[Pathophysiology of ischemic cardiac pain.]

Cardiac pain is a conscious experience that can be explored only indirectly with experimental approaches. The exact machanisms eliciting cardiac pain still remain obscure. The afferent fibres running in the cardiac sympathetic nerves are regarded as the essential pathway for the transmission of cardiac pain. Atria and ventricle are abundantly supplied with sympathetic sensory innervation. In the spinal cord, impulses transmitted by the sympathetic pathway converge with impulses from somatic thoracic structures onto the same ascending spinothalamic neuron which probably explains the mechanism of referred pain (=projection of pain to another organ). Two hypotheses have been put forward to explain the peripheral mechanism for nociception. The intensity mechanism assumes that pain results from an excessive stimulation of receptive structures normally stimulated at lower levels whereas a specific sensation is considered to result from an excitation of a well defined nociceptive apparatus. Ventricular sympathetic afferent fibres whether myelinated or unmyelinated, always possess some mechanosensitivity and respond to normal chemical and mechanical stimuli, thus displaying properties of polymodal receptors. Afferent vagal fibres may contribute to the mechanisms of cardiac nociception by modulating the threshold and characteristics of pain. Experimental studies identified three main mechanisms, which may be responsible for eliciting cardiac pain during ischemic periods in humans: a) nonphysiological motion of the ischemic left ventricular wall (bulging) and an excitation of mechanical receptors by passive stretching. b) The excitation of free sensory nerve endings by chemicals such as bradykinin, PGE(2), adenosin, histamin or potassium. c) A combination of a and b: algogenic chemicals may sensitize mechanical receptors and therefore lower their threshold for nociception.