Mechanisms of recurrent ventricular fibrillation in a rabbit model of pacing-induced heart failure
Mechanisms of recurrent ventricular fibrillation in a rabbit model of pacing-induced heart failure
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DOI：
10.1016/j.hrthm.2009.02.017
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发表时间：
2009-06-01
期刊：
影响因子：
5.5
通讯作者：
Chen, Peng-Sheng
中科院分区：
文献类型：
--
作者：
Ogawa, Masahiro;Morita, Norishige;Chen, Peng-Sheng
背景技术成功除颤后可能会出现复发性自发性心室颤动（VF）。电击后自发性心室颤动的机制尚不清楚。目的本研究的目的是确定兔心力衰竭（HF）模型初次成功除颤后自发性心室颤动的机制。方法对 12 只慢性起搏心力衰竭兔心脏、4 颗假手术心脏和 5 颗正常心脏进行细胞内钙（Ca-i）和膜电位（Vm）同步光学测绘。结果 在 4 颗衰竭心脏（SVF 组）初次成功除颤后，记录了 28 次自发性 VF 发作，但在其余 8 颗衰竭心脏（无 SVF 组）或正常或假手术心脏中没有记录到。起搏诱发 VF 之前的动作电位持续时间 (APD(80)) 在 SVF 组中为 209 +/- 9 ms，在无 SVF 组中为 212 +/- 14 ms (P = NS)。成功除颤后，SVF 组的 APD(80) 缩短至 147 +/- 26 ms，无 SVF 组缩短至 176 +/- 14 ms (P = .04)。然而，除颤后 Ca-i 的持续时间在两组之间没有差异（246 +/- 21 ms 与 241 +/- 17 ms，P = NS），导致动作电位第 3 相后期或第 4 相期间 Ca-i 升高。对另外 5 个衰竭心脏的标准玻璃微电极记录证实了电击后和去极化后 APD 缩短。正常心脏和假手术心脏的 APD(80) 在除颤后并未缩短。结论 心衰心脏在 VF 终止后，HF 会立即促进 APD 的急性缩短。动作电位缩短的第 3 相后期和第 4 相持续 Ca-i 升高导致去极化后、触发活动和自发性 VF。
BACKGROUND Successful defibrillation may be followed by recurrent spontaneous ventricular fibrillation (VF). The mechanisms of postshock spontaneous VF are unclear.OBJECTIVE The purpose of this study was to determine the mechanisms of spontaneous VF after initial successful defibrillation in a rabbit model of heart failure (HF).METHODS Simultaneous optical mapping of intracellular calcium (Ca-i) and membrane potential (Vm) was performed in 12 rabbit hearts with chronic pacing-induced heart failure, in 4 sham-operated hearts, and in 5 normal hearts during fibrillation-defibrillation episodes.RESULTS Twenty-eight spontaneous VF episodes were recorded after initial successful defibrillation in 4 failing hearts (SVF group) but not in the remaining 8 failing hearts (no-SVF group) or in the normal or sham-operated hearts. The action potential duration (APD(80)) before pacing-induced VF was 209 +/- 9 ms in the SVF group and 212 +/- 14 ms in the no-SVF group (P = NS). After successful defibrillation, APD(80) shortened to 147 +/- 26 ms in the SVF group and to 176 +/- 14 ms in the no-SVF group (P = .04). However, the duration of Ca-i after defibrillation was not different between the two groups (246 +/- 21 ms vs 241 +/- 17 ms, P = NS), resulting in elevated Ca-i during late phase 3 or phase 4 of the action potential. Standard glass microelectrode recording in an additional 5 failing hearts confirmed postshock APD shortening and after depolarizations. APD(80) of normal and sham-operated hearts was not shortened after defibrillation.CONCLUSION HF promotes acute shortening of APD immediately after termination of VF in failing hearts. Persistent Ca-i elevation during late phase 3 and phase 4 of the shortened action potential result in after depolarizations, triggered activity, and spontaneous VF.