Gustafsson U, Tibbling L
Astra Pain Control AB, Södertälje, Sweden.
Scand J Gastroenterol. 1997 Feb;32(2):104-7. doi: 10.3109/00365529709000178.
It is not known to what extent patients with non-cardiac chest pain have esophageal ischemia or motor dysfunction. The aim of this study was to investigate whether chest pain provoked by intravenous edrophonium chloride could be due to esophageal ischemia or to muscular spasm.
Sixteen patients with a history of non-cardiac chest pain took part. Ten patients (32-69 years old) who did not develop chest pain with intravenous edrophonium chloride were compared with six patients (50-71 years old) who did develop edrophonium-provoked chest pain. Esophageal motility was monitored manometrically. Changes in esophageal blood flow, assessed as the rewarming time after esophageal cooling, was measured with a thermistor technique.
The esophageal rewarming time after cooling was the same before and during the edrophonium test in both groups. The esophageal contraction amplitudes and contraction duration were significantly increased only in patients with edrophonium-provoked chest pain.
Strong esophageal contractions and not a decreased blood flow in the esophageal wall seem to be the cause of chest pain provoked by intravenous edrophonium chloride.
