Electroporation in a model of cardiac defibrillation. Export

@article{citeulike:749663, abstract = {INTRODUCTION: 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. 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 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. CONCLUSION: The electroporation-mediated anodal-break excitation mechanism may play an important role in electrical defibrillation.}, address = {First Department of Internal Medicine, Shiga University of Medical Science, Otsu, Japan. ash@belle.shiga-med.ac.jp}, author = {Ashihara, T. and Yao, T. and Namba, T. and Ito, M. and Ikeda, T. and Kawase, A. and Toda, S. and Suzuki, T. and Inagaki, M. and Sugimachi, M. and Kinoshita, M. and Nakazawa, K.}, citeulike-article-id = {749663}, citeulike-linkout-0 = {http://view.ncbi.nlm.nih.gov/pubmed/11797997}, citeulike-linkout-1 = {http://www.hubmed.org/display.cgi?uids=11797997}, issn = {1045-3873}, journal = {J Cardiovasc Electrophysiol}, keywords = {excitablegap}, month = {December}, number = {12}, pages = {1393--1403}, posted-at = {2008-05-05 14:33:41}, priority = {1}, title = {Electroporation in a model of cardiac defibrillation.}, url = {http://view.ncbi.nlm.nih.gov/pubmed/11797997}, volume = {12}, year = {2001} }

TY - JOUR ID - citeulike:749663 L3 - citeulike-article-id:749663 N2 - INTRODUCTION: 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. 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 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. CONCLUSION: The electroporation-mediated anodal-break excitation mechanism may play an important role in electrical defibrillation. IS - 12 JF - J Cardiovasc Electrophysiol SN - 1045-3873 AD - First Department of Internal Medicine, Shiga University of Medical Science, Otsu, Japan. ash@belle.shiga-med.ac.jp EP - 1403 TI - Electroporation in a model of cardiac defibrillation. VL - 12 SP - 1393 KW - excitablegap AU - Ashihara, T AU - Yao, T AU - Namba, T AU - Ito, M AU - Ikeda, T AU - Kawase, A AU - Toda, S AU - Suzuki, T AU - Inagaki, M AU - Sugimachi, M AU - Kinoshita, M AU - Nakazawa, K PY - 2001/12// UR - http://view.ncbi.nlm.nih.gov/pubmed/11797997 ER -