Mechanisms of recurrent ventricular fibrillation in a rabbit model of pacing-induced heart failure

Abstract

Successful defibrillation may be followed by recurrent spontaneous ventricular fibrillation (VF). The mechanisms of postshock spontaneous VF are unclear. 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). 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. 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. 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.