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(Circulation. 1995;92:3082-3088.)
© 1995 American Heart Association, Inc.
Articles |
Influence of Epicardial Patches on Defibrillation Threshold With Nonthoracotomy Lead Configurations
Presented in part at the 67th Scientific Sessions of the American Heart Association, Dallas, Tex, November 14-17, 1994, and published in abstract form (Circulation. 1994;90[pt 2]:I-123).
From the Medical Clinic I, Charité Hospital, Berlin, Germany (P.C.F.); Department of Medicine, University of Alabama at Birmingham (R.E.I., R.G.W.); Departments of Medicine and Pathology, Duke University Medical Center (R.L.C.), and the Engineering Research Center for Emerging Cardiovascular Technologies, Department of Biomedical Engineering of the School of Engineering, Duke University, Durham, NC (S.F.I.); and the I. Medical Clinic, Technische Universität, Munich, Germany (E.U.A.).
Correspondence to Raymond E. Ideker, MD, PhD, University of Alabama at Birmingham, Volker Hall G78A, 1670 University Blvd, Birmingham, AL 35294-0019.
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Abstract |
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 Top Abstract IntroductionMethods Results Discussion References |
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Background In previous studies, epicardial patch electrodes decreased transthoracic defibrillation efficacy. We studied the effects of two inactive epicardial 14-cm2 titanium mesh patches on defibrillation energy requirements with nonthoracotomy internal lead configurations.
Methods and Results A 6/6-millisecond biphasic shock waveform was
delivered via several electrode configurations 10 seconds after
ventricular fibrillation was initiated with a 60-Hz
generator. In two series, a total of 16 dogs (weight, 23.3±2.4 kg)
underwent an up-down defibrillation protocol. In the first series,
the defibrillation threshold (DFT) was determined for each electrode
configuration in the presence of two inactive epicardial patches. In
the second series, DFTs were determined in the presence of an inactive
right ventricular (RV) or left ventricular (LV)
patch alone. For several nonthoracotomy lead configurations tested in
the first 8 dogs, the mean±SD DFT energy increased 49% to 97% with
two inactive patches on the heart compared with no patches on the heart
as follows: RV to superior vena caval (SVC) electrode, from 8.9±2.6 to
18.0±14.3 J; RV to SVC plus subcutaneous array electrode, from
7.0±2.4 to 10.7±5.3 J; RV to subcutaneous pectoral plate
electrode,
from 6.2±1.3 to 11.4±4.0 J (P
.05). The lowest DFT
was
achieved by defibrillating between the epicardial patches (3.8±3.3 J).
The second series showed that DFT voltage requirements increased
significantly for all three nonthoracotomy lead configurations with the
inactive LV patch alone (P.05) but not with the inactive
RV patch alone.
Conclusions Inactive epicardial patches can significantly increase the defibrillation energy requirements for nonthoracotomy lead configurations. This negative impact may be due to an insulating effect of the patches and to a disturbance of the potential gradient field under the patches. If the same holds true in patients, these results have clinical implications. Functioning epicardial patch leads should be incorporated in the defibrillation lead system if already present. If the LV patch is nonfunctioning, such as because of a lead fracture, the marked increase in DFT due to an inactive LV patch calls for thorough DFT testing during surgery and, in selected patients, may necessitate patch removal to produce an effective transvenous-based system.
Key Words: defibrillation • death • sudden • fibrillation
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Introduction |
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TopAbstractIntroductionMethods Results Discussion References |
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Implanted defibrillators are a well-accepted therapy for patients with life-threatening ventricular arrhythmias.1 2 3 4 5 6 Most of these clinically implanted devices formerly had epicardial lead systems.1 2 7 With the introduction of nonthoracotomy transvenous and transvenous/subcutaneous lead configurations3 8 9 10 and the first clinical investigations using the defibrillator generator as an electrode,11 primary placement of epicardial patch electrode configurations can be avoided in the majority of patients. Patients who underwent implantation of epicardial systems and now require system replacement because of battery depletion, lead fracture, dislodgment, or infection of the patches12 13 are possible candidates for these new transvenous lead–based systems.
