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*

*Corresponding author for this work

Research output: Contribution to journalArticle

38 Scopus citations

Abstract

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
Pages (from-to)2595-2603
Number of pages9
JournalCirculation
Volume114
Issue number24
DOIs
StatePublished - 1 Dec 2006

Keywords

  • Arrhythmia
  • Cardioversion
  • Electrical stimulation
  • Electrocardiography
  • Electrophysiology

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    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. https://doi.org/10.1161/CIRCULATIONAHA.106.630509