Mechanisms of Recurrent Ventricular Fibrillation in a Rabbit Model of Pacing-Induced Heart Failure

Abstract

Background: Successful defibrillation may be followed by recurrent spontaneous ventricular fibrillation (VF). The mechanisms of postshock spontaneous VF are unclear. Objective: The purpose of this study was to determine the mechanisms of spontaneous VF after initial successful defibrillation in a rabbit model of heart failure (HF). Methods: Simultaneous optical mapping of intracellular calcium (Ca(i)) and membrane potential (Vm) was performed in 12 rabbit hearts with chronic pacing-induced heart failure, in 4 sham-operated hearts, and in 5 normal hearts during fibrillation-defibrillation episodes. Results: Twenty-eight spontaneous VF episodes were recorded after initial successful defibrillation in 4 failing hearts (SVF group) but not in the remaining 8 failing hearts (no-SVF group) or in the normal or sham-operated hearts. The action potential duration (APD(80)) before pacing-induced VF was 209 +/- 9 ms in the SVF group and 212 +/- 14 ms in the no-SVF group (P = NS). After successful defibrillation, APD(80) shortened to 147 +/- 26 ms in the SVF group and to 176 +/- 14 ms in the no-SVF group (P = .04). However, the duration of Ca(i) after defibrillation was not different between the two groups (246 +/- 21 ms vs 241 +/- 17 ms, P = NS), resulting in elevated Ca(i) during late phase 3 or phase 4 of the action potential. Standard glass microelectrode recording in an additional 5 failing hearts confirmed postshock APD shortening and afterdepolarizations. APD(80) of normal and sham-operated hearts was not shortened after defibrillation. Conclusion: HF promotes acute shortening of APD immediately after termination of VF in failing hearts. Persistent Ca(i) elevation during late phase 3 and phase 4 of the shortened action potential result in afterdepolarizations, triggered activity, and spontaneous VF.