Are the motility abnormalities of achalasia reversible? An experimental outflow obstruction in the feline model.

BACKGROUND: Experimental and clinical evidence suggests that the loss of esophageal body function in achalasia may be a result of the outflow obstruction of a nonrelaxing, hypertensive lower esophageal sphincter. The reversibility of such abnormalities has implications to the timing of therapeutic interventions. This study was designed to evaluate the evolution and reversibility of motility abnormalities resulting from esophageal outflow obstruction in cats.
METHODS: Twenty adult cats were divided into 2 groups. Group 1 consisted of 4 cats that underwent laparotomy as a sham procedure. Group 2 consisted of 16 cats that underwent surgical placement of a loose Gore-tex expanded polytetrafluoroethylene (W. L. Gore, Elkton, Md) band calibrated to 110% of the circumference of the gastroesophageal junction. The band was removed from 4 randomly selected cats each at 1, 2, 4, and 6 weeks after placement. Esophageal manometry was performed before placement of the band, at weekly intervals after placement of the band, and after removal of the band. The resting pressure and percent relaxation of the lower esophageal sphincter (LES), in addition to amplitude, duration, and propagation of esophageal body contractions, were measured at each interval. Data are expressed as median and interquartile range and compared with use of the Mann-Whitney U test for independent samples.
RESULTS: The LES resting pressure remained unchanged after placement of the band, but sphincter compliance was reduced, as manifested by a significant reduction in the percent of sphincter relaxation (98% prebanding, 65% postbanding, P < .05). The median amplitude of esophageal contraction decreased significantly after banding. By 6 weeks after banding the esophagus was markedly dilated and exhibited aperistaltic, low-amplitude esophageal motility typical of that seen in clinical achalasia. Importantly, removal of the bands resulted in a prompt return of both peristalsis and amplitude of contraction.
CONCLUSIONS: Loss of compliance of the lower esophageal sphincter produces outflow obstruction with the resultant loss of esophageal contraction amplitude and peristaltic waveform typical of achalasia in humans. These abnormalities were reversible after relief of obstruction in the feline model and may indicate that early relief of outflow obstruction in clinical achalasia may preserve esophageal function in patients.