Characterization of the relationship between preshock state and virtual electrode polarization-induced propagated graded responses resulting in arrhythmia induction.
BACKGROUND
Studies have demonstrated that failed defibrillation shocks often are followed by an electrically quiescent period (isoelectric window); however, the underlying mechanisms remain incompletely understood. We recently suggested a new mechanism termed "virtual electrode polarization-induced propagated graded responses" (VEPiPGRs) that might play a role in the origin of the global postshock activation following the isoelectric window.


OBJECTIVE
The purpose of this study to elucidate the circumstances under which VEPiPGR activations originate for shocks given to paced right ventricular preparations. Specifically, we examined the dependence of VEPiPGRs on coupling interval (CI) and shock polarity and whether VEPiPGRs emerge preferentially on the epicardium or the endocardium.


METHODS
Simultaneous endocardial and epicardial activity in isolated right ventricular preparations (n = 4) was imaged optically following shocks of strength +/-5A. All VEPiPGRs were analyzed, and the time T from shock end to activation onset was recorded (isoelectric window is the smallest T among activations that propagated globally).


RESULTS
VEPiPGR activations occurred for CIs in the range from 80 to 150 ms. Average duration of T was 64.5 +/- 18.15 ms, with T decreasing as CI increased (Tmax = 82 ms, Tmin = 46 ms, linear-fit slope = -0.675). The average earliest CI at which cathodal (+5A) shocks resulted in VEPiPGRs was 87 ms compared with 116 ms for anodal (-5A) shocks. All VEPiPGR activations emerged first on the epicardium in a focal pattern, and all induced ventricular fibrillation.


CONCLUSIONS
The global activation that terminates the isoelectric window could result from VEPiPGRs that find an exit pathway. VEPiPGRs originate at the sites of maximum action potential abbreviation by the shock, always on the epicardium for the preparation used here.
Bourn
David W
DW
Department of Biomedical Engineering, Tulane University, New Orleans, Louisiana 70118, USA.
Gray
Richard A
RA
Trayanova
Natalia A
NA
D000200:Action Potentials; D000818:Animals; D001145:Arrhythmias, Cardiac / Q000209:etiology* / Q000503:physiopathology*; D018780:Body Surface Potential Mapping; D002304:Cardiac Pacing, Artificial; D017147:Defibrillators, Implantable / Q000009:adverse effects; D004195:Disease Models, Animal; D004554:Electric Countershock / Q000009:adverse effects* / Q000295:instrumentation; D004558:Electric Stimulation; D004566:Electrodes / Q000009:adverse effects; D022062:Electrophysiologic Techniques, Cardiac; D004699:Endocardium / Q000503:physiopathology; D006329:Heart Conduction System / Q000503:physiopathology*; D010496:Pericardium / Q000503:physiopathology; D012032:Refractory Period, Electrophysiological; D012107:Research Design; D012756:Sheep; D017180:Tachycardia, Ventricular / Q000209:etiology / Q000503:physiopathology; D014693:Ventricular Fibrillation / Q000209:etiology / Q000503:physiopathology