Davy J M, Sirinelli A, Le Guludec D, Sebag C, Motté G
Service de Cardiologie, Hôpital A. Beclère, Clamart, France.
Eur Heart J. 1988 Feb;9 Suppl B:5-12. doi: 10.1093/eurheartj/9.suppl_b.5.
The mode of antiarrhythmic action of drugs usually cannot be extrapolated from their electrophysiologic properties despite extensive in vitro and in vivo assessment: in most cases, the mechanism of arrhythmias remains uncertain and cannot be established by clinical evaluation including electrophysiologic study; in specific cases where the arrhythmia substrate is fully described, the exact origin of antiarrhythmic action is unknown, especially when chronic preventive treatment is considered where triggering events are probably important. Nevertheless, the profound electrophysiologic changes resulting from antiarrhythmic drugs alter several delicate balances, at the cellular level (repolarizing and depolarizing currents) and at the tissue level (refractory period/conduction time ratio). Some afterdepolarizations can be elicited, especially when repolarization is delayed by long cycle lengths and K+ current inhibition; reentry is enhanced when conduction impairment occurs without similar change in refractoriness. Proarrhythmic effects of drugs seem to relate to these alterations and caution should be exerted when ECG shows drug-induced QT or QRS prolongations.
尽管进行了广泛的体外和体内评估，但药物抗心律失常作用的模式通常不能从其电生理特性推断出来：在大多数情况下，心律失常的机制仍然不确定，并且不能通过包括电生理研究在内的临床评估来确定；在心律失常基质被充分描述的特定情况下，抗心律失常作用的确切起源尚不清楚，特别是在考虑慢性预防性治疗时，触发事件可能很重要。然而，抗心律失常药物引起的深刻电生理变化会改变细胞水平（复极化和去极化电流）和组织水平（不应期/传导时间比）的几个微妙平衡。可以诱发一些后除极，特别是当复极化因长周期长度和钾电流抑制而延迟时；当传导受损而不应期无类似变化时，折返会增强。药物的促心律失常作用似乎与这些改变有关，当心电图显示药物引起的QT或QRS延长时应谨慎。
