1053
ENDOSCOPIC GASTRIC ABLATION TO MODULATE SLOW-WAVE ACTIVITY
Date
May 21, 2024
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Background: Gastric slow-wave dysrhythmias are associated with gastrointestinal disorders, including functional dyspepsia and gastroparesis. Gastric radiofrequency ablation has been used in pre-clinical feasibility trials to create targeted lesions that block slow-wave propagation. These were open surgical trials and the lesions were on the gastric serosal surface. This study aimed to translate gastric ablation to minimally-invasive endoscopic application on the mucosal surface.
Methods: Ethical approval was obtained from the University of Auckland Animal Ethics Committee. Anesthetized pigs (n=6) underwent midline laparotomy to expose the stomach. With minimal handling of the stomach, high-resolution mapping electrodes (256 electrodes, 4 mm spacing) were placed on the serosal surface, and baseline slow-wave activity was recorded. Electrodes were removed, and the abdominal wall was approximated using surgical clamps. An irrigated catheter (ThermoCool; Biosense Webster) was introduced down the instrument channel of a gastroscope inserted into the lumen of the stomach (Fig. 1A). With the catheter in contact with the mucosal surface, ablation was performed with two settings (15 W and 20 W, each with 5 mL min-1 irrigation; n=3 each). A series of adjacent spot lesions were created to form a continuous line (n=6-8 lesions, 10 s per lesion; Fig. 1B), perpendicular to the greater curvature in the mid-corpus. High-resolution mapping was then repeated to confirm a post-ablation conduction block (Fig. 1C). Histological injury was graded using full thickness gastric wall samples through the ablation site and stained with H&E.
Results: In all cases, ablation induced a conduction block characterized by a lack of propagation through the lesion, with slow waves instead rotating around the end of the lesion site (Fig. 1D). Frequency was similar between baseline and post-ablation recordings (P=0.30) suggesting that activity still originated from the same pacemaker. The post-ablation slow-wave velocities and amplitudes were significantly higher immediately distal to the lesion (P<0.001), consistent with a conduction block induced by ablation. Histological analysis revealed that both settings successfully created transmural lesions through the entire gastric wall (Fig. 1E).
Conclusions: Endoscopic gastric ablation from the mucosal surface successfully created conduction blocks capable of modulating slow-wave patterns. Delivery of the ablation catheter via an endoscope avoids the need for general anesthesia and open surgery. This study demonstrates the feasibility of this minimally invasive electrophysiological intervention for treatment of gastric dysrhythmias.
Methods: Ethical approval was obtained from the University of Auckland Animal Ethics Committee. Anesthetized pigs (n=6) underwent midline laparotomy to expose the stomach. With minimal handling of the stomach, high-resolution mapping electrodes (256 electrodes, 4 mm spacing) were placed on the serosal surface, and baseline slow-wave activity was recorded. Electrodes were removed, and the abdominal wall was approximated using surgical clamps. An irrigated catheter (ThermoCool; Biosense Webster) was introduced down the instrument channel of a gastroscope inserted into the lumen of the stomach (Fig. 1A). With the catheter in contact with the mucosal surface, ablation was performed with two settings (15 W and 20 W, each with 5 mL min-1 irrigation; n=3 each). A series of adjacent spot lesions were created to form a continuous line (n=6-8 lesions, 10 s per lesion; Fig. 1B), perpendicular to the greater curvature in the mid-corpus. High-resolution mapping was then repeated to confirm a post-ablation conduction block (Fig. 1C). Histological injury was graded using full thickness gastric wall samples through the ablation site and stained with H&E.
Results: In all cases, ablation induced a conduction block characterized by a lack of propagation through the lesion, with slow waves instead rotating around the end of the lesion site (Fig. 1D). Frequency was similar between baseline and post-ablation recordings (P=0.30) suggesting that activity still originated from the same pacemaker. The post-ablation slow-wave velocities and amplitudes were significantly higher immediately distal to the lesion (P<0.001), consistent with a conduction block induced by ablation. Histological analysis revealed that both settings successfully created transmural lesions through the entire gastric wall (Fig. 1E).
Conclusions: Endoscopic gastric ablation from the mucosal surface successfully created conduction blocks capable of modulating slow-wave patterns. Delivery of the ablation catheter via an endoscope avoids the need for general anesthesia and open surgery. This study demonstrates the feasibility of this minimally invasive electrophysiological intervention for treatment of gastric dysrhythmias.
Figure 1: A) Schematic of the experimental set-up. Catheter (blue) is inserted through the instrument channel of the gastroscope and into the stomach through the mouth (red arrow). B) Endoscopic view of the ablation lesions (white). C) Electrode array on the gastric serosal surface during post-ablation mapping. D) Activation map showing slow-wave propagation over time from early (red) to late (blue). Arrows indicate slow-wave direction around the lesion (black bar). E) Lesion (black lines) visible on H&E stained tissue section.
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