缺血性心脏病中心律失常的药物治疗应以了解有关机制为基础。晚近急性或慢性心肌缺血的动物实验指明,不同的机制,如折返、自律性增强(4相除极)、边界电流、和触发活动(迟发性后除极)可以在冠状动脉阻塞后引起心律失常。某些机制可能与缺血开始后的时距,以及有无部分再灌注有关。在人体心脏,冠状动脉阻塞后迅速变化着的电生理状况使缺血早期研究心律失常的机制有困难。只有在心肌梗塞的慢性期出现反复发作持续性心动过速的患者,才有可能进行诱发 Arrhythmic drug therapy in ischemic heart disease should be based on an understanding of the mechanisms involved. Recent animal studies of acute or chronic myocardial ischemia have shown that different mechanisms such as reentry, increased self-regulation (quadrupole depolarization), border currents, and triggering activities (late post-depolarization) can be caused after occlusion of the coronary artery Arrhythmia. Some mechanisms may be related to the time interval after the onset of ischemia, with or without partial reperfusion. In the human heart, rapidly changing electrophysiological conditions after coronary occlusion make it difficult to study early arrhythmia mechanisms of ischemia. Only in the chronic phase of myocardial infarction recurrence of recurrent tachycardia in patients only possible to be induced