早期后除极与再灌注心律失常机理的实验研究

再灌注心律失常已引起日益广泛的重视,但其发生机理尚未完全阐明。笔者应用心内膜接触电极导管,记录犬缺血及再灌注时在体心脏左室心内膜单相动作电位(MAPs)。10只犬,建立缺血(20分钟)—再灌注模型18次,66％(12/18)于再灌注时记录到早期后除极(EADs),其平均振幅为3.9±1.2mV,占MAPs振幅的22％。其中75％(9/12)发生与EADs有关的心律失常,EADs的耦联间期与室性早搏的耦联间期高度相关(r=0.71,P<0.01)。3只犬EADs振幅呈高低变化时,伴有左心腔电图T波电压交替变化。研究结果表明,EADs诱发的触发活动可能为再灌注心律失常的主要发生机理。MAPs技术是研究在体心脏触发活动的可靠方法。在某些特殊病例,EADs振幅的交替变化,可能是体表心电图T波电交替的发生机理。

Investigation of Mechanisms for Early Afterdepolarizations and Reperfusion Arrhythmias in Vivo

To investigate whether early afterdepolarizations (EADs) develop during myocardial ischemia and reperfusion, the monphasic action potentials (MAPs) were recorded by endocardial contact electrode in 10 anesthetized dogs when arrhythmias (RA) occur. Eighteen trials of 20 minutes occlusion of the left descending artery were followed by reperfusion. In 12/18 (66％) trials EADs with a mean amplitude of 3.9±1.2mV (22％ of MAPs amplitude) developed at the moment of reperfusion. In 9 of 12 (75％) cases in which EADs was associated with RA, the coupling interval of the EADs and of premature ventricular contractions showed a significant correlation (r=0.71, P<0.01). In three trials, the beat-to-beat changes in amplitude of EADs were observed, which were reflected on the left intracavitary electrocardiogram as T wave alternations. These findings suggested that triggered activity played a major role in the genesis of RA in vivo. MAPs technique is a reliable method in studing arrhythmiaa associated with triggered activity. The changes in amplitude of EADs may represent one of the mechanism for T wave alternations.