Copyright 2002 American Medical Association. All Rights Reserved. Applicable FARS/DFARS Restrictions Apply to Government Use.2002
We appreciate the comments of Drs Ringel, Shaheen, and Drossman.
Our article dealt with all causes of chest pain in patients with purported normal coronary angiograms, and space constraints did not permit an exhaustive review of individual causes. Nonetheless, we acknowledge our omission of the entity of esophageal hyperalgesia in the absence of reflux esophagitis and/or motility disorders. This, indeed, may be associated with chest pain that is central and not of a burning quality and potentially more difficult to distinquish from cardiac pain than other esophageal pathophysiologic mechanisms. Its true prevalence in comparison with other esophageal disorders such as gastroesophageal reflux is difficult to estimate but reflux appears to be somewhat more common, representing the primary mechanism in almost 50% of cases.1 These various motor and sensory esophageal disorders may coexist. A practical approach to patients with noncardiac chest pain of presumed esophageal origin is a therapeutic trial of a short (1 week) course of maximal acid suppression achieved by combining a twice-daily proton pump inhibitor (eg, 40 mg of omeprazole before breakfast and 20 mg before dinner) with a bedtime dose of ranitidine.2,3 For patients who respond, it can be concluded that acid esophagitis is the primary mechanism (with or without associated motility and/or sensory disorder) and long-term acid suppression therapy can be instituted. On the other hand, for those who do not respond and particularly if there is evidence of hypersensitivity of other viscera, such as the irritable bowel syndrome, then as Ringel and colleagues suggest, tricyclic antidepressants such as imipramine and trazodone hydrochloride (Desyrel)2 can be tried.
Schwartz L, Bourassa MG. Functional Chest Pain of Presumed Esophageal Origin—Reply. Arch Intern Med. 2002;162(3):366. doi: