Postshock arrhythmogenesis in a slice of the canine heart.
BACKGROUND
Recent evidence has demonstrated that defibrillation shocks terminate or reset reentrant activity in the myocardium through the generation of virtual electrode polarization (VEP). Previous research has revealed that the shock establishes phase singularities (PSs) in the tissue via the VEP mechanism. The aim of this study was to examine, as a function of shock strength and electrode configuration, the relationship between end-shock PSs and the reentrant circuits established after failed defibrillation attempts.


RESULTS
The study uses a complex three-dimensional finite-element bidomain model of a slice of the canine heart characterized by realistic geometry and fiber architecture and undergoing a single scroll wave. Defibrillation shocks of increasing strength are delivered through three different electrode configurations. The results demonstrated that >98% of all PSs have a lifetime of half a reentrant cycle or less. Stronger shocks result in a faster rate of annihilation of postshock PSs. For failed shocks, the surviving PSs underlie the activity of one or more scroll waves, which remain stationary in the slice. For all electrode configurations tested, the increase in shock strength leads to a rapid initial increase in the number of postshock reentries followed by a slower decrease; similar behavior is observed with regard to end-shock PSs.


CONCLUSIONS
These results present new evidence regarding the mechanisms underlying failure of defibrillation shocks.
Hillebrenner
Matthew G
MG
Department of Biomedical Engineering, Tulane University, New Orleans, Louisiana 70118, USA.
Eason
James C
JC
Campbell
Craig A
CA
Trayanova
Natalia A
NA
D000818:Animals; D001145:Arrhythmias, Cardiac / Q000503:physiopathology*; D004285:Dogs; D004554:Electric Countershock; D004597:Electroshock; D006321:Heart / Q000503:physiopathology*; D066298:In Vitro Techniques; D008564:Membrane Potentials / Q000502:physiology; D008954:Models, Biological; D009206:Myocardium / Q000166:cytology; D032383:Myocytes, Cardiac / Q000502:physiology