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KMID : 1011920150160010011
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International Journal of Arrhythmia
2015 Volume.16 No. 1 p.11 ~ p.18
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Calcium Dynamics and the Mechanisms of Ventricular Tachycardia to Ventricular Fibrillation Transition in Cryoablated Rabbit Ventricles
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Hwang Gyo-Seung
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Abstract
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Background and Objectives: An electrical shock applied on the T wave can induce a brief period of ventricular tachycardia (VT), orWiggers’ stage I ventricular fibrillation (VF), which degenerates into VF through the development of wavebreaks. The role of intracellular calcium (Cai) dynamics on VT to VF transition remains unclear.
Subjects and Methods: We simultaneously mapped epicardial membrane potential (Vm) and Cai after a T-wave shock in 10 Langendorffperfused rabbit ventricles. Optical mapping was performed on the thin (0.5 mm) layer of the surviving left ventricular epicardium after endocardial cryoablation. A biphasic waveform shock (117 ± 62 V) was applied on the T wave with a S1-shock coupling interval of 142 ± 25 ms to induce VT.
Results: A total of 145 episodes of new wavebreaks occurred from within the mapped region, 1122 ± 647 ms after the shock, resulting in VT to VF transition. In 135 of 145 episodes (93%), the wavebreaks occurred when a wavefront visited an area with persistent Cai elevation. In 103 of the 135 episodes, this area was co-localized within the wavebreak site and appeared to surround part of a Cai sinkhole. In 4 episodes (3%), the wavebreak occurred when a wavefront visitedan area already depolarized by another wavefront, without concomitant Cai elevation. However, 6 (4%) wavebreak episodes developed spontaneously regardless of the presence of another wavefront and Cai dynamics.
Conclusion: Wavebreaks occurring in high Cai areas are the most common phenomenon associated with VT to VF transition and continuing VF after a T-wave shock.
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KEYWORD
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ventricular tachycardia, ventricular fibrillation, calcium
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