Cardiac pain: anatomic pathways and physiologic mechanisms.

Abstract

It may be concluded that the pathways of cardiac pain have been thoroughly established, with the exception of the conduction of anginal attacks occasionally referred to the neck and jaws. Afferent impulses traverse axons that travel in the cervical and thoracic sympathetic cardiac nerves. In the case of the cervical pathway, all impulses on entering the paravertebral ganglionated chain in the neck must descend to the upper thoracic level before they can gain access to the spinal cord. Other impulses reach the 3 superior thoracic ganglia via the more direct thoracic cardiac nerves. Both the cervical and thoracic fibers join the spinal nerves over the communicant sympathetic rami. After passing through the intervertebral foramina, they enter the posterior roots and terminate in the lateral horn of the spinal cord. Here they establish synapses with secondary afferent neurons of the spinothalamic tract, decussate to the opposite anterior column, and are carried rostrally to the nucleus ventralis posterolateralis of the thalamus. This is the principal locus in the brain for the perception of visceral pain. In contrast to well-defined cutaneous sensibility, there is no cortical area for exact visceral localization in the postcentral region of the cerebral cortex. Another factor in the poor localization of cardiac pain is the paucity of sensory endings in the heart. A third appears to be the limited number of secondary sensory fibers in the spinothalamic tracts. These central axons must be shared with other impulses from the surface of the body. As a result, pain from the heart is in large part referred to the cutaneous distribution of the upper 4 thoracic spinal segments. Accounting for the superficial reference of visceral pain by Mackenzie's theory of a viscerocutaneous reflex is no longer justifiable. Even after cutaneous afferent fibers are interrupted by procaine or amputation of the arm, pain from the heart can still be felt over its previous distribution. Neither stimulation of the vagi nor interruption of transmission in these nerves has been found to have any beneficial effect in patients suffering from angina pectoris. Sensory denervation of the heart must therefore be carried out by destruction of the upper ganglia in the thoracic sympathetic trunks or by severing the corresponding posterior spinal roots.