Effects of pacing parameters on entrainment of gastric slow
waves in patients with gastroparesis
Z. Y.
Lin1,
R. W.
McCallum1,
B. D.
Schirmer1, and
J. D. Z.
Chen2
2 Thomas N. Lynn Institute
for Healthcare Research, INTEGRIS Baptist Medical Center,
Oklahoma City, Oklahoma 73112; and
1 University of Virginia Health
Science Center, Charlottesville, Virginia 22908
 |
ABSTRACT |
The aim of this
study was to investigate the effect of pacing parameters on the
entrainment of gastric slow waves in patients with gastroparesis. Four
pairs of cardiac pacing wires were placed on the serosal surface of the
stomach in 13 patients with gastroparesis. After a baseline recording
for 30 min, gastric pacing was performed in a number of sessions with
different effective parameters, each lasting for 30 min. The following
parameters were found to be effective for the entrainment of the
gastric slow wave: a pacing frequency 10% higher than the intrinsic
gastric slow wave frequency (IGF), 300 ms pulse width, and 4 mA pacing
amplitude. A reduction of pacing amplitude from 4 to 2 mA and 1 mA
reduced the percentage of entrainment of the gastric slow wave to 79 ± 10% and 50 ± 11%, respectively. Pacing with a pulse width
of 30 or 3 ms was not able to entrain the gastric slow wave in any of
the patients. An ectopic pacemaker of tachygastria found in three
patients was reversed with gastric pacing. It was concluded that
gastric pacing at a frequency up to 10% higher than the IGF and with
an amplitude of 4 mA and a pulse width of 300 ms is able to completely
entrain the gastric slow wave and normalize gastric dysrhythmias in
patients with gastroparesis.
gastric pacing; electrical stimulation; gastrointestinal motility; gastric emptying; electrogastrography
 |
INTRODUCTION |
AS IN THE HEART, there is a pacemaker in the stomach,
located in the midcorpus along the greater curvature. It paces gastric myoelectrical activity generated by smooth muscles, yielding so-called "slow waves" propagating circumferentially and distally toward the pylorus with an increasing amplitude and velocity. The gastric slow
wave is omnipresent, and its frequency in humans is about three cycles
per minute (cpm) (2, 12, 16). The frequency and propagation of gastric
contractions are determined by the gastric slow wave. This is because
second or spike potentials are phase-locked with the gastric slow wave.
Gastroparesis is a chronic disorder of gastric motility, defined as
delayed gastric emptying of a solid meal in the absence of any organic
or structural etiology. Gastroparesis may be attributed to impaired
motor activity and/or impaired myoelectrical activity (1, 3,
6). These include gastric hypomotility, uncoordinated antral
contractions, and uncoupled or dysrhythmic gastric myoelectrical activity. It is known that tachygastria is associated with gastric hypomotility and that uncoupled or dysrhythmic gastric myoelectrical activity leads to a lack of coordinated gastric contractions or peristalsis.
Electrical stimulation has made a recognized therapeutic contribution
in the field of cardiology. However, the role for electrical stimulation in the gastrointestinal tract remains controversial, and
conflicting results have been reported (2, 7, 9, 13, 14, 17-19,
21, 22, 24, 25, 27, 28). No systematic studies have been performed in
humans to derive effective parameters for gastric pacing. Without
optimization of pacing parameters, some investigators claimed success
in entraining the gastric slow wave with gastric pacing, whereas others
reported failure. Only in very few patients with gastroparesis was
electrical stimulation performed (13). The aim of this study was to
derive effective pacing parameters and attempt to entrain the gastric
slow waves in patients with gastroparesis.
 |
MATERIALS AND METHODS |
Subjects.
Thirteen patients (3 male, 10 female, ages 19-52 yr) with a
history of severe gastroparesis participated in the study. Gastric emptying of a solid test meal (4) was performed in nine of the 13 patients, and all showed delayed gastric emptying, a percentage of
retention in 2 h equal to or larger than 70%, a gastric half-emptying time
(t1/2) greater
than 150 min, or both (see Table 1). Four
patients were either not able to eat the solid test meal or vomited
during the test. The common symptoms of these patients were severe
nausea, vomiting, abdominal pain, weight loss, and anorexia. All
patients were refractory to standard medical therapy and underwent
abdominal surgery for the placement of a jejunostomy feeding tube for
nutritional support. The study protocol was approved by the Human
Investigation Committee at the University of Virginia Health Science
Center, and written consent forms were signed by all subjects before
the study.
