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Original Research: SLEEP MEDICINE |

Upper Esophageal Sphincter and Gastroesophageal Junction Pressure Changes Act to Prevent Gastroesophageal and Esophagopharyngeal Reflux During Apneic Episodes in Patients With Obstructive Sleep Apnea

Shiko Kuribayashi, MD; Benson T. Massey, MD; Muhammad Hafeezullah, MBBS; Lilani Perera, MD; Syed Q. Hussaini, MD; Linda Tatro; Ronald J. Darling, MD; Rose Franco, MD, FCCP; Reza Shaker, MD
Author and Funding Information

From the Dysphagia Institute, Division of Gastroenterology and Hepatology (Drs Kuribayashi, Massey, Hafeezullah, Perera, Hussaini, and Shaker, and Ms Tatro), the Department of Otolaryngology (Dr Darling), and the Department of Sleep Medicine (Dr Franco), Medical College of Wisconsin, Milwaukee, WI.

Correspondence to: Reza Shaker, MD, Division of Gastroenterology and Hepatology, Medical College of Wisconsin, 9200 W Wisconsin Ave, Milwaukee, WI 53226; e-mail: rshaker@mcw.edu


For editorial comment see page 747

Funding/Support: This study was supported in part by Esophageal Motor Function in Health and Disease [Grant 5R01DK025731-28] and Program Project [Grant 5P01DK068051-03].

Reproduction of this article is prohibited without written permission from the American College of Chest Physicians (www.chestpubs.org/site/misc/reprints.xhtml).


© 2010 American College of Chest Physicians


Chest. 2010;137(4):769-776. doi:10.1378/chest.09-0913
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Background:  Gastroesophageal reflux (GER) is thought to be induced by decreasing intraesophageal pressure during obstructive sleep apnea (OSA). However, pressure changes in the upper esophageal sphincter (UES) and gastroesophageal junction (GEJ) pressure during OSA events have not been measured. The aim of this study was to determine UES and GEJ pressure change during OSA and characterize the GER and esophagopharyngeal reflux (EPR) events during sleep.

Methods:  We studied 15 controls, nine patients with GER disease (GERD) and without OSA, six patients with OSA and without GERD, and 11 patients with both OSA and GERD for 6 to 8 h postprandially during sleep. We concurrently recorded the following: (1) UES, GEJ, esophageal body (ESO), and gastric pressures by high-resolution manometry; (2) pharyngeal and esophageal reflux events by impedance and pH recordings; and (3) sleep stages and respiratory events using polysomnography. End-inspiration UES, GEJ, ESO, and gastric pressures over intervals of OSA were averaged in patients with OSA and compared with average values for randomly selected 10-s intervals during sleep in controls and patients with GERD.

Results:  ESO pressures decreased during OSA events. However, end-inspiratory UES and GEJ pressures progressively increased during OSA, and at the end of OSA events were significantly higher than at the beginning (P < .01). The prevalence of GER and EPR events during sleep in patients with OSA and GERD did not differ from those in controls, patients with GERD and without OSA, and patients with OSA and without GERD.

Conclusions:  Despite a decrease in ESO pressure during OSA events, compensatory changes in UES and GEJ pressures prevent reflux.

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