critical components of VT circuits.
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Acknowledgments |
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The authors wish to acknowledge the careful work of Carol Wood in the preparation of this manuscript.
Received May 16, 1994; revision received August 2, 1994; accepted November 26, 1994.
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