Autonomic nervous system in ventricular arrhythmia

In spite of recent advances in cardiovascular medicine, sudden cardiac death (SCD) remains a major public health problem. Because there is increased risk of SCDs in patients with coronary artery diseases and myocardial infarction (MI), the electrical and anatomical remodeling created by infarction has been a focus of research in the mechanisms of SCD. There is a circadian variation of the incidence of SCD. Beta blocker therapy abolishes this circadian pattern. These data suggest that, in addition to anatomical and electrical remodeling, neural remodeling may also play a role in the generation of SCD. We propose that nerve sprouting occurs after myocardial infarction, and that the increased sympathetic nerve activity contributes to the development of SCD. Histopathological studies showed that there are increased sympathetic nerve densities in the heart, consistent with cardiac nerve sprouting. Direct stellate ganglion nerve activity (SGNA) recording showed that there is a direct temporal relationship between SGNA and the development of ventricular arrhythmias and SCD in ambulatory dogs. These findings suggest that autonomic nervous system remodeling and sympathetic nerve activities directly contribute to the development of SCD.