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Chapter 5:
Esophagus

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11. The Esophagus as a Cause of Angina-Like Chest Pain page 119

At least one-third of the patients referred to a cardiologist or admitted to a coronary care unit because of angina-like chest pain will have cardiac causes excluded. In most, an alternative etiology is not apparent. Lack of a specific diagnosis may lead to ongoing anxiety, changes in lifestyle and frequent medical consultations if the patient continues to worry that serious heart disease may be present. Such patients should be evaluated for esophageal disease, although the cost-effectiveness of this approach is not known.

Initial investigations include a barium esophagogram and/or upper GI endoscopy to screen for gross esophageal dysmotility and esophagitis. These studies, however, are frequently negative. For this reason, esophageal motility studies with provocative testing (acid perfusion, drug provocation with edrophonium or bethanechol, intraesophageal balloon distention) are usually required to establish an esophageal cause for the pain (Figure 8). In many of these patients, abnormalities of esophageal motility can be documented, suggesting that esophageal dysfunction may be responsible for the pain. Of more diagnostic importance, however, is the demonstration that "provoking" the esophagus with acid perfusion, balloon distention or cholinergic stimulation reproduces the patient's pain.

The pathophysiology of this angina-like chest pain of esophageal origin is poorly understood. In some patients acid reflux is the cause: these patients experience angina-like chest pain under circumstances in which most people would experience heartburn. In others, the pain is caused by abnormal "spastic" contractions of the esophagus that either occur spontaneously or are secondary to acid reflux. In most cases there is a poor correlation between spastic esophageal contractions and the occurrence of pain. Many of these patients appear to have an abnormal esophageal pain threshold; pain episodes may be triggered by multiple different stimuli that in normal subjects would not be perceived as painful.

Both pH and esophageal pressure can be monitored over 24 hours. This method is probably more sensitive and specific than conventional tests, but the equipment is expensive and the test is of limited value in patients with infrequent pain attacks.

Management of angina-like chest pain of esophageal origin should be directed at the specific pathophysiological process. If the pain is triggered by gastroesophageal reflux, then antireflux treatment may be quite helpful. If the pain is due to esophageal spasm, smooth-muscle relaxants such as nitrates, calcium channel blockers, hydralazine and anticholinergics should help, although few controlled clinical trials have demonstrated any significant benefit. Tricyclic antidepressants in relatively low dosage have been shown to be beneficial and should be tried in patients with incapacitating symptoms when other forms of treatment have failed. These are most likely to be useful in patients with abnormal visceral nociception, or the so-called irritable esophagus. Many of these patients will have a significant functional overlay with many other somatic complaints. Simple reassurance is probably the most important part of treatment. Symptoms usually improve once the patient is given a positive diagnosis and no longer fears that underlying heart disease is the cause. 

 

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