Antzelevitch Charles
Masonic Medical Research Laboratory, Utica, NY 13501, USA.
J Electrocardiol. 2004;37 Suppl:15-24. doi: 10.1016/j.jelectrocard.2004.08.004.
Torsade de Pointes (TdP) is an atypical ventricular arrhythmias associated with the acquired and congenital forms of the long QT syndrome. The substrate for the arrhythmia develops 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. A wide variety of drugs are capable of reducing net repolarizing current and thus amplifying the intrinsic spatial dispersion of repolarization, so as to create 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 TdP. Recent studies demonstrate that prolongation of the QT interval is not the sole determinant of the potential of a drug to cause TdP; agents that do not increase transmural dispersion of repolarization have little or no potential to induce the arrhythmia despite their ability to prolong the QT interval. Moreover, drugs such as sodium pentobarbital, which reduce transmural dispersion of repolarization, can diminish the likelihood of TdP, despite their ability to prolong the QT interval.
尖端扭转型室性心动过速（TdP）是一种与获得性和先天性长QT综合征相关的非典型室性心律失常。心律失常的基质是由于心室心肌固有的电不均一性放大所致。这些不均一性的存在是因为构成心室心肌的三种主要细胞类型复极化时间进程不同，从而产生跨壁电压梯度和复极化离散，这导致心电图T波的形成。多种药物能够降低净复极电流，从而放大复极化的固有空间离散，进而为折返的发生创造基质。结果是QT间期延长、T波异常以及出现具有TdP特征的多形性折返性室性心动过速。最近的研究表明，QT间期延长并非药物导致TdP可能性的唯一决定因素；尽管能够延长QT间期，但不增加复极化跨壁离散的药物诱发心律失常的可能性很小或没有。此外，戊巴比妥钠等药物可减少复极化跨壁离散，尽管它们能够延长QT间期，但可降低TdP发生的可能性。