Placement of pacing electrodes.
Four pairs of temporary 28-gauge cardiac pacing wires (A&E Medical,
Farmingdale, NJ) were placed on the serosal surface of the stomach
during the scheduled surgery for the placement of a feeding jejunostomy
tube. The pacing wires were arranged in an arching line along the
greater curvature from the corpus to the pylorus. The distance between
two electrodes in the pair was 1 cm, and the distance between adjacent
pairs of electrodes was 4 cm. The most distal electrodes were 2-4
cm above the pylorus. The pacing electrodes were affixed to the gastric
serosa by partially embedding the wire in the seromuscular layer of the
stomach. The wires were brought out through the abdominal wall
percutaneously and placed under a sterile dressing. One of the pairs
was used for gastric pacing, and the rest were to record gastric
myoelectrical activity.
Protocol for gastric pacing.
Three days or more after the surgery and the placement of the pacing
wires, while the patients were still in the hospital, myoelectrical
activity of the stomach was recorded via the pacing wires in the
fasting state for at least 1 h to confirm that the pacing wires were in
the right position and functioning.
The study on gastric pacing was initiated 1 wk or more after the
surgery, when the patients had recovered. On the day of the study, each
patient was fasted for 6 h or more and given no medications with known
effects on gastrointestinal motility. First, a 30-min baseline
recording was made via all the pacing wires. Then an adjustable
electrical stimulator (model A310; World Precision Instruments,
Sarasota, FL) was used in a constant current mode, and the stimulus
consisted of periodic rectangular pulses with adjustable frequency,
amplitude, and pulse width. To optimize gastric pacing for the
entrainment of the gastric slow waves, a series of sessions with
different pacing parameters was performed in the fasting state, each
lasting for 30 min. There was a sham pacing for 5-10 min between
two consecutive study sessions. The pacing frequencies tested included
frequencies 10% lower and 10% higher than the intrinsic gastric slow
wave frequency (IGF), and 4, 5.5, and 12 cpm. Three different pulse
width values were used: 3, 30, and 300 ms. The amplitude of the pulse
changed from 1 to 4 mA.
Recording and analysis of gastric myoelectrical activity.
Gastric myoelectrical activity was recorded from the electrodes distal
to the pacing electrodes during the entire study. All signals were
displayed on a Dynograph chart recorder and simultaneously recorded on
a tape recorder. The low and high cutoff frequencies were 0.02 to 30 Hz, respectively. All recorded signals were subjected to both visual
analysis and computerized spectral analysis. For the computerized data
analysis, all recorded signals were played back from the tape recorder,
digitized by a 12-bit analog-to-digital converter, and stored in ASCII
files on an IBM-AT computer. The sampling frequency was 60 Hz. To
reduce the volume of data, the digitized serosal recording was filtered
by a digital low-pass filter with a cutoff frequency of 0.5 Hz and
sampled again at 2 Hz. A smoothed power spectral analysis method called
the periodogram method (23) was applied to compute the power spectrum
of the recording. The frequency of the gastric slow wave with and
without gastric pacing was obtained from the power spectrum. The
gastric slow wave was defined as bradygastria if its frequency was
lower than 2 cpm and had a duration of longer than 2 min. Similarly, the gastric slow wave was defined as tachygastria if its frequency was
greater than 4 cpm.
Percent entrainment was defined to quantitatively assess the effect of
pacing parameters. Percent entrainment was defined as the ratio of the
difference between the recorded slow wave frequency during pacing and
the intrinsic baseline frequency, and the difference between the pacing
frequency and the intrinsic baseline frequency. Entrainment was defined
as 100% if the recorded frequency was exactly the same as the pacing
frequency. If the intrinsic frequency was 3.0 cpm, the pacing frequency
was 3.3 cpm, and the recorded frequency during pacing was 3.2 cpm, the percent entrainment would be 67% [(3.2
3.0)/(3.3
3.0)].
 |
RESULTS |
Entrainment of the gastric slow wave and normalization of gastric
dysrhythmia.
Effective pacing parameters for the complete entrainment of the gastric
slow wave were found to be as follows: pacing frequency, 10% higher
than the IGF; pacing pulse amplitude, 4 mA; pacing pulse width, 300 ms.
With these parameters, the entrainment of the gastric slow wave was
achieved in all 13 patients. The entrainment usually occurred a few
minutes after gastric pacing was initiated (see Figs.
