The etiology of noncardiac chest pain (NCCP) is poorly understood. Some evidence suggests that it may be related to sustained esophageal contractions (SECs) of longitudinal smooth muscle. This study attempts to evaluate whether SECs play a role in symptom production in NCCP patients.Methods
This was a prospective double-blind study comparing NCCP patients to healthy controls. Subjects underwent high-resolution esophageal manometry followed by infusions of normal saline and 0.1N hydrochloric acid into the esophagus. Pain intensity was recorded during each minute of the infusion using a visual analog scale between 0 and 10. Two blinded investigators measured the esophageal length at the end of the saline and acid infusion periods as well as the point at which esophageal shortening began using the computer based manometry software.Key Results
Seventeen NCCP patients and 16 controls completed the study. 64% of study subjects demonstrated esophageal shortening in response to acid infusion with mean shortening of 0.4 ± 0.54 cm. The mean decrease in esophageal length with acid was similar between the groups (1.9% ± 2.6% for NCCP patients vs 1.7% ± 2.4% for controls, P = .82). There was no correlation between pain onset and esophageal shortening.Conclusions and Inferences
NCCP patients did not appear to have an exaggerated esophageal shortening response to intraluminal acid. As well, there was poor temporal correlation between esophageal shortening and symptoms. Thus, acid-induced SECs may not play a significant role in pain production in NCCP patients.