This study was supported in part by Grant-in-Aid for Scientific Research (A) from The Ministry of Education, Science, Sports and Culture (12308046); Grant-in-Aid for Scientific Research (C) from The Ministry of Education, Science, Sports and Culture (12670660); Grant-in-Aid for Scientific Research (C) from The Ministry of Education, Science, Sports and Culture (12670698); and Grant-in-Aid for Research and Development for Applying Advanced Computational Science and Technology (12B-1).
Electroporation in a Model of Cardiac Defibrillation
Article first published online: 13 AUG 2003
© Futura Publishing Company, Inc. 2001
Journal of Cardiovascular Electrophysiology
Volume 12, Issue 12, pages 1393–1403, December 2001
How to Cite
ASHIHARA, T., YAO, T., NAMBA, T., ITO, M., IKEDA, T., KAWASE, A., TODA, S., SUZUKI, T., INAGAKI, M., SUGIMACHI, M., KINOSHITA, M. and NAKAZAWA, K. (2001), Electroporation in a Model of Cardiac Defibrillation. Journal of Cardiovascular Electrophysiology, 12: 1393–1403. doi: 10.1046/j.1540-8167.2001.01393.x
- Issue published online: 13 AUG 2003
- Article first published online: 13 AUG 2003
- Manuscript received 27 June 2001; Accepted for publication 26 October 2001.
- Cited By
- ventricular fibrillation;
- electrical shock;
- spiral wave;
- bidomain model;
- virtual electrode;
- upper limit of vulnerability;
Electroporation in a Model of Cardiac Defibrillation. Introduction: It is known that highstrength 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.
Methods and 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 highstrength 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.
Conclusion: The electroporation-mediated anodal-break excitation mechanism may play an important role in electrical defibrillation.