1 and
2). The entrainment of the gastric slow
wave was demonstrated by the fact that the slow waves were phase-locked with the pacing stimulus a few minutes after the initiation of pacing,
as seen in Fig. 1. The mean time required for the complete entrainment
was 5 min (see Fig. 2). It was also observed that the stomach exhibited
a brief memory, with the gastric slow wave remaining entrained for a
few cycles after the termination of gastric pacing. After that brief
period, the frequency of the gastric slow wave was reduced to a level
below the IGF for a few cycles and then returned to the baseline
frequency before pacing. In the baseline recording, the gastric slow
wave showed a regular pattern in nine of the subjects. As shown in Fig.
3, the gastric slow wave propagated
distally with an increasing amplitude and velocity. The frequency of
the gastric slow wave in these patients ranged from 2.60 to 3.0 cpm,
with a mean value of 2.86 ± 0.06 cpm (mean ± SE).

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Fig. 1.
Gastric myoelectrical recording from the most distal pair of electrodes
in 1 patient. A: gastric slow wave
before and after initiation of gastric pacing.
B: gastric slow wave before and after
gastric pacing was stopped. Dots indicate artifacts of gastric pacing
stimulus. During pacing, both gastric slow waves and pacing stimulus
were observed. Slow waves were phase-locked with the pacing stimulus,
demonstrating entrainment. A transient period of entrainment was seen
when pacing was initiated. A transient bradygastria was noted at
cessation of pacing.
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Fig. 2.
Entrainment of the gastric slow wave by gastric pacing as a function of
time in 13 patients. Five minutes after initiation of gastric pacing,
frequency of gastric slow wave was completely entrained. Pacing
frequency, 10% higher than intrinsic gastric slow wave frequency
(IGF); pacing amplitude, 4 mA; pacing pulse width, 300 ms.
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Fig. 3.
Gastric myoelectrical activity recorded in 1 patient along the greater
curvature of the stomach. Propagation of the gastric slow wave from the
corpus (S1;
A) to the distal antrum
(S4;
D) was observed.
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Tachygastria of higher than 4 cpm was observed in four of the patients.
Three patients showed ectopic gastric dysrhythmia in the antrum. As
shown in Fig. 4, the gastric slow wave in
the proximal stomach had a regular frequency of 3 cpm, whereas the gastric slow wave in the antrum showed tachygastria of higher than 4 cpm. Table 2 summarizes the frequencies of
the gastric slow waves in these three patients before, during, and
after gastric pacing. The proximal stomach had regular frequency and
the distal stomach exhibited tachygastria or dysrhythmia. Pacing at a
frequency higher than the IGF of the proximal stomach was able to
entrain the proximal stomach as well as the distal stomach. The time
required for the entrainment (or normalization) varied from 2 to 10 min. It took more time to entrain the distal stomach than the proximal stomach. More importantly, the gastric slow wave remained in regular rhythm even when gastric pacing was terminated. Typical tracings illustrating the normalization of tachygastria are presented in Fig.
5.

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Fig. 4.
Uncoupled gastric slow waves observed in 1 patient. Recording from
proximal stomach (S2;
A) showed a gastric slow wave of 3 cycles per minute (cpm), whereas recording in distal stomach
(S4;
C) revealed tachygastria of 7 cpm.
Similar ectopic tachygastria was observed in the other 2 patients.
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Table 2.
Effects of gastric pacing on frequency of the gastric slow wave in 3 patients with ectopic gastric dysrhythmia
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Fig. 5.
Normalization of ectopic tachygastria with gastric pacing.
A: tachygastria of 7 cpm in the
baseline recording. B: normalized 3 cpm gastric slow waves a few minutes after gastric pacing.
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The fourth patient showed tachygastria of 4.0 to 4.2 cpm on
postoperative days
3 and
5. Unlike in the other three patients, the tachygastria observed in this particular patient was not ectopic and did not originate in the antrum but originated in the pacemaker area and propagated distally toward the pylorus. Gastric pacing at a
frequency of 3.2 cpm was not able to reduce this elevated frequency of
the gastric slow wave on postoperative
days
5 and 7. After postoperative
day
7, however, the gastric slow wave in this patient was reduced spontaneously to 3.2 cpm, and gastric pacing
at a frequency 10% higher than the IGF was able to entrain the gastric
slow wave.
Effects of pacing parameters.
