Reinduction of atrial fibrillation immediately after termination of the arrhythmia is mediated by late phase 3 early afterdepolarization-induced triggered activity
Reinduction of atrial fibrillation immediately after termination of the arrhythmia is mediated by late phase 3 early afterdepolarization-induced triggered activity
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DOI：
10.1161/01.cir.0000065578.00869.7c
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发表时间：
2003-05-13
期刊：
影响因子：
37.8
通讯作者：
Antzelevitch, C
中科院分区：
文献类型：
--
作者：
Burashnikov, A;Antzelevitch, C
背景-房颤(AF)有时在心律失常终止后立即复发。重新诱发房颤的早搏机制(S)在很大程度上还不清楚。我们假设动作电位时程的缩写可以允许非常快的兴奋速率，从而引起细胞内钙负荷，进而促进延迟和/或早期后除极(EADs)。方法和结果：乙酰胆碱(ACh，1 mumol/L)被用来缩短心房动作电位时程，并允许在冠脉灌流的犬右心房快速诱发房颤。记录跨膜动作电位、伪心电信号和张力变化。房颤或快速起搏与紧张性张力增加有关。房颤的终止或快速起搏(周期150~80ms)导致相张力显著升高，在正常频率(周期长度为700ms)下的起搏复极延长，并出现晚期3型EADS和早搏。15例(9个右房)在房颤终止或快速起搏后11s内发生房颤。这种新的EAD机制仅与标记的apd缩写相关联。钙通道阻滞剂硝苯地平减少，肌浆网钙释放阻滞剂ryanodine消除，快速起搏后诱发的时相张力增加、晚期3型EADs和启动房颤的早搏。结论这些数据提示迷走神经介导的房颤终止后出现的钙超载状态有助于晚期3型EAD诱发的触发活动的发生，这一机制可能是重新启动房颤的早搏活动的机制之一。
Background-Atrial fibrillation (AF) at times recurs immediately after termination of the arrhythmia. The mechanism(s) responsible for the extrasystole that reinduces AF is largely unknown. We hypothesized that abbreviation of action potential duration (APD) would permit very rapid rates of excitation, known to induce intracellular calcium loading, which in turn could promote delayed and/or early afterdepolarizations (EADs).Methods and Results-Acetylcholine (ACh, 1 mumol/L) was used to abbreviate atrial APD and permit rapid-pacing induction of AF in isolated coronary-perfused canine right atria. Transmembrane action potentials, pseudo-ECG, and tension development were recorded. AF or rapid pacing was associated with an increase in tonic tension. Termination of AF or rapid pacing (cycle length, 150 to 80 ms) resulted in a dramatic rise of phasic tension, prolongation of repolarization of the initial beats at the regular rate (cycle length, 700 ms), and the development of late phase 3 EADs and extrasystoles. These extrasystoles initiated AF in 15 cases (involving 9 right atria) within the first 11 seconds after termination of AF or rapid pacing. This novel EAD mechanism is observed only in association with marked APD abbreviation. The calcium channel blocker nifedipine reduced, and the sarcoplasmic reticulum calcium release blocker ryanodine eliminated, the post-rapid pacing-induced increase in phasic tension, late phase 3 EADs, and extrasystoles that initiate AF.Conclusions-These data suggest that calcium overload conditions present after termination of vagally mediated AF contribute to the development of late phase 3 EAD-induced triggered activity and that this mechanism may be responsible for the extrasystolic activity that reinitiates AF.