BACKGROUND - The role of intracellular calcium (Cai) in defibrillation and vulnerability is unclear. METHODS AND RESULTS - We simultaneously mapped epicardial membrane potential and Cai during shock on T-wave episodes (n=104) and attempted defibrillation episodes (n=173) in 17 Langendorff-perfused rabbit ventricles. Unsuccessful and type B successful defibrillation shocks were followed by heterogeneous distribution of Cai, including regions of low Cai surrounded by elevated Cai ("Cai sinkholes") 31±12 ms after shock. The first postshock activation then originated from the Cai sinkhole 53±14 ms after the shock. No sinkholes were present in type A successful defibrillation. A Cai sinkhole also was present 39±32 ms after a shock on T that induced ventricular fibrillation, followed 22±15 ms later by propagated wave fronts that arose from the same site. This wave propagated to form a spiral wave and initiated ventricular fibrillation. Thapsigargin and ryanodine significantly decreased the upper limit of vulnerability and defibrillation threshold. We studied an additional 7 rabbits after left ventricular endocardial cryoablation, resulting in a thin layer of surviving epicardium. Cai sinkholes occurred 31±12 ms after the shock, followed in 19±7 ms by first postshock activation in 63 episodes of unsuccessful defibrillation. At the Cai sinkhole, the rise of Cai preceded the rise of epicardial membrane potential in 5 episodes. CONCLUSIONS - There is a heterogeneous postshock distribution of Cai. The first postshock activation always occurs from a Cai sinkhole. The Cai prefluorescence at the first postshock early site suggests that reverse excitation-contraction coupling might be responsible for the initiation of postshock activations that lead to ventricular fibrillation.
- Electrical stimulation
ASJC Scopus subject areas
- Cardiology and Cardiovascular Medicine
- Physiology (medical)