[Esophageal angina]

Angina-like chest pain, caused by alterations of esophageal function, is an increasingly common occurrence confronting cardiologists: advances in pathogenetic knowledge and in diagnostic possibilities in this field have in fact shed light on the prevalence of esophageal angina, which is present in approximately 60% of patients with angiographically intact coronaries (11% of anginal patients overall). Classically, esophageal chest pain is attributed to alterations of motility or to mucosal disease (pathologic gastro-esophageal reflux of the acid, mixed or alkaline type): this last cause prevails quantitatively. Little is known of the nociceptive mechanisms triggered by these alterations: as far as mucous disease is concerned, activation of the chemosensitive receptors has been postulated, while esophageal mechanoreceptors may be activated, in the course of a motor disorder, by distension of the wall. A recently proposed additional mechanism consists in the induction of parietal esophageal ischemia by chemical or mechanical injury: it is a fascinating and potentially resolvable mechanism, which however requires further investigation. Moreover, elements of psychological nature are also involved in the genesis of esophageal pain. A diagnosis of esophageal angina, heavily conditioned by obvious considerations of prognostic order, must necessarily aim for "certainty". Prolonged monitoring of the endoluminal pH and the adoption of provocative tests, in the course of pH monitoring and manometry, play an important role in achieving this aim (ergometric test, distension induced with a balloon, edrophonium, electrostimulation, seem most effective). A promising outlook is supported by the recent introduction of prolonged manometry. Finally, diagnostic attitude must necessarily abandon its limited specialistic horizon to consider the patient's profile in its entirety.