Burashnikov Alexander, Antzelevitch Charles
Masonic Medical Research Laboratory, Utica, New York 13501, USA.
Pacing Clin Electrophysiol. 2006 Mar;29(3):290-5. doi: 10.1111/j.1540-8159.2006.00336.x.
Early (EAD) and delayed (DAD) afterdepolarizations-induced triggered activity is capable of initiating and maintaining cardiac arrhythmias. EAD-induced triggered responses are traditionally thought to be involved in the generation of ventricular arrhythmias under long QT conditions and are precipitated by bradycardia or long pauses. In contrast, DAD-induced triggered activity commonly underlies arrhythmias precipitated by tachycardia. Spontaneous release of calcium from the sarcoplasmic reticulum (SR) secondary to cellular calcium overload induces DADs and some forms of EADs. Recent studies from our laboratory have uncovered a novel mechanism giving rise to triggered activity, termed "late-phase 3 EAD," which combines properties of both EAD and DAD, but has its own unique character. Late-phase 3 EAD-induced triggered extrasystoles represent a new concept of arrhythmogenesis in which abbreviated repolarization permits "normal SR calcium release" to induce an EAD-mediated closely coupled triggered response, particularly under conditions permitting intracellular calcium loading. This review briefly describes the mechanisms and properties of late-phase 3 EADs, how they differ from conventional EADs and DADs, as well as their role in the initiation of cardiac arrhythmias, such as atrial fibrillation.
早期后除极（EAD）和延迟后除极（DAD）所诱发的触发活动能够引发并维持心律失常。传统观点认为，EAD诱发的触发反应参与了长QT间期情况下室性心律失常的发生，且由心动过缓或长间歇所促发。相比之下，DAD诱发的触发活动通常是心动过速所诱发心律失常的基础。继发于细胞钙超载的肌浆网（SR）钙自发性释放可诱发DAD和某些形式的EAD。我们实验室最近的研究发现了一种引发触发活动的新机制，称为“3期晚期EAD”，它兼具EAD和DAD的特性，但有其自身独特之处。3期晚期EAD诱发的触发期前收缩代表了一种心律失常发生的新概念，即缩短的复极化允许“正常的SR钙释放”诱发EAD介导的紧密耦联触发反应，尤其是在允许细胞内钙负荷的情况下。本文简要描述了3期晚期EAD的机制和特性，它们与传统EAD和DAD的不同之处，以及它们在诸如心房颤动等心律失常起始中的作用。