Several studies have shown an increase of transthoracic defibrillation requirements due to epicardial patches.14 15 One explanation for this elevation is the insulation of the heart covered by the patches.14 15 Little is known of the impact of epicardial patches on the DFT when transvenous systems are used. In a recent study,16 our group showed a significant increase in defibrillation energy requirements caused by an inactive LV epicardial patch when an endocardial lead configuration was used. However, this epicardial patch was placed in that position of the ventricle in which the potential gradient generated by the shock was believed to be weakest. It is not known if inactive epicardial electrodes on the RV and LV in locations in which they are placed clinically increase defibrillation requirements for electrode configurations that are or soon will be in clinical use. On the basis of our previous findings,16 we investigated the effect of an epicardial patch system on several clinically used endocardial, subcutaneous, and epicardial lead configurations1 3 8 11 17 18 19 20 in one series of animals. In a second series of animals, we examined the impact of the RV or LV patch alone on these lead configurations.
A second clinically relevant scenario we wanted to investigate in animals was based on the fact that patients receiving defibrillators with nonthoracotomy-based lead systems frequently undergo a later open-chest procedure for other medical reasons. Studies21 22 have investigated the effect of a thoracotomy on transthoracic and epicardial defibrillation but not on defibrillation with nonthoracotomy electrode systems. Kallok21 showed no significant change in the DFT between an open and a surgically closed chest when epicardial electrodes were used. Kerber et al22 showed a significantly lower impedance for a surgically closed chest compared with an intact chest but did not determine a DFT. We investigated the effect on defibrillation requirements and impedance of opening and surgically closing the chest using nonthoracotomy-based lead systems.
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Methods |
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TopAbstractIntroductionMethods Results Discussion References |
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This study was approved by the Institutional Animal Care and Use Committees at Duke University and the University of Alabama at Birmingham. It conforms to the guidelines of the American Heart Association on research animal use adopted November 11, 1984.
Animal Preparation
In 16 mongrel dogs (weight,
23.3±2.4 kg; 8 dogs in each
series), anesthesia was induced with pentobarbital (30 to
35 mg/kg body weight IV) and maintained with a continuous infusion of
pentobarbital at a rate of approximately 0.05 mg/kg per
minute.23 24 Succinylcholine (1 mg/kg) was also given
intravenously at the time of anesthesia
induction. Supplemental doses of succinylcholine (0.25 to 0.5 mg/kg)
were given as needed to maintain muscle relaxation. The animals were
intubated with a cuffed endotracheal tube and ventilated with room air
and oxygen through a Harvard respirator (Harvard Apparatus
Co). A peripheral intravenous line was
inserted, and normal saline was continuously infused. A femoral
arterial line was placed for hemodynamic
monitoring as well as for arterial blood gas
analysis and electrolyte measurements. Normal
metabolic status was maintained throughout the study by
taking blood samples every 30 to 60 minutes and correcting any abnormal
values. ECG leads were applied for continuous ECG monitoring of lead
II. R2 patches (R2 Medical Systems Inc) were placed for external
defibrillation. Body temperature was measured via an esophageal
temperature probe and maintained at 35°C to 37°C with a thermal
mattress and heat lamp. At the end of the study, euthanasia was induced
with a potassium chloride injection. The heart was removed and
weighed.
Electrodes
One 11F defibrillation catheter (Cardiac
Pacemakers Inc) with a
distal 3.7-cm RV coil electrode, a 6.8-cm SVC coil electrode 9 cm
proximal to the distal coil, and a pacing electrode tip 5 mm distal
from the RV coil was placed through a right jugular vein incision.
Under fluoroscopic guidance, the distal coil was advanced in the RV
apex and the proximal coil was positioned in the SVC to serve as an
anode for the first phase of the biphasic shock. A three-wire array
(each wire 18 cm long) with a surface area of 6
cm225 26 27 28 29
was tunneled subcutaneously on
the left lateral chest wall (Fig 1
) to serve in
conjunction with the SVC electrode as a second anode for the first
phase of the biphasic shock (configurations 2, 5, and 8 in Table
1). A stainless steel plate (8.2x7.6x0.62 cm) was
placed in a left upper anteroaxillary line position (Fig 1) to
serve as
a third first-phase anode (configurations 3, 6, and 9). The
endocardial lead and subcutaneous electrodes were left in place;
electrode positions were unchanged for all configurations during the
study (Fig 1).
