Importance of Intracellular Calcium-Membrane Voltage Coupling Gain in Post-Shock Ventricular Arrhythmias

Mitsunori Maruyama, Takao Katoh, Kyoichi Mizuno, Boyoung Joung, Su Kiat Chua, Shien Fong Lin, Peng Sheng Chen

Research output: Contribution to journalArticle

Abstract

Objective: Ventricular tachycardia/fibrillation (VT/VF) can recur repeatedly after defibrillation (i.e. electrical storm). We tested the hypothesis that intracellular Ca2+ (Cai overload during VF and sensitivity of membrane voltage (Vm) to Cai (Cai-Vm coupling gain) is important for post-shock arrhythmias. Methods and Results: We simultaneously mapped Cai and Vm on epicardial (n=14) or endocardial (n=14) surfaces of Langendorff-perfused rabbit ventricles. Spontaneous Cai elevation (SCaE) was noted after defibrillation in 32% of VT/VF at baseline, 83% during isoproterenol infusion. SCaE was reproducibly induced by rapid ventricular pacing and inhibited by ryanodine. We found triggered activities (TAs) originating from 6 of 14 endocardial surfaces but none from epicardial surfaces, despite similar SCaEs between epicardial and endocardial surfaces. This was because delayed afterdepolarizations induced by SCaEs were larger on endocardial surfaces due to higher Cai-Vm coupling gain. Purkinje-like potentials preceded the TAs. /K1 suppression with CsCl or BaCl2 enhanced Cai-Vm coupling gain and enabled epicardium to also generate TAs. Further enhancement of Cai overload and Cai-Vm coupling gain by low [K+]o induced post-shock VTs and spontaneous VF recurrences leading to electrical storm. Conclusions: Cai-Vm coupling gain is important for the genesis of post-shock VT/VF and electrical storm. Purkinje fibers serve as arrhythmogenic substrate because of its higher Cai-Vm coupling gain. /K1 is a major determinant for Cai-Vm coupling gain.

Original languageEnglish
Number of pages1
Journaljournal of arrhythmia
Volume27
Issue number4
DOIs
Publication statusPublished - 2011 Jan 1

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Intracellular Membranes
Cardiac Arrhythmias
Shock
Calcium
Purkinje Fibers
Ryanodine
Pericardium
Ventricular Fibrillation
Ventricular Tachycardia
Isoproterenol
Rabbits
Recurrence
Membranes

All Science Journal Classification (ASJC) codes

  • Cardiology and Cardiovascular Medicine

Cite this

Maruyama, Mitsunori ; Katoh, Takao ; Mizuno, Kyoichi ; Joung, Boyoung ; Chua, Su Kiat ; Lin, Shien Fong ; Chen, Peng Sheng. / Importance of Intracellular Calcium-Membrane Voltage Coupling Gain in Post-Shock Ventricular Arrhythmias. In: journal of arrhythmia. 2011 ; Vol. 27, No. 4.
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title = "Importance of Intracellular Calcium-Membrane Voltage Coupling Gain in Post-Shock Ventricular Arrhythmias",
abstract = "Objective: Ventricular tachycardia/fibrillation (VT/VF) can recur repeatedly after defibrillation (i.e. electrical storm). We tested the hypothesis that intracellular Ca2+ (Cai overload during VF and sensitivity of membrane voltage (Vm) to Cai (Cai-Vm coupling gain) is important for post-shock arrhythmias. Methods and Results: We simultaneously mapped Cai and Vm on epicardial (n=14) or endocardial (n=14) surfaces of Langendorff-perfused rabbit ventricles. Spontaneous Cai elevation (SCaE) was noted after defibrillation in 32{\%} of VT/VF at baseline, 83{\%} during isoproterenol infusion. SCaE was reproducibly induced by rapid ventricular pacing and inhibited by ryanodine. We found triggered activities (TAs) originating from 6 of 14 endocardial surfaces but none from epicardial surfaces, despite similar SCaEs between epicardial and endocardial surfaces. This was because delayed afterdepolarizations induced by SCaEs were larger on endocardial surfaces due to higher Cai-Vm coupling gain. Purkinje-like potentials preceded the TAs. /K1 suppression with CsCl or BaCl2 enhanced Cai-Vm coupling gain and enabled epicardium to also generate TAs. Further enhancement of Cai overload and Cai-Vm coupling gain by low [K+]o induced post-shock VTs and spontaneous VF recurrences leading to electrical storm. Conclusions: Cai-Vm coupling gain is important for the genesis of post-shock VT/VF and electrical storm. Purkinje fibers serve as arrhythmogenic substrate because of its higher Cai-Vm coupling gain. /K1 is a major determinant for Cai-Vm coupling gain.",
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Importance of Intracellular Calcium-Membrane Voltage Coupling Gain in Post-Shock Ventricular Arrhythmias. / Maruyama, Mitsunori; Katoh, Takao; Mizuno, Kyoichi; Joung, Boyoung; Chua, Su Kiat; Lin, Shien Fong; Chen, Peng Sheng.

