Recent insights into the roles of critical sarcolemmal ion channels in ventricular fibrillation provide hope for developing personalized therapies to prevent sudden cardiac death.
Sudden cardiac death (SCD) causes 4 to 5 million deaths each year globally. Electrical vortices (tornadoes or rotors) are the origin of ventricular fibrillation (VF), which often causes SCD. Cardiac electrical vortices have complex dynamics and have been shown in many mammalian species. During VF, the heart fails to contract suitably and is unable to pump blood. Once VF is initiated, drug treatments are ineffective and even make things worse. The only effective treatment is electrical shock to the ventricles. Our current understanding of VF mechanisms is fragmentary, hindering the development of personalized therapies. Yet recent insights into the roles of the most critical sarcolemmal ion channels in VF in controlling the excitation-recovery process provide hope. Substantial evidence indicates that the molecular interplay between the main cardiac sodium channel (Na
Cruz et al. (Wed,) conducted a review in Sudden cardiac death and ventricular fibrillation. Recent insights into the roles of critical sarcolemmal ion channels in ventricular fibrillation provide hope for developing personalized therapies to prevent sudden cardiac death.