Is chest pain in achalasia always due to spasm?

Chest pain is a common symptom in achalasia, particularly in younger patients, those with a shorter disease duration, and type III achalasia. Its frequency and intensity vary, sometimes resembling angina. It may occur independently of eating, drinking, or sleeping. Despite treatment, long-term resolution rates are only 20-25 %, and up to 8 % of treated patients develop new-onset pain. The mechanisms behind chest pain in achalasia remain unclear. Pain occurs both before and after treatment and is not always linked to esophageal spasms. Possible causes include food retention, gas trapping, esophageal hypersensitivity, and persistent high-amplitude contractions in type III achalasia. Mechanisms may involve esophageal mechanoreceptor stimulation, nociceptor activation, and longitudinal muscle hyperactivity. However, in type I and II achalasia, contractions are weak or absent, and many pain episodes are not preceded by esophageal spasms. Studies indicate that air and saliva accumulation can provoke pain, sometimes relieved by endoscopic food removal or supragastric belching. Balloon distension tests and impedance-pH monitoring support the role of esophageal distension in pain generation. Attributing chest pain solely to esophageal spasms oversimplifies the issue. Once cardiovascular causes are ruled out, endoscopy, manometry, and pH monitoring help identify underlying mechanisms. Attributing chest pain solely to esophageal spasm oversimplifies the issue. Once cardiovascular causes are ruled out, diag nostic tools such as endoscopy, manometry, and pH monitoring help identify the underlying mechanism. A tailored treatment approach is essential to avoid ineffective or unnecessary therapies, such as prolonged use of antispasmodics or neuromodulators, ensuring better long-term symptom management.