Regulation of cardiac vulnerability by the cerebral defense system.
Psychosocial stressors are risk factors for sudden cardiac death. A theoretical model of the brain mechanism that links defined environmental events (stressors) to cardiac vulnerability (initiation of ventricular fibrillation) has been developed. In the model, a stressor event evokes a set of electrochemical responses in the frontal cortex. Depending on the state of acquisition of these electrochemical responses to the stressor, activity will or will not be initiated in the frontocortical-brainstem pathway. Activity in this pathway, either alone or in combination with myocardial ischemia, triggers a state of increased vulnerability of the heart to the initiation of ventricular fibrillation. Three independent interventions have been shown to prevent the initiation of ventricular fibrillation after acute coronary artery occlusion in the psychologically stressed pig: 1) learned behavioral adaptation to the stressor, 2) cryogenic blockade of the frontocortical-brainstem pathway, and 3) intracerebral (but not intravenous) injection of a beta-receptor blocking agent (levo-propranolol).
D000818:Animals; D000889:Anti-Arrhythmia Agents / Q000494:pharmacology; D001145:Arrhythmias, Cardiac / Q000503:physiopathology; D001921:Brain / Q000503:physiopathology*; D001923:Brain Chemistry / Q000187:drug effects; D003645:Death, Sudden / Q000209:etiology*; D004563:Electrochemistry; D005625:Frontal Lobe / Q000503:physiopathology; D000882:Haplorhini; D006801:Humans; D008954:Models, Biological; D009638:Norepinephrine / Q000502:physiology; D011311:Pressoreceptors / Q000502:physiology; D011433:Propranolol / Q000494:pharmacology; D013315:Stress, Psychological / Q000503:physiopathology; D013552:Swine; D014693:Ventricular Fibrillation / Q000503:physiopathology*
D000889:Anti-Arrhythmia Agents; D011433:Propranolol; D009638:Norepinephrine