Zipes D P
Am J Cardiol. 1987 Apr 30;59(11):26E-31E. doi: 10.1016/0002-9149(87)90198-6.
Antiarrhythmic agents can worsen existing arrhythmias by increasing their duration or frequency, increasing the number of premature complexes or couplets, altering the rate of the arrhythmia or causing new, previously unexperienced arrhythmias. QT prolongation occurs in many settings, not all of which are associated with increased arrhythmia development. Arrhythmogenesis in the setting of a long QT interval may be related to marked asynchrony of repolarization. The role of afterdepolarizations is still being investigated. No correlation has been established between the occurrence of torsades de pointes, a specific degree of QT prolongation and either the dose or serum concentration of any of the antiarrhythmic agents. In 30 patients who experienced drug-induced ventricular fibrillation, the median time to ventricular fibrillation was only 3 days after drug treatment began. Significant caution must be exercised in determining the need for antiarrhythmic therapy and in monitoring patients after treatment has begun.
抗心律失常药物可通过延长心律失常的持续时间或频率、增加早搏或成对搏动的数量、改变心律失常的速率或引发新的、先前未出现过的心律失常，从而使现有心律失常恶化。QT间期延长在多种情况下都会发生，但并非所有情况都与心律失常发生率增加相关。长QT间期情况下的心律失常发生可能与复极的显著不同步有关。后除极的作用仍在研究中。尖端扭转型室速的发生、特定程度的QT间期延长与任何抗心律失常药物的剂量或血清浓度之间均未建立相关性。在30例发生药物性室颤的患者中，发生室颤的中位时间仅在药物治疗开始后3天。在确定是否需要抗心律失常治疗以及治疗开始后监测患者时必须格外谨慎。
