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Published on: August 25, 2015
Differences in esophageal corpus motility in patients with pathological and non-pathological gastroesophageal reflux
Maria Klopocka1, Jacek Budzyński, Maciej Swiatkowski
1Department of Gastroenterology, Vascular Diseases, and Internal Medicine, Nicolaus Copernicus University, Collegium Medicum in Bydgoszcz, Poland. mariaklopocka@wp.pl
Background:
First- and second-order esophageal contractions are important factors responsible for esophageal clearance of refluxed gastric content. The aim of this study was to estimate the influence of acid reflux on second-order esophageal peristalsis.
Material/Methods:
Simultaneous 24-h esophageal pH-metry and 24-h motility monitoring was performed in 213 patients with non-cardiac chest pain. Pathological gastroesophageal acid reflux (pGER) was defined as pH <4 for more than 4.5% of the total monitoring time.
Results:
The group of pGER patients (n=65, 31%) had a lower percentage of complete and effective peristalsis, a higher percentage of incomplete peristalsis, and a lower mean contraction amplitude than the group of patients with normal esophageal acid exposure (nGER). Analysis of motility parameters in three periods, i.e. during acid reflux and 2 min before and 10 min after episodes (second-order peristalsis), showed that the pGER group had a lower percentage of effective peristalsis (20.6 +/- 13.3 vs. 29.6 +/- 16.2%, p = 0.002) and a higher percentage of ineffective peristalsis both during and after acid reflux, a lower mean contraction amplitude (56.5 +/- 30.3 vs. 70.0 +/- 32.8 mmHg, p=0.025), and a lower contraction frequency during acid reflux (1.6 +/- 0.7 vs. 2.6 +/- 3.1/min, p=0.001) and 10 min after (1.9 +/- 1.9 vs. 20.6 +/- 30.2/min, p=0.002), which indicated a lack of esophageal peristalsis acceleration after acid reflux in the pGER group.
Conclusions:
(1) pGER patients had ineffective esophageal peristalsis more frequently than nGER patients. (2) Impaired second-order peristalsis in pGER patients may be an important factor determining prolonged exposure of the esophageal mucosa to gastric content in addition to lower esophageal sphincter function.
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