Antzelevitch Charles, Shimizu Wataru
Masonic Medical Research Laboratory, Utica, New York, USA; National Cardiovascular Center, Osaka, Japan.
Curr Opin Cardiol. 2002 Jan;17(1):43-51. doi: 10.1097/00001573-200201000-00007.
QT prolongation is commonly associated with life-threatening torsade de pointes arrhythmias that develop as a consequence of the amplification of electrical heterogeneities intrinsic to the ventricular myocardium. These heterogeneities exist because of differences in the time course of repolarization of the three predominant cell types that make up the ventricular myocardium, giving rise to transmural voltage gradients and a dispersion of repolarization responsible for the inscription of the electrocardiographic T wave. Agents and conditions that reduce net repolarizing current amplify the intrinsic spatial dispersion of repolarization, thus creating the substrate for the development of re-entry. The result is a prolongation of the QT interval, abnormal T waves, and development of polymorphic re-entrant ventricular tachycardia displaying characteristics of torsades de pointes. These conditions also predispose M cells and Purkinje fibers to develop early afterdepolarization-induced extrasystoles, which are thought to trigger episodes of torsades de pointes. Agents that prolong the QT interval but do not increase transmural dispersion of repolarization are not capable of inducing torsades de pointes. The available data suggest that that the principal problem with the long QT syndrome is not long QT intervals but rather the dispersion of repolarization that often accompanies prolongation of the QT interval.
QT间期延长通常与危及生命的尖端扭转型室性心律失常相关，这种心律失常是由于心室肌固有的电不均一性增强所致。这些不均一性的存在是因为构成心室肌的三种主要细胞类型复极时间进程不同，从而产生跨壁电压梯度和复极离散，这导致了心电图T波的形成。减少净复极电流的药物和情况会放大复极的固有空间离散，从而为折返的发生创造了基质。结果是QT间期延长、T波异常以及出现具有尖端扭转型室性心动过速特征的多形性折返性室性心动过速。这些情况还使M细胞和浦肯野纤维易于发生早期后除极诱发的期前收缩，后者被认为可触发尖端扭转型室性心动过速发作。延长QT间期但不增加复极跨壁离散的药物不能诱发尖端扭转型室性心动过速。现有数据表明，长QT综合征的主要问题不是QT间期延长，而是常伴随QT间期延长的复极离散。
