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Electroporation in a Model of Cardiac Defibrillation
Author(s) -
ASHIHARA TAKASHI,
YAO TAKENORI,
NAMBA TSUNETOYO,
ITO MAKOTO,
IKEDA TAKANORI,
KAWASE AYAKA,
TODA SUNAO,
SUZUKI TORU,
INAGAKI MASASHI,
SUGIMACHI MASARU,
KINOSHITA MASAHIKO,
NAKAZAWA KAZUO
Publication year - 2001
Publication title -
journal of cardiovascular electrophysiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.193
H-Index - 138
eISSN - 1540-8167
pISSN - 1045-3873
DOI - 10.1046/j.1540-8167.2001.01393.x
Subject(s) - defibrillation , electroporation , bidomain model , medicine , fibrillation , ventricular fibrillation , shock wave , shock (circulatory) , biomedical engineering , cardiology , mechanics , neuroscience , atrial fibrillation , physics , chemistry , biochemistry , biology , gene
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.