Anatomic dilatation of the cardia and competence of the lower esophageal sphincter: A clinical and experimental study

Anatomic and clinical data suggest that the gastroesophageal junction or cardia in patients with gastroesophageal reflux disease (GERD) may be dilated. We hypothesized that anatomic dilatation of the cardia induces a lower esophageal sphincter dysfunction that may be corrected by narrowing the gastroesophageal junction (i.e., calibration of the cardia). We measured the perimeter of the cardia during surgery in control subjects and patients with GERD and Barrett’s esophagus. We then tested our hypothesis in a mechanical model. The model was based on a pig gastroesophageal specimen with perpendicularly placed elastic bands around the cardia simulating the action of the “sling” and “clasp” fibers. “Dilatation” of the cardia was induced by displacing the sling band laterally and decreasing its tension. “Calibration” of the cardia was performed by reapproximation of the sling band toward the esophagus but maintaining the same tension as the dilated model. In the “basal,” “dilated,” and “calibrated” states, the perimeter of the cardia was noted and rapid mechanized pullback manometry with a water-perfused catheter was performed. The opening pressure was determined, and three-dimensional sphincter pressure images were analyzed. The average cardia perimeter was 6.3 cm in control subjects, 8.9 cm in GERD patients, and 13.8 cm in patients with Barrett’s esophagus. The arrangement of the bands in the experimental model generated a manometric high-pressure zone similar to that in the human lower esophageal sphincter. Dilatation of the cardia resulted in a decrease in the resting pressure, length, and vector volume of the high-pressure zone, and reduced the opening pressure. Calibration restored the resting and opening pressure, and normalized the three-dimensional pressure image. In patients with GERD and Barrett’s esophagus, the cardia is dilated. Our model supports the hypothesis that lower esophageal sphincter function is compromised by anatomic dilatation of the cardia and can be restored by approximarion of the “sling” fibers toward the lesser curvature (“clasp” fibers). This provides evidence for a correlation between gastroesophageal sphincter dysfunction in reflux disease and its correction by antireflux surgery.