Although gastric pacing at a frequency 10% higher than the IGF was
able to entrain the gastric slow wave, it was found that there was an
upper limit beyond which the gastric slow wave could not be driven. As
shown in Fig. 6, there was no linear
relationship between the pacing frequency and the actual driven
frequency. Gastric pacing at a frequency equal to or higher than 4 cpm
was able to increase the frequency of the gastric slow wave but was not
able to completely entrain the gastric slow wave. The percentage of
entrainment was substantially reduced as the pacing frequency was
further away from the intrinsic baseline frequency. The maximum driven
frequency of the gastric slow wave was found to be 4.3 cpm, achieved at
a pacing frequency of 5.5 cpm. One of the patients showed gastric
arrhythmia during gastric pacing at a frequency of 5.5 cpm and vomited
during gastric pacing at a frequency of 12 cpm. Gastric pacing at a
frequency 10% lower than the IGF was not able to entrain the gastric
slow wave but slightly reduced the frequency by 3.0 ± 0.1%.

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Fig. 6.
Effect of pacing frequency on entrainment of gastric slow wave in 13 patients. A: pacing frequency and
recorded frequency during pacing with different pacing frequencies.
B: percent entrainment with gastric
pacing at different frequencies. 100% entrainment was achieved when
pacing frequency was 10% higher than IGF. Percent entrainment was
reduced when pacing frequency increased.
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Figure 7 shows the effect of pacing pulse
amplitude on the entrainment of the gastric slow wave. An amplitude of
4 mA yielded 100% entrainment, whereas amplitudes of 2 and 1 mA
resulted in 79 ± 10% and 50 ± 11% entrainment,
respectively.

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Fig. 7.
Effect of pacing pulse amplitude on entrainment of the gastric slow
wave. With a pacing frequency 10% higher than the IGF and a pulse
width of 300 ms, gastric pacing completely entrained the gastric slow
wave with an amplitude of 4 mA but only partially entrained the gastric
slow wave with an amplitude of 2 or 1 mA.
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The pulse width of the pacing stimulus was also found to affect the
entrainment of the gastric slow wave. With a fixed pacing frequency
10% higher than the IGF and a fixed pacing pulse amplitude of 4 mA,
gastric pacing with a pulse width of 300 ms was able to entrain the
gastric slow wave completely, whereas gastric pacing with pulse widths
of 30 and 3 ms only entrained the gastric slow wave by 45 ± 15%
and 14 ± 8%, respectively.
 |
DISCUSSION |
This study has shown that the result of gastric pacing was associated
with every pacing parameter, including pacing frequency, pacing
amplitude, and pulse width. The gastric slow wave in patients with
gastroparesis was successfully entrained using the parameters derived
in this study. Ectopic tachygastria or dysrhythmia in the antrum could
be normalized by gastric pacing at a frequency of ~3 cpm.
It is conceivable that the variable success of gastric pacing in the
literature can be attributed to variabilities in the pacing parameters
incorporated. In a well-designed experiment, Kelly (15) studied the
effect of different pacing parameters on the performance of gastric
pacing and derived appropriate pacing parameters for the entrainment of
the gastric slow wave in dogs. The effect of gastric pacing parameters
on the entrainment of the gastric slow wave in patients with
gastroparesis has not previously been investigated. The pacing
parameters used in human studies were usually chosen on the basis of
animal studies, which might have contributed to conflicting results
reported previously in the literature. A few studies suggested that the
entrainment of the gastric slow wave became more difficult with
increased time after surgery (14, 20). With the optimized pacing
parameters, we have found that the entrainment of the gastric slow wave
was possible even 1 wk or more after surgery. This study also indicates that the entrainment of the gastric slow wave was possible only when
the pacing frequency was slightly higher than the IGF. One of the early
studies, however, reported the entrainment of the gastric slow wave
with a pacing frequency lower than the IGF (18). Although gastric
pacing was able to entrain the gastric slow wave, our data showed that
the entrainment lasted only for a few cycles when gastric pacing was
terminated. This was in agreement with the findings reported in the
literature (14). These data suggest that a permanent stimulation device
would be necessary if gastric pacing is to be considered as a
therapeutic approach.
Although gastric pacing was not able to entrain the gastric slow wave
to a frequency lower than the IGF, it was capable of overriding ectopic
tachygastria originating in the antrum. In the three patients with
ectopic tachygastria in the distal stomach, the gastric slow wave in
the proximal stomach had normal rhythms but apparently was not able to
propagate distally and not able to override the antral dysrhythmia.
