Virtual electrode-induced phase singularity: a basic mechanism of defibrillation failure. Export

@article{citeulike:478614, abstract = {Delivery of a strong electric shock to the heart remains the only effective therapy against ventricular fibrillation. Despite significant improvements in implantable cardioverter defibrillator (ICD) therapy, the fundamental mechanisms of defibrillation remain poorly understood. We have recently demonstrated that a monophasic defibrillation shock produces a highly nonuniform epicardial polarization pattern, referred to as a virtual electrode pattern (VEP). The VEP consists of large adjacent areas of strong positive and negative polarization. We sought to determine whether the VEP may be responsible for defibrillation failure by creating dispersion of postshock repolarization and reentry. Truncated exponential biphasic and monophasic shocks were delivered from a bipolar ICD lead in Langendorff-perfused rabbit hearts. Epicardial electrical activity was mapped during and after defibrillation shocks and shocks applied at the plateau phase of a normal action potential produced by ventricular pacing. A high-resolution fluorescence mapping system with 256 recording sites and a voltage-sensitive dye were used. Biphasic shocks with a weak second phase (<20\% leading-edge voltage of the second phase with respect to the leading-edge voltage of the first phase) produced VEPs similar to monophasic shocks. Biphasic shocks with a strong second phase (>70\%) produced VEPs of reversed polarity. Both of these waveforms resulted in extra beats and arrhythmias. However, biphasic waveforms with intermediate second-phase voltages (20\% to 70\% of first-phase voltage) produced no VEP, because of an asymmetric reversal of the first-phase polarization. Therefore, there was no substrate for postshock dispersion of repolarization. Shocks producing strong VEPs resulted in postshock reentrant arrhythmias via a mechanism of phase singularity. Points of phase singularity were created by the shock in the intersection of areas of positive, negative, and no polarization, which were set by the shock to excited, excitable, and refractory states, respectively. Shock-induced VEPs may reinduce arrhythmias via a phase-singularity mechanism. Strong shocks may overcome the preshock electrical activity and create phase singularities, regardless of the preshock phase distribution. Optimal defibrillation waveforms did not produce VEPs because of an asymmetric effect of phase reversal on membrane polarization.}, address = {Department of Cardiology, Cleveland Clinic Foundation, Ohio 44195, USA. efimovi@cesmtp.ccf.org}, author = {Efimov, I. R. and Cheng, Y. and Van Wagoner, D. R. and Mazgalev, T. and Tchou, P. J.}, citeulike-article-id = {478614}, citeulike-linkout-0 = {http://view.ncbi.nlm.nih.gov/pubmed/9576111}, citeulike-linkout-1 = {http://www.hubmed.org/display.cgi?uids=9576111}, day = {4}, issn = {0009-7330}, journal = {Circ Res}, keywords = {aha, fellowship, octwedge}, month = {May}, number = {8}, pages = {918--925}, posted-at = {2006-07-14 22:21:46}, priority = {4}, title = {Virtual electrode-induced phase singularity: a basic mechanism of defibrillation failure.}, url = {http://view.ncbi.nlm.nih.gov/pubmed/9576111}, volume = {82}, year = {1998} }

TY - JOUR ID - citeulike:478614 L3 - citeulike-article-id:478614 N2 - Delivery of a strong electric shock to the heart remains the only effective therapy against ventricular fibrillation. Despite significant improvements in implantable cardioverter defibrillator (ICD) therapy, the fundamental mechanisms of defibrillation remain poorly understood. We have recently demonstrated that a monophasic defibrillation shock produces a highly nonuniform epicardial polarization pattern, referred to as a virtual electrode pattern (VEP). The VEP consists of large adjacent areas of strong positive and negative polarization. We sought to determine whether the VEP may be responsible for defibrillation failure by creating dispersion of postshock repolarization and reentry. Truncated exponential biphasic and monophasic shocks were delivered from a bipolar ICD lead in Langendorff-perfused rabbit hearts. Epicardial electrical activity was mapped during and after defibrillation shocks and shocks applied at the plateau phase of a normal action potential produced by ventricular pacing. A high-resolution fluorescence mapping system with 256 recording sites and a voltage-sensitive dye were used. Biphasic shocks with a weak second phase (<20% leading-edge voltage of the second phase with respect to the leading-edge voltage of the first phase) produced VEPs similar to monophasic shocks. Biphasic shocks with a strong second phase (>70%) produced VEPs of reversed polarity. Both of these waveforms resulted in extra beats and arrhythmias. However, biphasic waveforms with intermediate second-phase voltages (20% to 70% of first-phase voltage) produced no VEP, because of an asymmetric reversal of the first-phase polarization. Therefore, there was no substrate for postshock dispersion of repolarization. Shocks producing strong VEPs resulted in postshock reentrant arrhythmias via a mechanism of phase singularity. Points of phase singularity were created by the shock in the intersection of areas of positive, negative, and no polarization, which were set by the shock to excited, excitable, and refractory states, respectively. Shock-induced VEPs may reinduce arrhythmias via a phase-singularity mechanism. Strong shocks may overcome the preshock electrical activity and create phase singularities, regardless of the preshock phase distribution. Optimal defibrillation waveforms did not produce VEPs because of an asymmetric effect of phase reversal on membrane polarization. IS - 8 JF - Circ Res SN - 0009-7330 AD - Department of Cardiology, Cleveland Clinic Foundation, Ohio 44195, USA. efimovi@cesmtp.ccf.org EP - 925 TI - Virtual electrode-induced phase singularity: a basic mechanism of defibrillation failure. VL - 82 SP - 918 KW - aha KW - fellowship KW - octwedge AU - Efimov, IR AU - Cheng, Y AU - Van Wagoner, DR AU - Mazgalev, T AU - Tchou, PJ PY - 1998/05/04/ UR - http://view.ncbi.nlm.nih.gov/pubmed/9576111 ER -