Direct evidence of the role of virtual electrode-induced phase singularity in success and failure of defibrillation.
BACKGROUND
We recently demonstrated that virtual electrode-induced phase singularity is responsible for arrhythmogenesis during T wave shocks and explains the upper and lower limits of vulnerability. Furthermore, we suggested that the same mechanism might be responsible for defibrillation failure. The aim of this study was to experimentally support this hypothesis.


RESULTS
We used the voltage-sensitive dye di-4-ANEPPS and fast imaging to assess electrical activity in Langendorff-perfused rabbit hearts. Ventricular arrhythmias were induced by monophasic shocks applied during T wave. Three types of defibrillation shocks (n = 79) were delivered from an intravenous right ventricular electrode: monophasic (8 msec), optimal biphasic (8/8 msec, 2/1 leading-edge voltage ratio), and nonoptimal biphasic (8/8 msec, 1/1 leading-edge voltage ratio). We found that a monophasic shock extinguished arrhythmic pattern of electrical activity via a virtual electrode polarization effect. However, the virtual electrode polarization was likely to produce phase singularities, leading to another arrhythmia and defibrillation failure. Nonoptimal biphasic shocks produced similar effects. Optimal biphasic shocks were successful because the first phase of the shock erased the arrhythmia via the virtual electrodes effect, whereas the second phase canceled the virtual electrodes, eliminating the substrate for phase singularities and arrhythmia resulting from them.


CONCLUSIONS
Our data provide the first experimental support of the hypothesis implicating virtual electrode-induced phase singularity in defibrillation failure in the Langendorff-perfused rabbit heart. Optimal biphasic shock has a higher defibrillation efficacy because it does not produce virtual electrode-induced phase singularities.
Efimov
I R
IR
Department of Cardiology, Cleveland Clinic Foundation, Ohio 44195, USA. efimov@ieee.org
Cheng
Y
Y
Yamanouchi
Y
Y
Tchou
P J
PJ
D000818:Animals; D001145:Arrhythmias, Cardiac / Q000209:etiology / Q000503:physiopathology / Q000628:therapy; D004554:Electric Countershock / Q000009:adverse effects / Q000295:instrumentation* / Q000592:standards*; D004566:Electrodes; D004594:Electrophysiology; D005260:Female; D005456:Fluorescent Dyes; D006321:Heart / Q000503:physiopathology; D066298:In Vitro Techniques; D008297:Male; D010477:Perfusion; D011726:Pyridinium Compounds; D011817:Rabbits; D017211:Treatment Failure; D016896:Treatment Outcome; D014584:User-Computer Interface
D005456:Fluorescent Dyes; D011726:Pyridinium Compounds; C050019:1-(3-sulfonatopropyl)-4-(beta)(2-(di-n-butylamino)-6-naphthylvinyl)pyridinium betaine