Abstract
Introduction
This study evaluates the modeling of gastric electrophysiology tracings during long-term gastric electrical stimulation for gastroparesis. We hypothesized that serosal electrogastrogram may change over time representing gastric remodeling from gastric stimulation.
Patients
Sixty-five patients with gastroparesis underwent placement of gastric stimulator for refractory symptoms. Mean age at initial stimulator placement was 44 years (range, 8–76), current mean age was 49, and the majority of the subjects were female (n = 51, 78 %). Only a minority had diabetes-induced gastroparesis (n = 16, 25 %); the remainder were either idiopathic or postsurgical.
Methods
At the time of stimulator placement, electrogastrogram was performed after the gastric leads were placed but before stimulation was begun. Patients underwent continuous stimulation until pacer batteries depleted. At the time of replacement, before the new pacemaker was attached, electrogastrogram was again performed.
Results
After a mean of 3.9 years of stimulation therapy, the mean of baseline frequency before stimulation therapy was 5.06 cycles/min and declined to 3.66 after replacement (p = 0.0000002). The mean amplitude was 0.33 mV before stimulation therapy and decreased to 0.31 mV (p = 0.73). The frequency/amplitude ratio was 38.4 before stimulation therapy and decreased to 21.9 (p = 0.001).
Conclusion
Long-term gastric electrical stimulation causes improvement in basal unstimulated gastric frequency to near normal.
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Dr. John T. Mullen (Boston, MA): Dr. Williams and colleagues are to be congratulated on their many contributions to the study of GES for gastroparesis, including this investigation into a possible mechanism explaining how GES leads to improved gastric motility and symptom resolution—namely, quantitative improvement in the baseline frequency of gastric slow waves after chronic GES therapy. My major critique of this study is the failure to include symptom score data and thus the inability to correlate changes in symptom scores with EGG changes. I have four questions for the authors:
1. By my calculation, approximately 25 % of the patients had little or no improvement in gastric slow-wave frequency with long-term GES. Do you have any preliminary data as to whether these individuals were less likely to enjoy symptomatic benefit from GES?
2. The EGG tracings that you obtained were done so at a snapshot in time and one in which gastric motility is least likely to be physiologic—under general anesthesia at the time of laparotomy. Did you consider leaving the serosal leads in place for several days, or even weeks, to obtain more physiologic data, such as what the EGG tracings look like at the time of eating and at the time of severe symptoms to see if there are any correlations, much as we do with 24-h pH probe monitoring in reflux patients?
3. Did you obtain full-thickness gastric biopsies at the time of initial lead placement and replacement, and if so, do you have any preliminary data correlating normalization of gastric slow-wave frequency with histologic findings, such as the density of interstitial cells of Cajal?
4. Assuming that achieving normalization of the gastric slow-wave frequency is a goal in itself (because it correlates with symptom improvement), are there individuals whose gastric slow waves become “entrained” by long-term GES and thus may not need battery replacement and further GES?
Closing discussant
Dr. Patrick A. Williams:
1. We have not looked at this for all patients. Preliminary results have shown no correlation, but the data are incomplete.
2. No, we have not done this application, although others have suggested it as well. We have a current multicenter proposed to look at this.
3. We obtained full-thickness biopsies only at the initial placement operation but not at the replacement operation. We do not have any preliminary data on this but are curious to analyze the density of the ICC, as multiple studies have shown a correlation between tachygastria and decreased ICC counts. Furthermore, the degree if ICC depletion has also been shown to correlate with a poorer likelihood of response to GES therapy (Lin Z, Sarosiek I, Forster J, Damjanov I, Hou Q, McCallum RW. Association of the status of interstitial cells of Cajal and electrogastrogram parameters, gastric emptying and symptoms in patients with gastroparesis32).
4. This is an interesting point. Clinically speaking, there have been some patients who will come for their follow-up appointment, in which adjustments to their pacemakers are made (voltage, impedance, current, etc.), and in some patients the device is found to be dead, yet the patient feels no worse. This implies that indeed the long-term GES therapy has “entrained” their stomach. Likewise, there have been patients who have called the clinic urgently requesting an appointment because they are certain their pacemaker battery has expired; they can often point to a specific day that the pacemaker ceased to function. Anecdotally speaking, some of these latter patients also tend to be those with diabetic gastroparesis.
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Williams, P.A., Nikitina, Y., Kedar, A. et al. Long-Term Effects of Gastric Stimulation on Gastric Electrical Physiology. J Gastrointest Surg 17, 50–56 (2013). https://doi.org/10.1007/s11605-012-2020-5
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DOI: https://doi.org/10.1007/s11605-012-2020-5