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Long-Term Effects of Gastric Stimulation on Gastric Electrical Physiology

  • 2012 SSAT Plenary Presentation
  • Published:
Journal of Gastrointestinal Surgery Aims and scope

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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References

  1. Yin J, Abell TL, McCallum RW, Chen JDZ. Gastric neuromodulation with Enterra system for nausea and vomiting in patients with gastroparesis. Neuromodulation 2012; doi:10.1111/j.1525-1403.2012.00429.x.

  2. Hocking MP, Vogel SB, Sninsky CA. Human gastric myoelectric activity and gastric emptying following gastric surgery and with pacing. Gastroenterology 1992; 103:1811–1816.

    PubMed  CAS  Google Scholar 

  3. McCallum RW, Chen JD, Lin Z, Schirmer BD, Williams RD, Ross RA. Gastric pacing improves emptying and symptoms in patients with gastroparesis. Gastroenterology 1998; 114:456–461.

    Article  PubMed  CAS  Google Scholar 

  4. Lin ZY, McCallum RW, Schirmer BD, Chen JD. Effects of pacing parameters on entrainment of gastric slow waves in patients with gastroparesis. American Journal of Physiology 1998; 274:G186–G191.

    PubMed  CAS  Google Scholar 

  5. Maranki JL, Lytes V, Meilahn JE, Harbison S, Friedenberg FK, Fisher RS, Parkman HP. Predictive factors for clinical improvement with Enterra gastric electric stimulation treatment for refractory gastroparesis. Digestive Diseases and Sciences 2008; 53:2072–2078.

    Article  PubMed  Google Scholar 

  6. McCallum RW, Lin Z, Forster J, Roeser K, Hou Q, Sarosiek I. Gastric electrical stimulation improves outcomes of patients with gastroparesis for up to 10 years. Clinical Gastroenteroly and Hepatology 2011; 9:314–319.

    Article  Google Scholar 

  7. Runnels JEW, Johnson W, Abell TL. Long-term follow up double masked temporary GES study: the importance of baseline physiologic measures. Neurogastroenterology and Motility 2008; 20:A30.

    Google Scholar 

  8. Thompson JJW, Minocha A, Abell TL. Double blinded randomized study of temporary gastric electrical stimulation (GES): preliminary results of the Endostim study (Endoscopic Stimulation Temporarily Implanted Mucosally). Gastroenterology 2007; 132 (Suppl. 2):780.

    Google Scholar 

  9. McCallum RW, Snape W, Brody F, Wo J, Parkman HP, Nowak T. Gastric electrical stimulation with Enterra therapy improves symptoms from diabetic gastroparesis in a prospective study. Clinical Gastroenterology and Hepatology 2010 Nov;8(11):947–954. quiz e116.

    Article  PubMed  Google Scholar 

  10. O’Grady G, Egbuji JU, Du P, Cheng LK, Pullan AJ, Windsor JA. High-frequency gastric electrical stimulation for the treatment of gastroparesis: a meta-analysis. World Journal of Surgery 2009; 33:1693–1701.

    Article  PubMed  Google Scholar 

  11. Bortolotti M. Gastric electrical stimulation for gastroparesis: a goal greatly pursued, but not yet attained. World Journal of Gastroenterology 2011; 17:273–282.

    Article  PubMed  Google Scholar 

  12. Hasler WL. Methods of gastric electrical stimulation and pacing: a review of their benefits and mechanisms of action in gastroparesis and obesity. Neurogastroenterology and Motility 2009; 21:229–243.

    Article  PubMed  CAS  Google Scholar 

  13. Abell T, McCallum R, Hocking M, Koch K, Abrahamsson H, Leblanc I, Lindberg G, Konturek J, Nowak T, Quigley EM, Tougas G, Starkebaum W. Gastric electrical stimulation for medically refractory gastroparesis. Gastroenterology 2003; 125:421–428.

    Article  PubMed  Google Scholar 

  14. Stanghellini V. Unfulfilled wishes by gastric electrical stimulation. Clinical Gastroenterology and Hepatology 2011; 9:447–448.

    Article  PubMed  Google Scholar 

  15. McCallum RW, Dusing RW, Sarosiek I, Cocjin J, Forster J, Lin Z. Mechanisms of symptomatic improvement after gastric electrical stimulation in gastroparetic patients. Neurogastroenterology and Motility 2010; 22:161–167. e150–161.

    Article  PubMed  CAS  Google Scholar 

  16. Cutts TF, Luo J, Starkebaum W, Rashed H, Abell TL. Is gastric electrical stimulation superior to standard pharmacologic therapy in improving GI symptoms, healthcare resources, and long-term health care benefits? Neurogastroenterology and Motility 2005; 17:35–43.

    Article  PubMed  CAS  Google Scholar 

  17. Chen JD, Xu X, Zhang J, Abo M, Lin X, McCallum RW, Ross B. Efficiency and efficacy of multi-channel gastric electrical stimulation. Neurogastroenterology and Motility 2005; 17:878–882.

    PubMed  CAS  Google Scholar 

  18. Song G, Hou X, Yang B, Liu J, Qian W, Chen JD. Two-channel gastric electrical stimulation accelerates delayed gastric emptying induced by vasopressin. Digestive Diseases and Sciences 2005; 50:662–668.

    Article  PubMed  CAS  Google Scholar 

  19. Mintchev MP, Sanmiguel CP, Amaris M, Bowes KL. Microprocessor-controlled movement of solid gastric content using sequential neural electrical stimulation. Gastroenterology 2000; 118:258–263.

