Cardiac pain, sympathetic afferents, and life-threatening arrhythmias

Myocardial ischemia activates receptors of sympathetic and vagal afferent fibers. Although both afferent pathways are excited, this article primarily focuses on the sympathetic pathways. Increased sympathetic afferent activity to cells of the spinal cord can lead to cardiac pain and reflex sympathetic hyperactivity that can be quite arrhythmogenic. Complicating factors that affect the relationship arises from activation of vagal afferent fibers. Sympathetic afferent fibers in the ventricle appear to be composed of mechanosensitive and chemosensitive receptors. Sympathetic afferent fibers excite cells of origin of the spinothalamic tract, the classical pain pathway that transmits information about noxious somatic and visceral episodes to areas of the brain involved with pain perception. Activation of selected brainstem nuclei, the vagus, and the dorsal columns can suppress afferent information from the heart that excites spinothalamic tract cells. Excitation of sympathetic afferent fibers initiates a series of cardiovascular reflexes, some of which may affect cardiac electrical stability significantly. Increased arrhythmogenesis can be reduced when C₈-T₅ dorsal roots are transected. Stimulation of cardiac nerves that involve the left stellate ganglion can produce life-threatening arrhythmias, particularly if combined with myocardial ischemia or infarction. Through reflex mechanisms, activation of sympathetic afferent fibers can suppress activity of vagal efferent fibers. If prevention of cardiac pain through reduced firing or inhibition of cells in the spinothalamic tract reduces afferent sympathetic activity that occurs during acute myocardial ischemia, it would be logical to surmise that another significant benefit would follow, namely reduced risk for malignant arrhythmias.