Sudden cardiac death: biobehavioral perspective.
Increasing evidence indicates that sudden death resulting from ventricular fibrillation may be triggered in some patients by behavioral and neural factors. In animal preparations, diverse psychologic stressors and augmented sympathetic neural traffic to the heart lower the vulnerable period threshold for ventricular fibrillation. Epidemiologic studies have demonstrated increased cardiac fatality after bereavement and unemployment, as it relates to social class and cultural dislocation, and as a function of level of education, psychologic stress, and social isolation. Ventricular premature beats (VPBs), which may be risk indicators of susceptibility to sudden death, are not affected by perturbations of the peripheral autonomic nervous system. However, differing psychologic stressors increase, whereas their abatement diminishes, VPB frequency and grade. The most potent stressors relate to the recall of emotionally charged experiences. Such stressors are uniquely individual and cannot be readily replicated. Among the most significant factors to reduce VPBs are non-rapid eye movement sleep and increases in vagal neural activity. Psychological precipitants are demonstrable in about 20% of patients experiencing malignant ventricular arrhythmias. A promising new avenue for investigation relates to the role of various central neurotransmitters and their dietary precursors in cardiac neural traffic. Augmenting central serotonin by administering its tryptophan precursor reduces sympathetic neural activity and protects the heart against ventricular fibrillation.