O. Korn et al., Anatomic dilatation of the cardia and competence of the lower esophageal sphincter: A clinical and experimental study, J GASTRO S, 4(4), 2000, pp. 398-406
Anatomic and clinical data suggest that the gastroesophageal junction or ca
rdia hi patients with gastroesophageal reflux disease (GERD) may be dilated
. We hypothesized that anatomic dilatation of die cardia induces a lower es
ophageal sphincter dysfunction that may be corrected by narrowing the gastr
oesophageal junction (i.e., calibration of the cardia). We measured the per
imeter of the cardia during surgery In control subjects and patients with G
ERD and Barett's esophagus. We then tested our hypothesis in a mechanical m
odel. The model was based on a pig gastroesophageal specimen with perpendic
ularly placed elastic bands around the cardia simulating the action of the
"sling" and "clasp" fibers. "Dilatation" of the cardia was induced by displ
acing the sling band laterally and decreasing its tension. "Calibration" of
the cardia was performed by reapproximation of the sling band toward the e
sophagus but maintaining the same tension as the dilated model. In the "bas
al," "dilated," and "calibratrd" states, the perimeter of the cardia was no
ted and rapid mechanized pullback manometry with a water-perfused catheter
was performed. The opening pressure was determined, and three-dimensional s
phincter 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 I-nanometric high-pressure zone similar to that in the hu
man lower esophageal sphincter Dilatation of the cardia resulted in a decre
ase in the resting pressure, length, and vector volume of the high-pressure
zone, and reduced the opening pressure. Calibration restored the resting a
nd opening pressure, and normalized the three-dimensional pressure image. I
n patients with GERD and Barrett's esophagus, the cardia is dilated. Our mo
del supports the hypothesis that lower esophageal sphincter function is com
promised by anatomic dilatation of the cardia and can be restored by approx
imation of the "sling" fibers toward die lesser curvature ("clasp" fibers).
This pro t ides evidence for a correlation between gastroesophageal sphinc
ter dysfunction in reflux disease and its correction by antireflux surgery.