title: Ventricular fibrillation: dynamics and ion channel determinants.
abstract: Ventricular fibrillation (VF) is the leading cause of sudden cardiac death. This brief review addresses issues relevant to the dynamics of the rotors responsible for functional reentry and VF. It also makes an attempt to summarize present-day knowledge of the manner in which the dynamic interplay between inward and outward transmembrane currents and the heterogeneous cardiac structure establish a substrate for the initiation and maintenance of rotors and VF. The fragmentary nature of our current understanding of ionic VF mechanisms does not even allow an approach toward a "Theory of VF". Yet some hope is provided by recently obtained insight into the roles played in VF by some of the sarcolemmal ion channels that control the excitation-recovery process. For example, strong evidence supports the idea that the interplay between the rapid-inward sodium current and the inward-rectifier potassium current controls rotor formation, as well as rotor stability and frequency. Solid evidence also exists for an involvement of L-type calcium current in the control of rotor frequency and in determining VF-to-ventricular tachycardia conversion. Less clear, however, is whether or not time dependent outward currents through voltage-gated potassium channels affect the fibrillatory process. Hopefully, taking advantage of currently available approaches of structural, molecular and cellular biology, together with computational and imaging techniques, will afford us the opportunity to further advance knowledge on VF mechanisms.
authors.affiliation: Department of Pharmacology and Institute for Cardiovascular Research, SUNY Upstate Medical University, Syracuse, NY 13210, USA.
authors.forename: Sami F
authors.initials: SF
authors.lastname: Noujaim
authors.forename: David S
authors.initials: DS
authors.lastname: Auerbach
authors.forename: José
authors.initials: J
authors.lastname: Jalife
mesh_terms: D000200:Action Potentials; D000818:Animals; D000889:Anti-Arrhythmia Agents / Q000627:therapeutic use; D056966:Excitation Contraction Coupling; D006329:Heart Conduction System / Q000187:drug effects / Q000378:metabolism* / Q000503:physiopathology; D006339:Heart Rate / Q000187:drug effects; D006801:Humans; D007473:Ion Channels / Q000187:drug effects / Q000378:metabolism*; D007700:Kinetics; D014693:Ventricular Fibrillation / Q000188:drug therapy / Q000378:metabolism* / Q000503:physiopathology
chemical_list: D000889:Anti-Arrhythmia Agents; D007473:Ion Channels