In: journal of arrhythmia, Vol. 27, No. 4, 01.01.2011.

Research output: Contribution to journalArticle

TY - JOUR

T1 - Importance of Intracellular Calcium-Membrane Voltage Coupling Gain in Post-Shock Ventricular Arrhythmias

AU - Maruyama, Mitsunori

AU - Katoh, Takao

AU - Mizuno, Kyoichi

AU - Joung, Boyoung

AU - Chua, Su Kiat

AU - Lin, Shien Fong

AU - Chen, Peng Sheng

PY - 2011/1/1

Y1 - 2011/1/1

N2 - Objective: Ventricular tachycardia/fibrillation (VT/VF) can recur repeatedly after defibrillation (i.e. electrical storm). We tested the hypothesis that intracellular Ca2+ (Cai overload during VF and sensitivity of membrane voltage (Vm) to Cai (Cai-Vm coupling gain) is important for post-shock arrhythmias. Methods and Results: We simultaneously mapped Cai and Vm on epicardial (n=14) or endocardial (n=14) surfaces of Langendorff-perfused rabbit ventricles. Spontaneous Cai elevation (SCaE) was noted after defibrillation in 32% of VT/VF at baseline, 83% during isoproterenol infusion. SCaE was reproducibly induced by rapid ventricular pacing and inhibited by ryanodine. We found triggered activities (TAs) originating from 6 of 14 endocardial surfaces but none from epicardial surfaces, despite similar SCaEs between epicardial and endocardial surfaces. This was because delayed afterdepolarizations induced by SCaEs were larger on endocardial surfaces due to higher Cai-Vm coupling gain. Purkinje-like potentials preceded the TAs. /K1 suppression with CsCl or BaCl2 enhanced Cai-Vm coupling gain and enabled epicardium to also generate TAs. Further enhancement of Cai overload and Cai-Vm coupling gain by low [K+]o induced post-shock VTs and spontaneous VF recurrences leading to electrical storm. Conclusions: Cai-Vm coupling gain is important for the genesis of post-shock VT/VF and electrical storm. Purkinje fibers serve as arrhythmogenic substrate because of its higher Cai-Vm coupling gain. /K1 is a major determinant for Cai-Vm coupling gain.

AB - Objective: Ventricular tachycardia/fibrillation (VT/VF) can recur repeatedly after defibrillation (i.e. electrical storm). We tested the hypothesis that intracellular Ca2+ (Cai overload during VF and sensitivity of membrane voltage (Vm) to Cai (Cai-Vm coupling gain) is important for post-shock arrhythmias. Methods and Results: We simultaneously mapped Cai and Vm on epicardial (n=14) or endocardial (n=14) surfaces of Langendorff-perfused rabbit ventricles. Spontaneous Cai elevation (SCaE) was noted after defibrillation in 32% of VT/VF at baseline, 83% during isoproterenol infusion. SCaE was reproducibly induced by rapid ventricular pacing and inhibited by ryanodine. We found triggered activities (TAs) originating from 6 of 14 endocardial surfaces but none from epicardial surfaces, despite similar SCaEs between epicardial and endocardial surfaces. This was because delayed afterdepolarizations induced by SCaEs were larger on endocardial surfaces due to higher Cai-Vm coupling gain. Purkinje-like potentials preceded the TAs. /K1 suppression with CsCl or BaCl2 enhanced Cai-Vm coupling gain and enabled epicardium to also generate TAs. Further enhancement of Cai overload and Cai-Vm coupling gain by low [K+]o induced post-shock VTs and spontaneous VF recurrences leading to electrical storm. Conclusions: Cai-Vm coupling gain is important for the genesis of post-shock VT/VF and electrical storm. Purkinje fibers serve as arrhythmogenic substrate because of its higher Cai-Vm coupling gain. /K1 is a major determinant for Cai-Vm coupling gain.

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