Investigation of low-voltage defibrillation by standing waves in human ventricular tissue models

Nikolay Georgiev, Adam Connolly, Martin Bishop, Oleg Aslanidi
King's College London


Introduction. Ventricular arrhythmias are one of the primary causes of sudden cardiac death. Strong electric shocks remain the only reliable mechanism for the successful termination of ventricular fibrillation. However, despite the successes of such conventional defibrillation, it often predisposes to physiological and psychological post-injuries. The main objective of this study is testing a hypothesis that low-voltage shocks received at certain frequencies could result in phase locking (standing waves) of human ventricular tissue, and thus, to successful defibrillation.

Methods. 1D and 2D ventricular tissue models were based on the ventricular myocyte model by Ten Tusscher et al. In order to overcome the restriction of quick voltage decay imposed by a short electrical constant (~1 mm), we consider an extended version of the bidomain model with an external bathing solution, to which the electric shocks were delivered. Sinusoidal low-voltage (20 V) shocks of variable frequency were applied at opposite sides of 1D tissue strands and 2D square tissues of variable sizes; in 2D models, arrhythmia was induced in form of a single re-entrant wave.

Results. In 1D models, standing waves were observed at all frequencies in the range 10-50 Hz in short ventricular strands (1-2 cm, comparable to transmural distance in the human ventricles), but not in long strands (5-10 cm). Accordingly, in 2D tissue models of 5-10 cm linear dimensions, standing waves failed to form and terminate re-entry; on the contrary, in some cases electrical waves originating from the shock application sites led to the generation of additional re-entries.

Conclusion. Phase locking via the formation of standing waves due to periodic low-voltage stimulation (20 V, 10-50 Hz) of human ventricular tissue can lead to the successful defibrillation of transmural re-entrant waves, but not of rotors on the ventricular surface in human hearts.