The elusive link between transient myocardial ischemia and pain.

"There is perhaps no symptom familiar to clinicians that has given rise to more speculation than that of anginal pain."1 Lewis, the author of this sentence, was merited with having initiated a critical evaluation of the link between muscular ischemia and pain but, as often occurs, better knowledge was soon transformed into a choral certainty. Entire generations of physicians lived, and still perhaps do, with the conviction that acute myocardial ischemia, as a rule, leads to pain. Cardiac pain hence became a reliable warning symptom, reflecting tissue damage and its natural history. The purpose of this article is to outline the capital elements forming the traditional interpretation of cardiac pain and to consider them in relation to the new experimental findings. A great amount of uncertainty will be reestablished in the interpretation of this cornerstone symptom, and its reliability to supply a sound basis for deep clinical reasoning will be doubted. The hope is to contribute to a clinical method based on the contradictions of experimental pathophysiology rather than on more reassuring monolithic views.