title: Electroporation in a model of cardiac defibrillation.
abstract: BACKGROUND
  It is known that high-strength shock disrupts the lipid matrix of the myocardial cell membrane and forms reversible aqueous pores across the membrane. This process is known as "electroporation." However, it remains unclear whether electroporation contributes to the mechanism of ventricular defibrillation. The aim of this computer simulation study was to examine the possible role of electroporation in the success of defibrillation shock.
  
  
  RESULTS
  Using a modified Luo-Rudy-1 model, we simulated two-dimensional myocardial tissue with a homogeneous bidomain nature and unequal anisotropy ratios. Spiral waves were induced by the S1-S2 method. Next, monophasic defibrillation shocks were delivered externally via two line electrodes. For nonelectroporating tissue, termination of ongoing fibrillation succeeded; however, new spiral waves were initiated, even with high-strength shock (24 V/cm). For electroporating tissue, high-strength shock (24 V/cm) was sufficient to extinguish ongoing fibrillation and did not initiate any new spiral waves. Weak shock (16 to 20 V/cm) also extinguished ongoing fibrillation; however, in contrast to the high-strength shock, new spiral waves were initiated. Success in defibrillation depended on the occurrence of electroporation-mediated anodal-break excitation from the physical anode and the virtual anode. Some excitation wavefronts following electrical shock used a deexcited area with recovered excitability as a pass-through point; therefore, electroporation-mediated anodal-break excitation is necessary to block out the pass-through point, resulting in successful defibrillation.
  
  
  CONCLUSIONS
  The electroporation-mediated anodal-break excitation mechanism may play an important role in electrical defibrillation.
authors.affiliation: First Department of Internal Medicine, Shiga University of Medical Science, Otsu, Japan. ash@belle.shiga-med.ac.jp
authors.forename: T
authors.initials: T
authors.lastname: Ashihara
authors.forename: T
authors.initials: T
authors.lastname: Yao
authors.forename: T
authors.initials: T
authors.lastname: Namba
authors.forename: M
authors.initials: M
authors.lastname: Ito
authors.forename: T
authors.initials: T
authors.lastname: Ikeda
authors.forename: A
authors.initials: A
authors.lastname: Kawase
authors.forename: S
authors.initials: S
authors.lastname: Toda
authors.forename: T
authors.initials: T
authors.lastname: Suzuki
authors.forename: M
authors.initials: M
authors.lastname: Inagaki
authors.forename: M
authors.initials: M
authors.lastname: Sugimachi
authors.forename: M
authors.initials: M
authors.lastname: Kinoshita
authors.forename: K
authors.initials: K
authors.lastname: Nakazawa
mesh_terms: D000200:Action Potentials; D016880:Anisotropy; D001145:Arrhythmias, Cardiac / Q000503:physiopathology / Q000628:therapy*; D003198:Computer Simulation; D004554:Electric Countershock; D018274:Electroporation / Q000295:instrumentation / Q000379:methods*; D006801:Humans; D008564:Membrane Potentials; D008955:Models, Cardiovascular; D009206:Myocardium / Q000166:cytology* / Q000473:pathology