    Article  PubMed  CAS  Google Scholar 

  20. Mintchev MP, Sanmiguel CP, Otto SJ, Bowes KL. Microprocessor controlled movement of liquid gastric content using sequential neural electrical stimulation. Gut 1998; 43:607–611.

    Article  PubMed  CAS  Google Scholar 

  21. Lei Y, Chen JD. Effects of dual pulse gastric electrical stimulation on gastric tone and compliance in dogs. Digestive and Liver Diseases 2009; 41:277–282.

    Article  CAS  Google Scholar 

  22. Song GQ, Hou X, Yang B, Sun Y, Qian W, Chen JD. A novel method of 2-channel dual-pulse gastric electrical stimulation improves solid gastric emptying in dogs. Surgery 2008; 143:72–78.


    Article  PubMed  Google Scholar 

  23. Liu J, Qiao X, Chen JD. Therapeutic potentials of a novel method of dual-pulse gastric electrical stimulation for gastric dysrhythmia and symptoms of nausea and vomiting. American Journal of Surgery 2006; 191:255–261.

    Article  PubMed  Google Scholar 

  24. Chen J, Koothan T, Chen JD. Synchronized gastric electrical stimulation improves vagotomy-induced impairment in gastric accommodation via the nitrergic pathway in dogs. American Journal of Physiology and Gastrointestinal Liver Physiology 2009; 296:G310–G318.

    Article  CAS  Google Scholar 

  25. Song GQ, Chen JD. Synchronized gastric electrical stimulation improves delayed gastric emptying in nonobese mice with diabetic gastroparesis. Journal of Applied Physiology 2007; 103:1560–1564.

    Article  PubMed  Google Scholar 

  26. Zhu H, Sallam H, Chen DD, Chen JD. Therapeutic potential of synchronized gastric electrical stimulation for gastroparesis: enhanced gastric motility in dogs. American Journal of Physiology. Regulatory, Integrative, and Comparative Physiology 2007; 293:R1875–R1881.

    Article  CAS  Google Scholar 

  27. Lin Z, Forster J, Sarosiek I, McCallum RW. Treatment of gastroparesis with electrical stimulation. Digestive Diseases and Sciences 2003; 48:837–848.

    Article  PubMed  Google Scholar 

  28. Eagon JC, Soper NJ. Gastrointestinal pacing. The Surgical Clinics of North America 1993; 73:1161–1172.28.45.

    PubMed  CAS  Google Scholar 

  29. Bortolotti M. The “electrical way” to cure gastroparesis. American Journal of Gastroenterology 2002; 97:1874–1883.

    PubMed  Google Scholar 

  30. Lin Z, Forster J, Sarosiek I, McCallum RW. Effect of high-frequency gastric electrical stimulation on gastric myoelectric activity in gastoparetic patients. Neurogastroenterology and Motility 2004; 16:205–212.

    Article  PubMed  CAS  Google Scholar 

  31. Chen JD, Qian L, Ouyang H, Yin J. Gastric electrical stimulation with short pulses reduces vomiting but not dysrhythmias in dogs. Gastroenterology 2003; 124:401– 409.

    Article  PubMed  Google Scholar 

  32. O’Grady G, Egbuji JU, Du P, Cheng LK, Pullan AJ, Windsor JA. High-frequency gastric electrical stimulation for the treatment of gastroparesis: a meta-analysis. World J Surg. 2009 Aug;33(8):1693–701.

    Article  PubMed  Google Scholar 

  33. 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 gastroparesis. Neurogastroenterology and Motility 2010; 22:56–61. e10.

    PubMed  CAS  Google Scholar 

  34. Tack J, Piessevaux H, Coulie B, Caenepeel P, Janssens J. Role of impaired gastric accommodation to a meal in functional dyspepsia. Gastroenterology 1998; 115:1346–1352.

    Article  PubMed  CAS  Google Scholar 

  35. Undeland KA, Hausken T, Aanderud S, Berstad A. Lower postprandial gastric volume response in diabetic patients with vagal neuropathy. Neurogastroenterology and Motility 1997;9:19–24.

    Article  PubMed  CAS  Google Scholar 

  36. Samsom M, Roelofs JM, Akkermans LM, van Berge Henegouwen GP, Smout AJ. Proximal gastric motor activity in response to a liquid meal in types I diabetes mellitus with autonomic neuropathy. Digestive Diseases and Sciences 1998; 43:491–496

    Article  PubMed  CAS  Google Scholar 

  37. Xing JH, Chen JD. Gastric electrical stimulation with parameters for gastroparesis enhances gastric accommodation and alleviates distention-induced symptoms in dogs. Digestive Diseases and Sciences 2006; 51:2160–2164.

    Article  PubMed  CAS  Google Scholar 

  38. Qin C, Sun Y, Chen JD, Foreman RD. Gastric electrical stimulation modulates neuronal activity in nucleus tractus solitarii in rats. The Autonomic Neuroscience 2005; 119:1–8.

    Article  Google Scholar 

  39. Tang M, Zhang J, Chen JD. Central mechanisms of gastric electrical stimulation involving neurons in the paraventricular nucleus of the hypothalamus in rats. Obesity Surgery 2006; 16:344–352.

    Article  PubMed  Google Scholar 

  40. Gallas S, Sinno MH, Boukhettala N, Coëffier M, Dourmap N, Gourcerol G, Ducrotté P, Déchelotte P, Leroi AM, Fetissov SO. Gastric electrical stimulation increases ghrelin production and inhibits catecholaminergic brainstem neurons in rats. The European Journal of Neuroscience 2011; 33:276–284.

    Article  PubMed  Google Scholar 

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Authors and Affiliations

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Corresponding author

Correspondence to Thomas L. Abell.

Additional information

Discussant

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

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