Neurophysiological aspects of angina pectoris

Abstract

Several clinical characteristics of angina pectoris are reflected in the nature of the cardiac nervous system. The extent of silent ischemia, the slow onset of angina during the ischemic cascade, the diffuse character of the visceral component of the pain and the referred pain. Of putative myocardial pain messengers so far only adenosine fulfills Lewis criteria for a cardiac pain messenger. Dependent on the pattern of ischemic release, adenosine appears to stabilize or sensitize afferent cardiac nerves with silent or painful ischemia as a result. Through spatio-temporal summation sensitization may result in an alarm whereby the myocardium signals centrally its precarious state. The activity of adenosine-sensitized afferent nerves may become enhanced by additional stimuli such as potassium, protons, substance P and bradykinin. Primary and secondary afferents from the intrinsic and extrinsic intrathoracic cardiac nervous systems project towards the central nervous system via sympathetic and vagal elements. The main part of primary afferents have their cell bodies in extrinsic cardiac ganglia and only a minority in the dorsal root ganglia. No cardiotopical representation exists in the intrathoracic ganglia. The majority of neurons in intrinsic and extrinsic cardiac ganglia are interneurons integrating cardiac inotropic and vasomotor functions on a beat to beat basis. Multisynaptic transmission over secondary afferents may not only delay the anginal pain message; as somatic afferents also connect to the intrathoracic ganglia, these multisynaptic transmissions may also be a basis for referred pain or pain inhibition. Dorsal root afferents appear to convey only excitatory impulses. Probably due to interneurons, cardiac nodose ganglia activities can become either excitatory or inhibitory. Cardiocardiac reflexes occur from the axonal level up to the brain stem cerebral levels. The brain defense system including the basal ganglia and limbic system and the prefrontal but not the sensory cortex are activated during myocardial ischemia indicating its traumatic nature. The reflexogenic nature of angina pectoris is evident as in silent ischemia similar central nervous system activation occurs as in angina pectoris but with less intense prefrontal activation while in Syndrome X more intense activation occurs. Therapeutic interference of the reflex mechanism by sympathectomy, electrical stimulation or pharmacological interventions can counteract angina pectoris and relax the reflexogenic stress and vasomotor drive on the heart.