UCLA Cardiovascular Research Laboratory, Departments of Medicine (Cardiology), Physiology and Integrative Biology and Physiology, David Geffen School of Medicine at UCLA, Los Angeles, California 90095, USA.
Heart Rhythm. 2010 Dec;7(12):1891-9. doi: 10.1016/j.hrthm.2010.09.017. Epub 2010 Sep 22.
Early afterdepolarizations (EADs) are an important cause of lethal ventricular arrhythmias in long QT syndromes and heart failure, but the mechanisms by which EADs at the cellular scale cause arrhythmias such as polymorphic ventricular tachycardia (PVT) and torsades de pointes (TdP) at the tissue scale are not well understood. Here we summarize recent progress in this area, discussing (1) the ionic basis of EADs, (2) evidence that deterministic chaos underlies the irregular behavior of EADs, (3) mechanisms by which chaotic EADs synchronize in large numbers of coupled cells in tissue to overcome source-sink mismatches, (4) how this synchronization process allows EADs to initiate triggers and generate mixed focal reentrant ventricular arrhythmias underlying PVT and TdP, and (5) therapeutic implications.
早期后除极（EADs）是长 QT 综合征和心力衰竭中导致致命性室性心律失常的一个重要原因，但 EADs 在细胞尺度上引发心律失常（如多形性室性心动过速（PVT）和尖端扭转型室性心动过速（TdP））的机制尚不清楚。在这里，我们总结了这一领域的最新进展，讨论了（1）EADs 的离子基础，（2）确定性混沌是 EADs 不规则行为的基础的证据，（3）混沌 EADs 在组织中大量偶联细胞中同步的机制，以克服源-汇不匹配，（4）这种同步过程如何使 EADs 能够引发触发并产生混合局灶性折返性室性心律失常，从而导致 PVT 和 TdP，以及（5）治疗意义。