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Series I
At first, the
animal's chest was left intact. DFTs were
determined in random order for all three electrode configurations
(configurations 1, 2, and 3). Then the chest was opened through a
median sternotomy, and the heart was exposed and suspended in a
pericardial cradle. Depending on the outcome of a binary randomization
technique, two 14-cm2 titanium mesh epicardial patches
(Cardiac Pacemakers Inc) either were positioned (Fig 2)
on the anterolateral wall of the RV and the posterolateral wall of the
LV (configurations 7 through 12) or they were not so positioned
(configurations 4, 5, and 6). Chest tubes were placed, and constant
negative pressure was applied after the chest was closed in an airtight
manner. After determining the DFTs for the electrode configurations,
the patches were placed (if they had not been previously placed) or
removed (if they had been previously placed). Again, chest tubes were
placed, the chest was closed in an airtight manner, constant negative
pressure was applied, and DFTs were determined. For further
information, see Table 1
.
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Series II
In this series, the chest was opened at the beginning of the
study. On the basis of randomization, (1) no patch electrode
(configurations a, b, and c), (2) the RV patch (configurations d
through g), (3) the LV patch (configurations h through k), or (4) both
patches (configuration l) were placed. Surgical procedures were the
same as for the first series of animals. For further information, see
Table 2.
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Defibrillation Protocol and Data Acquisition
Defibrillation
success was determined by a threshold
value.24 30 31 In series I, DFTs were
determined first
with the chest intact in all animals (configurations 1, 2, and 3), then
the dogs were randomized to have the patches placed or not placed. In
all three groups (intact chest and surgically closed chest with and
without patches), the tested electrode configurations (Table 1)
were
randomized. In series II, the order in which the four groups (Table
2)
were tested was also randomized. On the basis of randomization, one or
two 14-cm2 titanium mesh patches were sutured securely to
the epicardium. In both series, the patches remained disconnected from
any electrical source when not used as electrodes. Defibrillation
testing was performed by following a modified up-down
protocol32 that started with a leading-edge voltage of
400 V. The initial step size was 40 V. If the first shock failed, then
incremental 40-V shocks were given until a defibrillation success
occurred. If the first shock succeeded, then decremental 40-V shocks
were performed until the shock failed. After a reversal point was
established, the step size was decreased to 20 V. DFT was defined as
the lowest voltage required to defibrillate.
Ventricular fibrillation was induced by 60-Hz alternating current through the pacing tip of the RV apex defibrillation lead, with the return electrode on the animal's chest wall. Fibrillation was allowed to continue for 10 seconds before attempting defibrillation. A failed shock was followed by a rescue shock of higher voltage delivered between the electrodes. If the rescue shock failed, it was followed by external defibrillation given by a Life-Pak 8 defibrillator (Physio-Control Corp). A minimum of 4 minutes elapsed between each fibrillation-defibrillation attempt. Fibrillation was not reinitiated until blood pressure and heart rate returned to normal.
The defibrillation electrodes were connected to a defibrillator (HVS-02, Ventritex Inc). The defibrillator delivered a single-capacitor biphasic shock from a 150-µF capacitor bank. The truncated exponential biphasic shock used a second phase of opposite polarity to the first, with the second phase leading-edge voltage equal to the first phase trailing-edge voltage rounded to the nearest 10 V. The duration of each of the two phases was 6 milliseconds with a 1-millisecond delay between phases. The actual current and voltage waveforms were digitized at 20 kHz and recorded by a Data Precision 6100 waveform analyzer. Signal analysis software within the analyzer was used to obtain impedance and energy measurements. Data were transferred to a Macintosh computer for analysis.
Statistical Analysis
Data are expressed as mean±SD for
energy, voltage, current, and
impedance for all DFT determinations. ANOVA was adjusted for repeated
measurements and was performed for the different electrode
configurations. Patch on/patch off data were compared by use of paired
t test. Comparison of the two animal series was done by use
of a t test. A value of P.05 was considered
significant.
