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

Research output: Contribution to journalArticle

35 Citations (Scopus)

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

Fingerprint

Rabbits
Calcium
Shock
Ventricular Fibrillation
Membrane Potentials
Excitation Contraction Coupling
Ryanodine
Cryosurgery
Thapsigargin
Pericardium

Keywords

  • Arrhythmia
  • Cardioversion
  • Electrical stimulation
  • Electrocardiography
  • Electrophysiology

ASJC Scopus subject areas

  • Physiology
  • Cardiology and Cardiovascular Medicine

Cite this

Intracellular calcium and vulnerability to fibrillation and defibrillation in Langendorff-perfused rabbit ventricles. / Hwang, Gyo Seung; Hayashi, Hideki; Tang, Liang; Ogawa, Masahiro; Hernandez, Heidy; Tan, Alex Y.; Li, Hongmei; Karagueuzian, Hrayr S.; Weiss, James N.; Lin, Shien-Fong; Chen, Peng-Sheng.

In: Circulation, Vol. 114, No. 24, 12.2006, p. 2595-2603.

Research output: Contribution to journalArticle

Hwang, GS, Hayashi, H, Tang, L, Ogawa, M, Hernandez, H, Tan, AY, Li, H, Karagueuzian, HS, Weiss, JN, Lin, S-F & Chen, P-S 2006, 'Intracellular calcium and vulnerability to fibrillation and defibrillation in Langendorff-perfused rabbit ventricles', Circulation, vol. 114, no. 24, pp. 2595-2603. https://doi.org/10.1161/CIRCULATIONAHA.106.630509
Hwang, Gyo Seung ; Hayashi, Hideki ; Tang, Liang ; Ogawa, Masahiro ; Hernandez, Heidy ; Tan, Alex Y. ; Li, Hongmei ; Karagueuzian, Hrayr S. ; Weiss, James N. ; Lin, Shien-Fong ; Chen, Peng-Sheng. / Intracellular calcium and vulnerability to fibrillation and defibrillation in Langendorff-perfused rabbit ventricles. In: Circulation. 2006 ; Vol. 114, No. 24. pp. 2595-2603.
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T1 - Intracellular calcium and vulnerability to fibrillation and defibrillation in Langendorff-perfused rabbit ventricles

AU - Hwang, Gyo Seung

AU - Hayashi, Hideki

AU - Tang, Liang

AU - Ogawa, Masahiro

AU - Hernandez, Heidy

AU - Tan, Alex Y.

AU - Li, Hongmei

AU - Karagueuzian, Hrayr S.

AU - Weiss, James N.

AU - Lin, Shien-Fong

AU - Chen, Peng-Sheng

PY - 2006/12

Y1 - 2006/12

N2 - 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.

AB - 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.

KW - Arrhythmia

KW - Cardioversion

KW - Electrical stimulation

KW - Electrocardiography

KW - Electrophysiology

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