Pretreatment of BAPTA-AM suppresses the genesis of repetitive endocardial focal discharges and pacing-induced ventricular arrhythmia during global ischemia

Tsu Juey Wu, Shien-Fong Lin, Yu Cheng Hsieh, Tung Chao Lin, Jiunn Cherng Lin, Chih Tai Ting

Research output: Contribution to journalArticle

2 Citations (Scopus)

Abstract

BAPTA-AM and Repetitive Endocardial Focal Discharges. Introduction: In isolated rabbit hearts, repetitive endocardial focal discharges (REFDs) were consistently observed during ventricular fibrillation (VF) with prolonged (>5 minutes) global ischemia (GI). We hypothesized that BAPTA-AM, a calcium chelator, can suppress these REFDs. Methods and Results: Using a two-camera optical mapping system, we simultaneously mapped endocardial (left ventricle, LV) and epicardial (both ventricles) activations during ventricular arrhythmia with GI. In 5 hearts (protocol I), we infused Tyrode's solution (no BAPTA-AM) for ≥30 minutes before the onset of no-flow GI. In 7 additional hearts (protocol II), BAPTA-AM (20 μmol/L) was infused for ≥30 minutes before the initiation of GI. In protocol I, sustained VF (>30 seconds) was successfully induced in all 5 hearts with prolonged GI. REFDs were present in >85 % of recording time. In protocol II, however, ventricular arrhythmia was not inducible and REFDs were not observed after 5-minute GI in 5 hearts. Effects of BAPTA-AM on intracellular calcium (Ca i) at the LV endocardium were also evaluated in 5 hearts (protocol III) using dual Ca i/membrane potential mapping. GI, both without and with BAPTA-AM pretreatment, caused a decrease of Ca i amplitude during S 1 pacing. However, this effect was more pronounced in the hearts with BAPTA-AM pretreatment (P < 0.001). GI, without BAPTA-AM pretreatment, caused broadening of Ca i transient. In contrast, GI, with BAPTA-AM pretreatment, caused narrowing of Ca i transient. Conclusions: BAPTA-AM pretreatment attenuates Ca i transient, suppressing the genesis of REFDs and pacing-induced ventricular arrhythmia during GI. These findings support the notion that Ca i dynamics is important in the maintenance of REFDs.

Original languageEnglish
Pages (from-to)1154-1162
Number of pages9
JournalJournal of Cardiovascular Electrophysiology
Volume22
Issue number10
DOIs
StatePublished - Oct 2011

Fingerprint

Cardiac Arrhythmias
Ischemia
Calcium
Ventricular Fibrillation
Heart Ventricles
1,2-bis(2-aminophenoxy)ethane N,N,N',N'-tetraacetic acid acetoxymethyl ester
Endocardium
Optical Devices
Membrane Potentials
Maintenance
Rabbits

Keywords

  • BAPTA-AM
  • calcium
  • ischemia
  • optical mapping
  • ventricular fibrillation

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine
  • Physiology (medical)

Cite this

Pretreatment of BAPTA-AM suppresses the genesis of repetitive endocardial focal discharges and pacing-induced ventricular arrhythmia during global ischemia. / Wu, Tsu Juey; Lin, Shien-Fong; Hsieh, Yu Cheng; Lin, Tung Chao; Lin, Jiunn Cherng; Ting, Chih Tai.

In: Journal of Cardiovascular Electrophysiology, Vol. 22, No. 10, 10.2011, p. 1154-1162.

Research output: Contribution to journalArticle

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abstract = "BAPTA-AM and Repetitive Endocardial Focal Discharges. Introduction: In isolated rabbit hearts, repetitive endocardial focal discharges (REFDs) were consistently observed during ventricular fibrillation (VF) with prolonged (>5 minutes) global ischemia (GI). We hypothesized that BAPTA-AM, a calcium chelator, can suppress these REFDs. Methods and Results: Using a two-camera optical mapping system, we simultaneously mapped endocardial (left ventricle, LV) and epicardial (both ventricles) activations during ventricular arrhythmia with GI. In 5 hearts (protocol I), we infused Tyrode's solution (no BAPTA-AM) for ≥30 minutes before the onset of no-flow GI. In 7 additional hearts (protocol II), BAPTA-AM (20 μmol/L) was infused for ≥30 minutes before the initiation of GI. In protocol I, sustained VF (>30 seconds) was successfully induced in all 5 hearts with prolonged GI. REFDs were present in >85 {\%} of recording time. In protocol II, however, ventricular arrhythmia was not inducible and REFDs were not observed after 5-minute GI in 5 hearts. Effects of BAPTA-AM on intracellular calcium (Ca i) at the LV endocardium were also evaluated in 5 hearts (protocol III) using dual Ca i/membrane potential mapping. GI, both without and with BAPTA-AM pretreatment, caused a decrease of Ca i amplitude during S 1 pacing. However, this effect was more pronounced in the hearts with BAPTA-AM pretreatment (P < 0.001). GI, without BAPTA-AM pretreatment, caused broadening of Ca i transient. In contrast, GI, with BAPTA-AM pretreatment, caused narrowing of Ca i transient. Conclusions: BAPTA-AM pretreatment attenuates Ca i transient, suppressing the genesis of REFDs and pacing-induced ventricular arrhythmia during GI. These findings support the notion that Ca i dynamics is important in the maintenance of REFDs.",
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AU - Wu, Tsu Juey

