Mechanism of Ventricular Fibrillation: Current Status and Problems

Nitaro Shibata, Shin Inada, Kazuo Nakazawa, Takashi Ashihara, Naoki Tomii, Masatoshi Yamazaki, Haruo Honjo, Hiroshi Seno, Ichiro Sakuma
Vol. 11 (2022) p.117-135

Ventricular fibrillation (VF) causes failure of synchronous contraction of the heart ventricles, resulting in cardiac collapse. Currently, VF is still the major cause of sudden cardiac death, and strategies such as prevention, prediction, and immediate termination are not yet established. This article reviews the progress of research on VF mechanism and proposes a future direction to elucidate it. Historical hypotheses proposed for VF mechanism were wandering wavelets, mother rotors, and multiple foci. Current concept is a combination of these hypotheses, but remains to be explicated. Rotor, a spiral shape of the excitation wavefront, plays a major role in VF. The mother rotor eventually breaks up and creates multiple unstable rotors by pathological and electrophysiological abnormalities, terminating as irreversible VF. The dynamics of rotors are influenced by many factors such as ion channel modification, alternance of intracellular calcium, and restitution characteristics of the repolarization duration. The break-up of a rotor is created by head–tail interaction of the rotor, or the area of the ischemic tissue zone. The advance of computer approach has realized simulation of the complex heart model, which provides deep insight into electrophysiological background of VF in three dimensional settings. Also, many mapping techniques including not only activation and repolarization mapping, but also phase variance analysis help understanding the rotor/filament mechanism during VF. Topological analysis and chaotic approach have been developed to evaluate the mechanism of VF, but it is still impossible to control the chaotic behavior of VF. Many cardiac and non-cardiac factors induce or reduce the VF characteristics. Cardiac factors include Purkinje fiber, intracellular calcium dynamics, ion channels, and gap junction. Interventions of these parameters have the potential to prevent or induce VF. Optimal control of cardiac factor(s) may be used as VF control therapy, but a clinically useful method is yet to be developed. Non-cardiac factors influencing VF include hypokalemia, hypothermia, heart failure, cardiac ischemia, and autonomic nerve. The detailed mechanisms of VF modification for each factor have been clarified; however, no universal mechanism related to VF is established. The mechanism of VF remains to be determined in order to accomplish VF therapy.