Angina pectoris is a pain syndrome caused by coronary arteriosclerosis but also by a number of other disorders, including microvascular angina, gastroesophageal reflux (GER), and esophageal dysmotility. The relationship between abnormal physiology and pain in these conditions is complex. Simultaneous ambulatory monitoring of esophageal pH and motility has demonstrated that patients may have identical episodes of chest pain with acid reflux, dysmotility, both types of events, or neither. Patients may have anginal chest pain with inflation of an esophageal balloon, and patients with microvascular angina may have pain with catheter manipulation in the right atrium. Recent evidence suggests that disorders of visceral pain perception may play a role in both chest pain of esophageal origin and microvascular angina. The physiology of visceral pain is reviewed, including concepts of convergence of somatic and visceral afferent input, descending modulation of pain perception, and sensitization of visceral pain afferents. An approach to evaluation and treatment of chest pain in patients with angiographically normal coronary arteries is outlined.
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