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Results |
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TopAbstractIntroductionMethods Results Discussion References |
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Series I
Table 3
shows the leading-edge
voltage,
leading-edge current, mean impedance of the first phase, and total
energy of both phases at DFT. The data show the mean (SD for the
RV–to–SVC (RV–SVC), RV–to–SVC plus subcutaneous
wire array
(RV–SVC+array), and RV–to–steel plate (RV–plate)
electrode
configurations in the intact chest model and in the surgically
closed-chest model with the inactive patches on and off the heart.
Opening the chest decreased the voltage requirements for defibrillation
as follows: 17% for the RV–SVC, 12% for the RV–SVC+array, and
10%
for the RV–plate. Total energy also decreased: 46% for the RV–SVC,
24% for the RV–SVC+array, and 24% for the RV–plate. There was
no
statistically significant difference for voltage and energy between
intact and surgically closed chest without patches. Mean values for
current increased between 2% and 14% from the intact chest to the
surgically closed chest. Impedance for the surgically closed–chest
model without patches was 22% to 24% lower than for the
intact-chest model with the three transvenous/transvenous plus
subcutaneous electrode configurations (P.001).
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Table
3 also shows the leading-edge DFT voltages for the three
transvenous/transvenous plus subcutaneous electrode configurations with
the patch on or off the heart. Voltage increased 34% with the inactive
patches on the heart for the RV–SVC configuration, 21% for the
RV–SVC+array, and 33% for the RV–plate (P.05). A
major
increase was seen in DFT energy requirements in the presence of the
inactive patches: 97% for the RV–SVC configuration, 49% for the
RV–SVC+array, and 81% for the RV–plate (P.05).
Changes
in DFT current were between 17% and 32% (P.05). In
contrast to the above-mentioned impedance changes of the
intact-chest comparison, impedance for the
patch-off/patch-on groups changed only insignificantly.
Table
4 shows the mean±SD for DFT voltage, energy,
current, and impedance for shocks delivered via the epicardial patch
configurations. Voltage, energy, and current were significantly lower
for the RV patch–LV patch configuration. Voltage was 62% higher for
the RV coil–LV patch and 66% higher for the RV coil–LV+RV
patch
compared with the RV patch–LV patch configuration. Energy was 150%
and 170% higher and current was 77% and 208% higher for the RV
coil–LV patch and the RV coil–LV+RV patch, respectively,
compared
with the RV patch–LV patch configuration. Impedance was 76% lower for
the RV coil–LV+RV compared with the RV patch–LV patch and 61%
lower
compared with the RV coil–LV patch configuration
(P.05).
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Series II
One animal had high defibrillation requirements in
all
configurations (including RV patch to LV patch) and could not be
defibrillated with several transvenous electrode configurations
(regardless of the presence of a patch) and was therefore excluded from
data analyses. On macroscopic examination, no obvious reason
for the high DFT was found.
Table 5 shows the
mean±SD for the remaining seven
animals. There was no statistically significant difference between the
two studies with regard to the three transvenous electrode
configurations (without patches) of each series (P=.9). For
all three transvenous lead systems, lowest defibrillation voltage,
energy, and current were achieved when no patches were on the heart.
Placing one inactive epicardial patch on the RV increased the voltage
for the RV–SVC configuration by 20% (43% for energy), for the
RV–SVC+array configuration by 12% (31% for energy), and for the
RV–plate configuration by 20% (32% for energy). These increases were
not statistically significant. Compared with no patch on the heart,
placement of an inactive LV patch on the epicardium resulted in an
increase in voltage of 34% (86% for energy) for the RV–SVC
configuration, 17% (33% for energy) for the RV–SVC+array, and 23%
(54% for energy) for the RV–plate configuration. The increase in
voltage was significant for all three transvenous lead configurations
(P.05). The increase in energy was not quite significant
(P=.06).
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Table 6 shows the mean (SD for
the configurations
involving epicardial electrodes. No difference was seen when
defibrillating between the RV coil and the RV patch regardless of the
presence of an inactive LV patch.
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No significant difference was seen when comparing the RV coil–LV patch with RV patch (series I) configuration to the RV coil–LV patch without RV patch (series II) configuration.
