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Intracellular calcium dynamics, shortened action potential duration, and late-phase 3 early afterdepolarization in Langendorff-perfused rabbit ventricles

Authors
 LIANG TANG ; BOYOUNG JOUNG ; SHIEN-FONG LIN ; PENG-SHENG CHEN ; MASAHIRO OGAWA 
Citation
 Journal of Cardiovascular Electrophysiology, Vol.23(12) : 1364~1371, 2012 
Journal Title
 Journal of Cardiovascular Electrophysiology 
ISSN
 1045-3873 
Issue Date
2012
Abstract
INTRODUCTION: To elucidate the mechanism of late-phase 3 early after depolarization (EAD) in ventricular arrhythmogenesis, we hypothesized that intracellular calcium (Ca(i) ) overloading and action potential duration (APD) shortening may promote late-phase 3 EAD and triggered activity, leading to development of ventricular fibrillation (VF). METHODS AND RESULTS: In isolated rabbit hearts, we performed microelectrode recording and simultaneous dual optical mapping of transmembrane potential (V(m) ) and Ca(i) transient on left ventricular endocardium. An I(KATP) channel opener, pinacidil, was used to abbreviate APD. Rapid pacing was then performed. Upon abrupt cessation of rapid pacing with cycle lengths of 60-200 milliseconds, there were APD(90) prolongation and the corresponding Ca(i) overloading in the first postpacing beats. The duration of Ca(i) transient recovered to 50% (DCaT(50) ) and 90% (DCaT(90) ) in the first postpacing beats was significantly longer than baseline. Abnormal Ca(i) elevation coupled with shortened APD produced late-phase 3 EAD induced triggered activity and VF. In additional 6 preparations, the heart tissues were treated with BAPTA-AM, a calcium chelator. BAPTA-AM significantly reduced the maximal Ca(i) amplitude (26.4 ± 3.5% of the control; P < 0.001) and the duration of Ca(i) transients in the mapped region, preventing the development of EAD and triggered activity that initiated VF. CONCLUSIONS: I (KATP) channel activation along with Ca(i) overloading are associated with the development of late-phase 3 EAD and VF. Because acute myocardial ischemia activates the I(KATP) channel, late-phase 3 EADs may be a mechanism for VF initiation during acute myocardial ischemia.
URI
http://ir.ymlib.yonsei.ac.kr/handle/22282913/90653
DOI
10.1111/j.1540-8167.2012.02400.x
Appears in Collections:
1. 연구논문 > 1. College of Medicine > Dept. of Internal Medicine
Yonsei Authors
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Link
 http://onlinelibrary.wiley.com/doi/10.1111/j.1540-8167.2012.02400.x/abstract
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