VIRTUAL ELECTRODE-INDUCED PHASE SINGULARITY - A BASIC MECHANISM OF DEFIBRILLATION FAILURE

Citation
Ir. Efimov et al., VIRTUAL ELECTRODE-INDUCED PHASE SINGULARITY - A BASIC MECHANISM OF DEFIBRILLATION FAILURE, Circulation research, 82(8), 1998, pp. 918-925
Citations number
32
Categorie Soggetti
Hematology,"Peripheal Vascular Diseas
Journal title
ISSN journal
00097330
Volume
82
Issue
8
Year of publication
1998
Pages
918 - 925
Database
ISI
SICI code
0009-7330(1998)82:8<918:VEPS-A>2.0.ZU;2-C
Abstract
Delivery of a strong electric shock to the heart remains the only effe ctive therapy against ventricular fibrillation. Despite significant im provements in implantable cardioverter defibrillator (ICD) therapy, th e fundamental mechanisms of defibrillation remain poorly understood. W e have recently demonstrated that a monophasic defibrillation shock pr oduces a highly nonuniform epicardial polarization pattern, referred t o as a virtual electrode pattern (VEP), The VEP consists of large adja cent areas of strong positive and negative polarization. We sought to determine whether the VEP may be responsible for defibrillation failur e by creating dispersion of postshock repolarization and reentry. Trun cated exponential biphasic and monophasic shocks were delivered from a bipolar ICD lend in Langendorff-perfused rabbit hearts. Epicardial el ectrical activity was mapped during and after defibrillation shocks an d shocks applied at the plateau phase of a normal action potential pro duced by ventricular pacing. A high-resolution fluorescence mapping sy stem with 256 recording sites and a voltage-sensitive dye were used. B iphasic shocks with a weak second phase (<20% lending-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 wi th a strong second phase (>70%) produced VEPs of reversed polarity. Bo th of these waveforms resulted in extra beats and arrhythmias. However , biphasic waveforms with intermediate second-phase voltages (20% to 7 0% of first-phase voltage) produced no VEP, because of an asymmetric r eversal of the first-phase polarization. Therefore, there was no subst rate for postshock dispersion of repolarization. Shocks producing stro ng VEPs resulted in postshock reentrant arrhythmias via a mechanism of phase singularity. Points of phase singularity were coated by the sho ck in the intersection of areas of positive, negative, and no polariza tion, which were set by the shock to excited, excitable, and refractor y states, respectively. Shock-induced VEPs may reinduce arrhythmias vi a a phase-singularity mechanism. Strong shocks may overcome the presho ck electrical activity and create phase singularities, regardless of t he preshock phase distribution. Optimal defibrillation waveforms did n ot produce VEPs because of an asymmetric effect of phase reversal on m embrane polarization.