|
|
||||||||
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
1 Department of Biomedical Engineering, Tulane University, New Orleans, LA, USA
* To whom correspondence should be addressed. E-mail: nataliat{at}tulane.edu.
Energy requirements for successful anti-arrhythmia shocks are arrhythmia specific. However, it remains unclear why probability of shock success decreases with increase in arrhythmia complexity. The goal of this research is to determine whether a diminished probability of shock success results from an increased number of functional reentrant circuits in the myocardium, and if so, what are the responsible mechanisms. To achieve this goal, we assess shock efficacy in a bidomain defibrillation model of a 4mm thick slice of canine ventricles. Shocks are applied between an RV cathode and a distant anode to terminate either a single scroll wave (SSW) or multiple scroll waves (MSW). From the 160 simulations conducted, dose-response curves are constructed for shocks given to SSW and MSW. The ED50 shock strength for SSW is found to be 13% less than that for MSW indicating that a larger number of functional reentries results in increased defibrillation threshold. The results also demonstrate that an isoelectric window exists following both failed and successful shocks, however, shocks of strength near ED50 given to SSW result in 16.3% longer isoelectric window durations as compared to the same shocks delivered to MSW. Mechanistic inquiry into these finding revealed that 1) smaller VEP in depth, and 2) difference in preshock tissue state are the two main factors underlying the observed relationships. As a result of these factors, -intramural excitable pathways leading to delayed breakthrough on the surface are formed earlier following shocks given to MSW as compared to SSW, thus resulting in lower defibrillation threshold for shocks given to SSW.
This article has been cited by other articles:
![]() |
J. F. Huizar, M. D. Warren, A. G. Shvedko, J. Kalifa, J. Moreno, S. Mironov, J. Jalife, and A. V. Zaitsev Three distinct phases of VF during global ischemia in the isolated blood-perfused pig heart Am J Physiol Heart Circ Physiol, September 1, 2007; 293(3): H1617 - H1628. [Abstract] [Full Text] [PDF] |
||||
![]() |
K. H.W.J. Ten Tusscher, R. Hren, and A. V. Panfilov Organization of Ventricular Fibrillation in the Human Heart Circ. Res., June 22, 2007; 100(12): e87 - e101. [Abstract] [Full Text] [PDF] |
||||
![]() |
N. Trayanova Defibrillation of the heart: insights into mechanisms from modelling studies Exp Physiol, March 1, 2006; 91(2): 323 - 337. [Abstract] [Full Text] [PDF] |
||||
![]() |
N. H. L. Kuijpers, R. H. Keldermann, T. Arts, and P. A. J. Hilbers Computer simulations of successful defibrillation in decoupled and non-uniform cardiac tissue Europace, January 1, 2005; 7(s2): S166 - S177. [Abstract] [Full Text] [PDF] |
||||
![]() |
B. Rodriguez, B. M. Tice, J. C. Eason, F. Aguel, J. M. Ferrero Jr., and N. Trayanova Effect of acute global ischemia on the upper limit of vulnerability: a simulation study Am J Physiol Heart Circ Physiol, June 1, 2004; 286(6): H2078 - H2088. [Abstract] [Full Text] [PDF] |
||||
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH |
| Visit Other APS Journals Online |