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J Thorac Cardiovasc Surg 2005;130:401-407
© 2005 The American Association for Thoracic Surgery

General Thoracic Surgery

On the pathogenesis of gastroesophageal reflux: The concept of gastroesophageal dyssynergia

Ahmed Shafik, MD, PhD a , * , Ismail Shafik, MD, MCh a , Olfat El-Sibai, MD, PhD b , Ali A. Shafik, MD, MCh a

a Department of Surgery and Experimental Research, Faculty of Medicine, Cairo University, Cairo
b Department of Surgery, Faculty of Medicine, Menoufia University, Shebin El-Kom, Egypt

Received for publication April 18, 2004; revisions received June 28, 2004; accepted for publication August 20, 2004.

* Address for reprints: Ahmed Shafik, MD, PhD, 2 Talaat Harb St, Cairo, 11121, Egypt (Email: shafik{at}ahmed-shafik.org).

OBJECTIVES: The cause of lower esophageal sphincter incompetence in gastroesophageal reflux disease is not clearly understood. We investigated the hypothesis that the esophagogastric junction incompetence results from failure of the gastric distention to produce the lower esophageal sphincter and crural diaphragm contraction caused by a disordered reflex action.

METHODS: The study was performed in 19 subjects (mean age, 42.6 ± 7.2 years; 11 men and 8 women) who had reflux esophagitis and hiatus hernia and were scheduled for a fundoplication operation. Eight control volunteers (mean age, 41.8 ± 6.9; 5 men and 3 women) who had huge supraumbilical ventral hernia but no reflux esophagitis or hiatus hernia were studied during operative hernia repair. The electromyographic activity and pressure response of the lower esophageal sphincter and crural diaphragm to separate esophageal and gastric distention were recorded.

RESULTS: In the control subjects (volunteers) esophageal distention caused diminished electromyographic activity of the crural diaphragm and lower esophageal sphincter with decreased esophagogastric junction pressure, whereas gastric distention increased the electromyographic activity of the crural diaphragm and lower esophageal sphincter with increased esophagogastric junction pressure. In the patients the crural diaphragm and lower esophageal sphincter showed diminished resting electromyographic activity, with either no response or a paradoxical response to esophageal or gastric distention.

CONCLUSION: The current study has demonstrated that the lower esophageal sphincter and crural diaphragm in patients with gastroesophageal reflux disease exhibited a diminished resting electric activity and either did not respond or reacted paradoxically to esophageal and gastric distention, constituting what we call esophagosphincteric and gastroesophageal paradox or dyssynergia. The cause of lower esophageal sphincter and crural diaphragm dysfunction is not known; a neurogenic cause was proposed. Further studies are required to investigate this point.






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