NEW LOOK TO AN OLD SYMPTOM - ANGINA-PECTORIS

At the turn of this century, it was proposed that ischemic cardiac pai n might be related to distension of the ventricular wall (''mechanical hypothesis''). Three decades later, it was hypothesized that ischemic pain might be elicited by the intramyocardial release of pain-produci ng substances induced by ischemia (''chemical hypothesis''). Studies c arried out in the past 10 years have given strong support to the chemi cal hypothesis, because they have consistently shown that adenosine is a mediator of ischemic cardiac pain. Adenosine-induced ischemic cardi ac pain is mediated primarily by stimulation of A(1) receptors located in cardiac nerve endings and is potentiated by substance P. Conversel y, the magnitude and rate of left ventricular dilation during ischemia do not predict the severity of angina. It is worth noting, however, t hat stretching of epicardial coronary arteries appears to potentiate t he severity of angina caused by myocardial ischemia. The nervous activ ity generated by myocardial ischemia is modulated in intrinsic cardiac , mediastinal, and thoracic ganglia. Then it is further modulated in t he central nervous system and projects bilaterally to the core-ex, as demonstrated in humans by positron emission tomography, where it is de coded as a painful sensation. The causes responsible for the lack of a ngina during myocardial ischemia are probably different in patients wh o present both pain-free and painful myocardial ischemia, in patients with predominantly painless ischemia, and in diabetic patients.