Phase singularities and termination of spiral wave reentry.
BACKGROUND
Recent defibrillation studies show that electric fields interact with reentrant activity in myocardial tissue through virtual electrode polarization (VEP). This study focuses on determining how VEP relates to the creation and survival of postshock phase singularities in cardiac tissue and demonstrating that interactions between VEP and preshock tissue state engender the probabilistic nature of defibrillation.


RESULTS
We constructed a two-dimensional tissue model representing a ventricular cross-section with fiber architecture and surrounding bath. We initiated spiral wave reentry and subjected the tissue to a monophasic shock. We estimated the shock success probability for a given strength by testing 16 coupling intervals throughout a single rotation of the wavefront. Over a range of shock strengths, our model exhibits dose-response behavior similar to experimental defibrillation efficacy curves. At the 50% effective strength (ED50), successful termination of reentry depends upon the interaction between preshock excitable gap and postshock phase singularities. We also found that increasing the stimulus strength toward ED50 increases the number of postshock singularities, whereas further strength increases above ED50 decrease the number of singularities.


CONCLUSIONS
Our results show for the first time that a computational model can account for the probabilistic nature of defibrillation as VEP interacts with the dynamics of an ongoing reentrant wavefront. Further, we demonstrate that success of a shock depends on the annihilation of the phase singularities that arise after any strong stimulus. Our findings imply that VEP completely overrides the preshock tissue state in shocks that are highly likely to defibrillate (ED95).
Department of Biomedical Engineering, Tulane University, New Orleans, Louisiana 70118, USA. James.Eason@tulane.edu
James
J
Eason
Natalia
N
Trayanova
D055592:Biophysical Phenomena; D001703:Biophysics; D003198:Computer Simulation; D004554:Electric Countershock / Q000379:methods*; D006329:Heart Conduction System / Q000503:physiopathology; D008955:Models, Cardiovascular; D011336:Probability; D014693:Ventricular Fibrillation / Q000503:physiopathology / Q000628:therapy*