How can we facilitate spontaneous termination of ventricular fibrillation and prevent sudden cardiac death? A working hypothesis.

Ventricular fibrillation (VF) is one of the most life-threatening arrhythmias encountered in daily clinical practice. Its occurrence cannot be completely prevented by currently used antiarrhythmic drugs, and, in most instances, VF is sustained and leads to the patient's death unless a successful DC defibrillation is applied. However, spontaneous reversion of VF to sinus rhythm has been observed in various animals and occasionally even in man. Hence, facilitation of self-ventricular defibrillation must be explored as an alternative therapeutic approach. In experimental studies using several mammalian species, we have found that self ventricular defibrillation requires a good intercellular coupling and well synchronized electrical activity in the ventricles, which, in untreated animals, depend on their myocardial catecholamine content. It can then be hypothesized that any agent that elevates the catecholamine level during VF would facilitate spontaneous ventricular defibrillation, and drugs inhibiting extraneuronal catecholamine reuptake have indeed been shown to possess this ability. It is suggested that their effects are mediated by an increase in the intracellular cAMP level, and any compounds sharing this property could well prove efficacious in making VF transient and in reducing sudden cardiac death.