INTRODUCTION

Recurring substernal chest pain, not due to coronary artery disease, is a common clinical problem. (See "Pathophysiology and clinical presentation of ischemic chest pain".) More than 50 percent of patients presenting to emergency facilities with unexplained chest pain will have coronary disease ruled out [1-3]. Unfortunately, these patients are usually sent home without a diagnosis and remain confused and concerned about the origin of their pain. Most of them are evaluated initially by a cardiologist or by emergency department physicians who often fail to pursue evaluation for other possible causes for the chest pain, since the overall risk of life-threatening events is so much higher with coronary disease [4].

There is ample documentation that this large group of patients with unexplained chest pain represents a major economic burden because of continued utilization of physician and emergency facilities for recurring pain attacks [5]. Even knowing that they have a negative coronary arteriogram fails to relieve concern or lead to sustained improvement in these patients. One report, for example, surveyed functional status in patients with chest pain and negative coronary arteriograms more than one year after the initial evaluation: 51 percent were unable to work, 47 percent noted limited activity because of their pain, and 44 percent still believed they had coronary disease [6].

PATHOPHYSIOLOGY OF ESOPHAGEAL CHEST PAIN

A potential esophageal origin for recurring "noncardiac" chest pain has been considered likely since William Osler first suggested in 1892 that esophageal spasm might cause these symptoms [7]. Thus, over the ensuing years, an empiric diagnosis of "esophageal spasm" has been applied to patients with unexplained chest pain.

However, more recent studies indicate that true spasm is not a likely cause for recurring unexplained chest pain. A study of 910 patients with negative coronary angiograms undergoing esophageal motility testing found that 28 percent of patients had abnormal motility while only 10 percent of those (ie, 2.8 percent of the total patients) had evidence of esophageal spasm [8]. Other studies have confirmed that spasm is identified in fewer than 10 percent of such patients [9-11]. In a series that included 140 patients with noncardiac chest pain, the most common esophageal motor abnormality was a hypotensive lower esophageal sphincter (61 percent of patients) while nutcracker esophagus and nonspecific motility disorders were present in only 10 percent of patients each [11]. (See "Diffuse esophageal spasm, nutcracker esophagus, and hypertensive lower esophageal sphincter".)

Esophageal chest pain may result from abnormal processes inside the esophagus, abnormal perception of otherwise normal stimuli due to decreased pain threshold (ie, esophageal hypersensitivity) or abnormal transmission of stimuli in the peripheral and central nervous system. Painful esophageal sensations are considered to result from the stimulation of chemoreceptors by acid or hyperosmolar substances, mechanoreceptors by distension or abnormal contractions and thermoreceptors by hot or cold food [12].