During and after pacing, however, the antral dysrhythmia was normalized
to a frequency identical to that in the proximal stomach, indicating
that the propagation of the gastric slow wave from the proximal stomach
to the distal stomach was restored. Similar findings on the
normalization of gastric dysrhythmia were previously reported in
postsurgical patients with and without gastroparesis (14). The
entrainment of the gastric slow wave and normalization of ectopic
tachygastria observed in this and previous studies suggest that gastric
pacing may be an effective therapeutical approach for the treatment of
patients with gastric dysrhythmia.
Although the gastric slow wave could be driven to a higher frequency,
there seemed to be a maximum driven frequency. The mean maximum driven
frequency in patients with gastroparesis found in this study was ~4.2
cpm. This maximum driven frequency may prevent the stomach from being
paced into the range of tachygastria (4-9 cpm). It is well known
that the stomach does not contract when tachygastria occurs. That is,
entrainment of the gastric slow wave at a frequency higher than 4 cpm
may lead to gastric hypomotility. Pacing at a frequency higher than 4 cpm may lead to improvement in symptoms but should not be aimed at
entrainment. A similar maximum driven frequency was previously observed
in dogs (18, 21). An early study reported that the frequency of the
gastric slow wave in dogs could be entrained from 5 to 8 cpm (18). In a
recent study, the gastric slow wave in dogs was entrained from 5 cpm to
a maximum of 6 cpm (10). Pacing at a frequency much higher than the IGF
was also reported (10, 11, 21, 24). Some investigators reported the
introduction of gastric contractions by gastric pacing at a frequency
of 30 or 1,200 cpm (10, 11). The earliest gastric pacing studies used a
pacing frequency of 50 Hz (or 3,000 cpm). However, there seemed to be
no significant improvement in the clinical symptoms with gastric pacing
at that high frequency (21, 24). A recent study revealed a dramatic
improvement in the symptoms of nausea and vomiting with gastric pacing
at a frequency of 12 cpm and a pulse width of 300 µs, 1,000 times
smaller than that used in our present study (10a). With a pulse width
of 300 ms, however, pacing at a frequency of 12 cpm may induce an
adverse effect such as gastric dysrhythmia or symptoms of nausea and
vomiting, as we observed in some patients. Side effects of excessive
belching were also reported in a previous study with a pacing frequency of 50 Hz (24).
The strength or energy of the pacing stimulus was found in this study
to be important in the entrainment of the gastric slow wave. The pacing
energy was determined by the pulse width and the pulse amplitude. Our
data indicated that an amplitude of 4 mA and a width of 300 ms are the
minimum requirements for the entrainment of the gastric slow wave in
patients with gastroparesis. Gastric pacing with energy below this
level may not be able to completely entrain the gastric slow wave. The
values of these two parameters used in some previous studies were lower
than those used in this study, which may explain the failure or partial
entrainment of the gastric slow wave.
The effects of gastric pacing on gastric emptying and symptoms were
investigated in nine of the 13 patients (5). Using the effective
parameters derived in this study, gastric pacing was performed daily
for 1 h before and 2 h after the meal for a period of 35 days or more
in these nine patients. A significant improvement in gastric emptying
and symptoms of gastroparesis was observed. This might be attributed to
the entrainment of the gastric slow wave and normalization of
dysrhythmia.
In summary, the entrainment of the gastric slow wave is associated with
the pacing frequency and energy. With enough pacing energy and a
frequency slightly higher than the IGF, the entrainment of the gastric
slow wave can be achieved in patients with gastroparesis. Ectopic
tachygastria or dysrhythmia may be normalized by gastric pacing at a
frequency of ~3 cpm. Appropriate gastric pacing may be a therapeutic
approach for the treatment of patients with gastric dysrhythmias.
 |
ACKNOWLEDGEMENTS |
We are grateful to the physicians and staff in the Dept. of Nuclear
Medicine and General Clinical Research Center for their support of the
study, and we thank Regina Randall and Loretta Dunnaway for assistance
in preparing the manuscript.
 |
FOOTNOTES |
This study was partially supported by a research grant from
Medtronic-Bakken Research Center B.V., Maastricht, The Netherlands.
Address for reprint requests: J. Chen, Thomas N. Lynn Institute for
Healthcare Research, INTEGRIS Baptist Medical Center, 3300 Northwest
Expressway, Oklahoma City, OK 73112.
Received 18 February 1997; accepted in final form 13 October 1997.
 |
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