Nostrant T T
Department of Internal Medicine, University of Michigan Hospital, Ann Arbor 48109-0362.
Am J Med. 1992 May 27;92(5A):56S-64S. doi: 10.1016/0002-9343(92)80058-8.
The ability to reproduce chest pain and to identify the esophagus as the source of this pain are the major reasons why provocation testing has become standard in the evaluation of patients with noncardiac chest pain. Recent studies that challenge the validity of performing provocation tests have polarized experts into two camps: those who would abandon such testing because of its low sensitivity and low specificity, and those who would use testing judiciously because of moderate increases in diagnostic yield. Use of 24-hour pH and pressure testing has shown a high number of chest pain events associated with acid reflux in patients with positive cholinergic stimulation tests and esophageal dysmotility, as well as pain with esophageal dysmotility in patients with positive acid infusion tests. Mechanisms of esophageal chest pain are not known. All provocation agents can decrease coronary flow reserve (i.e., induce microvascular angina), thus raising the question of a cardiac source of pain even in patients with positive presumed esophageal provocation. Acid infusion, cholinergic stimulation, and balloon distention are discussed in light of 24-hour pH and pressure monitoring. Esophageal distention and the role of acid in inducing chest pain are emphasized. The role of stress, the use of defined stressors to induce chest pain, and altered pain perception as a final common pathway for chest pain are examined.