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Esophageal hypercontractility is abolished by cholinergic blockade
Arash Babaei1,2, Sadaf Shad1, Benson T Massey1
1Division of Gastroenterology and Hepatology, Medical College of Wisconsin, Milwaukee, WI, USA.
Neurogastroenterology and Motility
|November 13, 2020
Summary
Esophageal hypercontractility (EHC) is driven by cholinergic hyperactivity, not loss of inhibition. Most EHC patients may benefit from anticholinergic treatments targeting excessive nerve signaling.
Area of Science:
- Gastroenterology
- Esophageal Physiology
- Neurogastroenterology
Background:
- Esophageal hypercontractility (EHC) is a significant esophageal motor disorder with an unknown cause.
- Proposed mechanisms include an imbalance in esophageal innervation.
- This study investigates if EHC patients experience cholinergic hyperactivity.
Purpose of the Study:
- To examine excitatory and inhibitory neurotransmission in EHC.
- To assess esophageal motor responses to atropine (ATR) and cholecystokinin (CCK) in EHC patients.
Main Methods:
- Retrospective review of 49 EHC patients undergoing high-resolution manometry (HRM) with pharmacologic challenge (2007-2017).
- Patients categorized by hypercontractile peristaltic sequence frequency.
- Analysis of pressure metrics and motor responses to IV ATR and CCK.
Main Results:
- Atropine administration eliminated hypercontractility in all studied groups.
- Nearly half of patients showed ineffective esophageal motility post-atropine.
- Abnormal CCK responses were mainly observed in patients with concurrent outflow obstruction.
Conclusions:
- Esophageal hypercontractility is mediated by cholinergic pathways.
- Isolated EHC is primarily linked to excessive cholinergic drive, not impaired inhibitory innervation.
- EHC patients may be suitable candidates for anticholinergic therapies.
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