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Discussion |
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TopAbstractIntroductionMethods Results Discussion References |
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Implantable defibrillators that use epicardial patches are an accepted therapy for patients with ventricular arrhythmias.1 2 3 4 5 6 Despite the beneficial effect of a defibrillator on survival of sudden cardiac death, the operative and postoperative risk of placement of epicardial patches is significant.2 33 34 With the development and approval of transvenous and transvenous/subcutaneous electrode–based devices8 11 18 35 and the clinical investigation of a pectorally implanted defibrillator used as an electrode,11 a decreasing percentage of patients will undergo defibrillator implants that use epicardial patches. Recent studies1 have shown acceptable DFTs36 with these transvenous and transvenous/subcutaneous devices.
The question arises of whether patients with epicardial patches who are undergoing device replacement should receive an epicardial or transvenous-based system. Several factors will influence this decision. Possible causes for replacement are end of battery life, pouch or lead infection, and epicardial lead and patch failure or fracture. This decision must be made for patients in whom epicardial patches were prophylactically placed during open-chest surgery without implanting a generator. Another consideration is the possibility that DFT can be lowered in patients with epicardial patches and high DFTs with the addition of an endocardial electrode. The decision to implant an epicardial or transvenous-based system will be made on the basis of the reason for replacement, the abdominal or pectoral implant experience of the surgeon or cardiologist, and the availability of improved leads and devices at that time.
On the basis of knowledge of the increase in transthoracic defibrillation requirements caused by epicardial patches14 15 and the impact of an inactive LV patch on an endocardial lead system,16 we investigated the effect on DFT of two clinically used epicardial patches that utilize transvenous and transvenous/subcutaneous electrode systems in the first group of animals (series I) . In the second group of animals (series II), we examined the effect on DFT of one epicardial patch in the transvenous lead systems and the effect on DFT of an inactive epicardial patch in lead configurations in which the other epicardial patch is incorporated in the defibrillation system. Despite the limitations of such an animal model for human application, we studied three configurations: a transvenous electrode configuration (RV–SVC), a transvenous/subcutaneous configuration (RV–SVC+subcutaneous array), and a configuration consisting of a RV catheter electrode and a stainless steel plate (RV–plate) placed in the left upper thorax to mimic pectoral placement of a defibrillator in which the generator serves as an electrode.8 9 10 11 17 20 35 Applicability of the results, especially for the last configuration, is limited by the anatomic differences between dogs and humans. The aim of the present study was not to find the best electrode location,37 38 39 achieve very low DFTs,40 or investigate the impact of cardiac diseases such as an acute myocardial infarct.41 42 Instead, our aim was to focus on the relative changes in DFT caused by the presence of electrically floating epicardial patches for these three nonthoracotomy lead systems.
The most likely explanation for the increase in defibrillation
requirements caused by the inactive epicardial electrodes is the
creation of an area of low potential gradient under the
patches16 43 44 45 46
because of current shunting through the
very low impedance of the patches. This is probably the primary effect
with a pure transvenous system. In configurations with a subcutaneous
electrode, the insulation on the back of the patches may also influence
DFT energy requirements by decreasing current flow through the LV from
the RV endocardial electrode to the array or plate. Because the area
subtended by the subcutaneous wire array is larger than that subtended
by the plate or the SVC electrode, the electric field for the array
might be larger and more evenly distributed throughout the LV.
Alternatively, the direction of the electric field may be more parallel
to the LV insulating patch than the field from the plate or the SVC
electrode, so that less current flow is blocked for the wire array.
These may be the reasons for the slightly larger increase in
defibrillation requirements of the RV–plate or RV–SVC
configurations
compared with the RV–SVC+array combination. The three
configurations
were not quite significantly different for energy and voltage
(P.06) but were significantly different for current and
impedance (P.05) in the configurations that used the
inactive epicardial patches. In series II, we showed that an inactive
LV patch caused a larger increase in the DFT than an inactive RV patch.
Interestingly, when defibrillating between the RV endocardial coil
electrode and the RV epicardial patch, the defibrillation requirements
are not altered by an inactive LV patch. In contrast, when
defibrillating between the RV endocardial electrode and the left
epicardial patch, the right inactive patch affects DFT. On the basis of
our data, the inactive RV patch seems to lower the DFT for the RV coil
to LV patch configuration. This might be due to current shunting from
the endocardial coil electrode to the right epicardial patch,
decreasing the very high potential gradients near the RV
coil.47
Our animal studies suggest that in patients with nonfunctioning epicardial patches, it may be advantageous to remove the patches before placing a transvenous system. If they hold true in patients, these results have clinical implications. Functioning epicardial patch leads should be incorporated in the defibrillation lead system if patches are already present. If the LV patch is nonfunctioning, eg, because of a lead fracture, the marked increase in DFT caused by an inactive LV patch calls for thorough DFT testing intraoperatively and, in selected patients, may necessitate patch removal to produce an effective transvenous-based system.
