We studied the primary and secondary esophageal peristalsis in 36 patients with heartburn and acid regurgitation and in 14 asymptomatic volunteers. Primary peristalsis was elicited by ten swallows of a 5-mL bolus of water and secondary peristalsis was elicited by intra-esophageal infusion of 5, 10, and 15 mL water, 0.1 N hydrochloric acid and air. Esophageal contractions were measured by an 8-lumen manometric catheter assembly incorporating a 6-cm sleeve device. Contractions were registered at 3, 9, and 15 cm from the upper margin of the sleeve and the infusion was done through a side hole located at 12 cm. Twenty patients had normal endoscopic esophageal examination, 10 with normal (group I) and 10 with abnormal pH-metric examination (group II), and 16 had esophagitis (group III). The amplitude of contractions after swallows was lower (97.8 ± 10.0 mmHg) in the distal esophagus of group III patients than in controls (142.3 ± 14.0 mmHg). Patients of group III had fewer secondary contractions (water: 25% of infusion) than patients of the other groups and controls (67% of infusion). Patients of group III also had a lower amplitude of secondary peristalsis in the distal esophagus (water: 70.1 ± 9.6 mmHg) than controls (129.2 ± 18.2 mmHg). We conclude that patients with esophagitis have an impairment of primary and secondary peristalsis in the distal esophagus.

Chagas' disease causes degeneration and reduction of the number of intrinsic neurons of the esophageal myenteric plexus, with consequent absent or partial lower esophageal sphincter relaxation and loss of peristalsis in the esophageal body. The impairment of esophageal motility is seen mainly in the distal smooth muscle region. There is no study about esophageal striated muscle contractions in the disease. In 81 patients with heartburn (44 with esophagitis) taken as controls, 51 patients with Chagas' disease (21 with esophageal dilatation) and 18 patients with idiopathic achalasia (11 with esophageal dilatation) we studied the amplitude, duration and area under the curve of esophageal proximal contractions. Using the manometric method and a continuous perfusion system we measured the esophageal striated muscle contractions 2 to 3 cm below the upper esophageal sphincter after swallows of a 5-ml bolus of water. There was no significant difference in striated muscle contractions between patients with heartburn and esophagitis and patients with heartburn without esophagitis. There was also no significant difference between patients with heartburn younger or older than 50 years or between men and women or in esophageal striated muscle contractions between patients with heartburn and Chagas' disease. The esophageal proximal amplitude of contractions was lower in patients with idiopathic achalasia than in patients with heartburn. In patients with Chagas' disease there was no significant difference between patients with esophageal dilatation and patients with normal esophageal diameter. Esophageal striated muscle contractions in patients with Chagas' disease have the same amplitude and duration as seen in patients with heartburn. Patients with idiopathic achalasia have a lower amplitude of contraction than patients with heartburn.