Ann Thorac Surg 2005;79:1131
© 2005 The Society of Thoracic Surgeons
Original article: General thoracic
INVITED COMMENTARY
Gail Darling, MD, FRCSC, FACS
Division of Thoracic Surgery, University Health Network, 200 Elizabeth St, Toronto, Ontario, M5G 2C4 Canada
(E-mail: gail.darling{at}uhn.on.ca).
Gastroesophageal reflux occurs due to an incompetent lower esophageal sphincter (LES) associated with hiatus hernia, spontaneous relaxations of the lower esophageal sphincter, and gastric distension. Increased esophageal peristalsis has been observed in association with acid reflux. This may be related to the presence of a bolus or the acid itself in the esophagus causing increased esophageal motor activity and secondary peristalsis, or the presence of the noxious stimulus of acid may stimulate salivation that in turn causes voluntary swallows and primary peristalsis. The authors suggest that it is the distension of the LES and not the presence of acid in the esophagus that causes the increase in peristalsis. However, instead of using a standard multi-channel manometry catheter, the authors have used a device with a single pressure transducer. Although a change in intra-esophageal pressure in response to balloon inflation was recorded, this cannot be equated with peristaltic activity because it is only a single measurement in time and space. Similarly, although electrical activity is recorded, it is not clear what this represents and it cannot be correlated with peristaltic activity. Therefore, their conclusion that peristalsis occurred cannot be confirmed by their study. Furthermore, there is no mention of any monitoring of swallowing activity, which would certainly affect the results of the pressure measurement.
Distension of the LES with a balloon does not replicate normal physiologic events and specifically cannot be equated with spontaneous relaxations. Balloon distension of the esophagus causes vigorous contractions above the balloon with inhibition of motor activity below the balloon. Spontaneous relaxations of the LES are recognized as a major cause of reflux symptomatology and are mediated through sensory input from the stomach to the brainstem, which through vagal pathways relaxes the LES and occurs with phrenic nerve inhibition causing perihiatal diaphragmatic relaxation. These events are well studied and are not associated with esophageal peristaltic activity.
Although the authors present an interesting idea, their results do not support their conclusions and they also ignore well known esophageal physiology.