More and more patients receive nonthoracotomy lead systems. Frequently, these patients later undergo open-chest procedures for other medical reasons, eg, bypass grafting. A clinically relevant question is, "How does opening the chest affect the defibrillation requirements of nonthoracotomy lead systems?" Two previous investigations21 22 showed the influence of opening the chest on impedance and on DFT. Kallok21 showed no difference in DFT for a closed-chest versus an open-chest determination. That comparison was made with epicardial patches; no endocardial or endocardial/subcutaneous configuration was tested. Kerber et al22 reported significantly lower transthoracic impedance in humans for an intact chest than for a surgically closed chest. They found no statistical difference between the measurement of impedance soon after surgery and several weeks after surgery. No DFT measurements were reported in their study.
In the present study, defibrillation requirements were determined first for the intact chest and then for the surgically closed chest for three nonthoracotomy electrode configurations. Like Kerber et al,22 we found that impedance was significantly decreased by surgically opening and then closing the chest, but we found only an insignificant decrease in DFT energy and voltage between the intact chest and the surgically closed chest for nonthoracotomy lead-based systems. Interestingly, the decrease in impedance did not affect DFT requirements, even in the two electrode configurations that used subcutaneous electrodes (RV–array, RV–plate). On the basis of the studies of Kerber et al22 and Kallok21 and our present findings, we conclude that opening the thorax does not increase the defibrillation energy requirements of nonthoracotomy lead-based systems.
We also determined the DFT for shocks (1) between the two epicardial patches, (2) from a RV endocardial coil electrode to a right epicardial patch, (3) from a RV endocardial electrode to a left epicardial patch, and (4) from a RV electrode to both epicardial patches. The purpose for these determinations was to see whether the DFT could be lowered by adding a transvenous RV electrode and defibrillating between it and one or both of the epicardial patches. The highest DFT was achieved by defibrillating between the RV coil electrode and the RV patch. The DFT energy, voltage, and current were significantly higher for the endocardial to epicardial configurations (RV coil–RV patch, RV coil–LV patch, and RV coil–LV patch+RV patch) than for the epicardial configuration (RV patch–LV patch). Even though the impedance was significantly lower for the RV coil–LV patch+RV patch compared with the RV patch–LV patch combination, the DFT was significantly higher. This may be because having two epicardial electrodes tied together at the same voltage created a region approximately halfway between these electrodes, near the anterior and posterior interventricular grooves, in which the shock electric field was very weak.48 Our animal data suggest that in patients with functioning epicardial patches, adding an endocardial lead and defibrillating between the RV electrode and the epicardial patches may not be beneficial.
Conclusion
Within the limitations of an animal model, our
results demonstrate
a significant increase in voltage, energy, and current defibrillation
requirements of nonthoracotomy lead systems in the presence of an
inactive LV epicardial patch. This may be due to an area of low
potential gradient under the patch, current shunting, and insulation by
the patch. Shocking from a RV catheter to one or both epicardial
patches resulted in a higher DFT than shocking between the two
epicardial patches alone. On the basis of these animal data, the
simultaneous use of nonthoracotomy lead systems and
inactive epicardial patches should be reconsidered. Opening the chest
does not significantly change the defibrillation energy, voltage, and
current of nonthoracotomy lead-based systems, despite a significant
decrease in impedance.
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Selected Abbreviations and Acronyms |
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Acknowledgments |
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This study was supported in part by American Heart Association Grant NC-93-SA-05, National Institutes of Health research grants HL-42760 and HL-44066, and National Science Foundation Engineering Research Center grant CDR-8622201. The authors wish to thank Ellen Dixon-Tulloch, Jenny Hagler, Sharon Melnick, Biyu Zheng, Danielle Winkler, and Kim Mulligan for their technical assistance.
Received May 23, 1994; revision received June 8, 1995; accepted July 5, 1995.
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