Intracellular calcium and vulnerability to fibrillation and defibrillation in Langendorff-perfused rabbit ventricles

Gyo Seung Hwang, Hideki Hayashi, Liang Tang, Masahiro Ogawa, Heidy Hernandez, Alex Y. Tan, Hongmei Li, Hrayr S. Karagueuzian, James N. Weiss, Shien Fong Lin, Peng Sheng Chen

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36 Scopus citations


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.

Original languageEnglish (US)
Pages (from-to)2595-2603
Number of pages9
Issue number24
StatePublished - Dec 1 2006



  • Arrhythmia
  • Cardioversion
  • Electrical stimulation
  • Electrocardiography
  • Electrophysiology

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine
  • Physiology (medical)

Cite this

Hwang, G. S., Hayashi, H., Tang, L., Ogawa, M., Hernandez, H., Tan, A. Y., Li, H., Karagueuzian, H. S., Weiss, J. N., Lin, S. F., & Chen, P. S. (2006). Intracellular calcium and vulnerability to fibrillation and defibrillation in Langendorff-perfused rabbit ventricles. Circulation, 114(24), 2595-2603.