Lucchesi B R
Am J Cardiol. 1984 Jul 30;54(2):14A-19A. doi: 10.1016/0002-9149(84)90812-9.
Experimental evidence suggests a number of pathologic and electrophysiologic mechanisms that may help initiate ventricular arrhythmias accompanying myocardial ischemia and infarction. Early and late phase events are associated with reentry or an enhancement of focal mechanisms, or both. These can initiate ventricular tachycardia (VT) or ventricular fibrillation (VF), or both. The presence of distinct mechanisms that may initiate and maintain life-threatening dysrhythmias early in myocardial ischemia suggest different pharmacologic approaches for their prevention or suppression. Another consideration concerns patients subjected to coronary artery angioplasty or thrombolytic therapy and the development of arrhythmias associated with reperfusion of the once ischemic myocardium. The electrophysiologic mechanisms associated with reperfusion arrhythmias are unknown, and little is known about appropriate therapy for each episode of cardiac dysrhythmia. Ventricular extrasystoles or VT usually precedes VF. These premonitory arrhythmias are poor criteria for the institution of antiarrhythmic drug therapy, because VF develops within 1 to 10 minutes after the appearance of the rhythmic disturbances. Some authorities suggest that all patients with acute myocardial infarction should receive prophylactic antiarrhythmic therapy, because warning arrhythmias either do not occur at all or provide insufficient time to intervene pharmacologically. Many of the new class I antiarrhythmic agents effectively reduce the frequency of premature ventricular depolarizations, but lack specific antifibrillatory activity. However, the recent introduction of bretylium into clinical cardiology opens a new approach to preventing life-threatening ventricular dysrhythmias. Along with other members of class III, bretylium exerts different cardiac electrophysiologic effects than do the other 3 classes of drugs.(ABSTRACT TRUNCATED AT 250 WORDS)
实验证据表明,有多种病理和电生理机制可能有助于引发伴随心肌缺血和梗死的室性心律失常。早期和晚期事件与折返或局灶机制增强或两者均有关联。这些可引发室性心动过速(VT)或心室颤动(VF),或两者皆有。在心肌缺血早期可能引发并维持危及生命的心律失常的不同机制的存在,提示了预防或抑制它们的不同药物治疗方法。另一个需要考虑的问题涉及接受冠状动脉血管成形术或溶栓治疗的患者,以及与曾经缺血的心肌再灌注相关的心律失常的发生。与再灌注心律失常相关的电生理机制尚不清楚,对于每一次心脏心律失常发作的适当治疗也知之甚少。室性期前收缩或VT通常先于VF出现。这些先兆性心律失常并非启动抗心律失常药物治疗的可靠标准,因为VF会在节律紊乱出现后的1至10分钟内发生。一些权威人士建议,所有急性心肌梗死患者都应接受预防性抗心律失常治疗,因为警示性心律失常要么根本不出现,要么没有足够的时间进行药物干预。许多新型I类抗心律失常药物能有效降低室性早搏的频率,但缺乏特异性的抗颤动活性。然而,近来溴苄铵引入临床心脏病学,为预防危及生命的室性心律失常开辟了一条新途径。与III类的其他成员一样,溴苄铵产生的心脏电生理效应与其他三类药物不同。(摘要截选至250词)