Although successful treatment of achalasia depends on alleviating the obstruction at the esophagogastric junction, the postintervention contractile and pressurization pattern may also play a role in outcome. To determine whether myotomy that alleviates the esophagogastric junction outflow obstruction in achalasia might improve peristalsis. Retrospective study from August 1, 2004, through January 30, 2012. Two tertiary care hospitals in Chicago and Lyon. We included 30 patients (18 male; mean age [range], 43 [17-78] years), of whom 8 had type 1 (26.6%), 17 had type 2 (56.7%), and 5 (16.7%) had type 3 achalasia according to the Chicago classification. Esophageal high-resolution manometry before and after laparoscopic or endoscopic myotomy. The integrity of peristalsis, characterized as intact, weak contractions; frequent failed peristalsis; or premature contractions. Although peristaltic fragments were evident only in patients with type 3 achalasia before treatment, intact, weak, or frequent failed peristalsis was encountered in 5 patients with type 1 (63%), 8 with type 2 (47%), and 4 with type 3 (80%) achalasia after myotomy. One patient with type 3 achalasia had distal esophageal spasm after treatment. In patients with a postmyotomy integrated relaxation pressure of less than 15 mm Hg, only 10 (40%) had persistent absent peristalsis. Panesophageal pressurization disappeared after myotomy in 16 of 19 patients. In the 5 patients with postmyotomy integrated relaxation pressure of more than 15 mm Hg, 4 had weak peristalsis and 1 had absent peristalsis. Reduction or normalization of the esophagogastric junction relaxation pressure achieved by myotomy in achalasia is associated with partial recovery of peristalsis in some patients, suggesting that the disease process progresses from the esophagogastric junction to the esophageal body. Whether the return of peristalsis is predictive of an improved therapeutic outcome requires further study.