[Cardiac mechanisms for the development of angina pectoris pain]

Despite numerous experimental and clinical investigations, the exact mechanisms involved in the development of cardiac pain are not completely understood. Sensory receptors for painful stimuli, presumably sympathetic sensory nerve endings, are located in the atria, the ventricles, and in the walls of the coronary arteries. These receptors fire at a background rate under normal hemodynamic conditions. They respond to chemical stimuli and are therefore similar to polymodal nociceptors. The afferent fibers (slow-conducting, unmyelinated group IV-fibers, or fast-conducting myelinated group III-fibers) run in the cardiac sympathetic nerves and converge with somatosensory fibers on the same ascending spinothalamic neurons, which may explain the phenomenon of "referred pain". Still unknown is the role of the afferent vagal fibers in pain perception; however, a modulating influence on pain threshold and characteristics seems possible. Two main mechanisms may be responsible for cardiac pain during ischemic periods: a) chemical excitation of free sensory nerve endings by substances such as bradykinin, PGE2, adenosine, histamine, serotonin, or K+; b) abnormal motion of ischemic segments (dyskinesia, bulging) during systole and excitation of mechanical receptors by passive stretching, and probably a combination of a) and b): the release of chemical substances sensitizes mechanical receptors and lowers their threshold for nociceptive stimuli. These can be suppressed at various spinal or supraspinal levels.