[Ionic currents and ventricular fibrillation dynamics].
Ventricular fibrillation is the principal immediate cause of sudden cardiac death. Yet, in contrast to other arrhythmias, ventricular fibrillation is considered to be inaccessible to pharmacologic therapy because of its characteristic and apparently never-ending disarray of electrical waves that seem to propagate chaotically throughout the ventricles. Its prevention has historically been focused on the suppression of ventricular ectopy, with the idea of eliminating potential triggers of fibrillation, which from a clinical standpoint has proven to be detrimental. During the last decade, the application of the theory of wave propagation in non-linear excitable media to the study of cardiac fibrillation has led to a dramatic increase in our understanding of its mechanisms. It is now clear that fibrillation is generated and maintained by rotors that gyrate at exceedingly high frequencies. From such rotors emanate spiral waves of excitation that propagate throughout the myocardium in very complex ways. Among the most important factors that determine rotor dynamics are the electrophysiological properties of the ventricular cells, established by their underlying transmembrane ionic currents. Thus, in recent years, studies have focused on the roles played by specific ionic mechanisms and their modulation by antiarrhythmic drugs in ventricular fibrillation dynamics. This review article summarizes the main findings of such studies, which pave the way for a better understanding of fibrillation, and for the development of new pharmacological approaches that aim to prevent rotor formation and maintenance rather than to suppress the triggering ectopic event.
Moreno
Javier
J
Unidad de Arritmias. Instituto Cardiovascular. Hospital Clínico San Carlos. Madrid. España.
Warren
Mark
M
Jalife
José
J
D000889:Anti-Arrhythmia Agents / Q000494:pharmacology; D002986:Clinical Trials as Topic; D006801:Humans; D007473:Ion Channels / Q000187:drug effects / Q000502:physiology*; D007477:Ions / Q000494:pharmacology; D008955:Models, Cardiovascular; D014693:Ventricular Fibrillation / Q000188:drug therapy / Q000209:etiology / Q000503:physiopathology*
D000889:Anti-Arrhythmia Agents; D007473:Ion Channels; D007477:Ions