AU - Lin, Shien-Fong

AU - Hsieh, Yu Cheng

AU - Lin, Tung Chao

AU - Lin, Jiunn Cherng

AU - Ting, Chih Tai

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N2 - BAPTA-AM and Repetitive Endocardial Focal Discharges. Introduction: In isolated rabbit hearts, repetitive endocardial focal discharges (REFDs) were consistently observed during ventricular fibrillation (VF) with prolonged (>5 minutes) global ischemia (GI). We hypothesized that BAPTA-AM, a calcium chelator, can suppress these REFDs. Methods and Results: Using a two-camera optical mapping system, we simultaneously mapped endocardial (left ventricle, LV) and epicardial (both ventricles) activations during ventricular arrhythmia with GI. In 5 hearts (protocol I), we infused Tyrode's solution (no BAPTA-AM) for ≥30 minutes before the onset of no-flow GI. In 7 additional hearts (protocol II), BAPTA-AM (20 μmol/L) was infused for ≥30 minutes before the initiation of GI. In protocol I, sustained VF (>30 seconds) was successfully induced in all 5 hearts with prolonged GI. REFDs were present in >85 % of recording time. In protocol II, however, ventricular arrhythmia was not inducible and REFDs were not observed after 5-minute GI in 5 hearts. Effects of BAPTA-AM on intracellular calcium (Ca i) at the LV endocardium were also evaluated in 5 hearts (protocol III) using dual Ca i/membrane potential mapping. GI, both without and with BAPTA-AM pretreatment, caused a decrease of Ca i amplitude during S 1 pacing. However, this effect was more pronounced in the hearts with BAPTA-AM pretreatment (P < 0.001). GI, without BAPTA-AM pretreatment, caused broadening of Ca i transient. In contrast, GI, with BAPTA-AM pretreatment, caused narrowing of Ca i transient. Conclusions: BAPTA-AM pretreatment attenuates Ca i transient, suppressing the genesis of REFDs and pacing-induced ventricular arrhythmia during GI. These findings support the notion that Ca i dynamics is important in the maintenance of REFDs.

AB - BAPTA-AM and Repetitive Endocardial Focal Discharges. Introduction: In isolated rabbit hearts, repetitive endocardial focal discharges (REFDs) were consistently observed during ventricular fibrillation (VF) with prolonged (>5 minutes) global ischemia (GI). We hypothesized that BAPTA-AM, a calcium chelator, can suppress these REFDs. Methods and Results: Using a two-camera optical mapping system, we simultaneously mapped endocardial (left ventricle, LV) and epicardial (both ventricles) activations during ventricular arrhythmia with GI. In 5 hearts (protocol I), we infused Tyrode's solution (no BAPTA-AM) for ≥30 minutes before the onset of no-flow GI. In 7 additional hearts (protocol II), BAPTA-AM (20 μmol/L) was infused for ≥30 minutes before the initiation of GI. In protocol I, sustained VF (>30 seconds) was successfully induced in all 5 hearts with prolonged GI. REFDs were present in >85 % of recording time. In protocol II, however, ventricular arrhythmia was not inducible and REFDs were not observed after 5-minute GI in 5 hearts. Effects of BAPTA-AM on intracellular calcium (Ca i) at the LV endocardium were also evaluated in 5 hearts (protocol III) using dual Ca i/membrane potential mapping. GI, both without and with BAPTA-AM pretreatment, caused a decrease of Ca i amplitude during S 1 pacing. However, this effect was more pronounced in the hearts with BAPTA-AM pretreatment (P < 0.001). GI, without BAPTA-AM pretreatment, caused broadening of Ca i transient. In contrast, GI, with BAPTA-AM pretreatment, caused narrowing of Ca i transient. Conclusions: BAPTA-AM pretreatment attenuates Ca i transient, suppressing the genesis of REFDs and pacing-induced ventricular arrhythmia during GI. These findings support the notion that Ca i dynamics is important in the maintenance of REFDs.

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