Fujimoto T, Peter T, Hamamoto H, Mandel W J
Am Heart J. 1983 Feb;105(2):201-9. doi: 10.1016/0002-8703(83)90514-8.
The threat of reperfusion fibrillation could potentially deter attempts of reperfusion in patients with acute myocardial infarction. Delineation of the mechanisms of this arrhythmia could pave the way to newer interventions designed as prevention or definitive treatment. Therefore the purpose of the present study was to investigate the features of initiation of reperfusion-induced ventricular fibrillation, and further to distinguish between episodic and sustained ventricular arrhythmias following reperfusion. Nine instances of reperfusion ventricular fibrillation and five instances of episodic tachyarrhythmia were analyzed in the study utilizing endocardial bipolar electrograms from normal, ischemic, reperfused, and border of these myocardial segments. In 11 of 14 instances, the site of initiation of the tachyarrhythmias was in the reperfused myocardium; however, maintenance of the arrhythmia defined as diastolic and or continuous electrical activity suggestive of reentry was not seen in the reperfused myocardium in any of these instances. Diastolic electrical activity was observed in 8 of 14 instances, and was seen either in the center or border of ischemic myocardium. Neither heart rate or mean aortic pressure was different between episodic and sustained arrhythmia groups; however, the initial beat of the fatal arrhythmia was significantly more premature than that of episodic arrhythmia. In addition, shorter cycle length, greater variations in the cycle length, and greater disparity in local activation during the tachyarrhythmia were seen in the sustained arrhythmia group compared to the episodic group; cycle length increased and the disparity in local activation improved gradually prior to the termination of the arrhythmia. There was no particular difference in conduction delay immediately prior to reperfusion between control and reperfusion ventricular fibrillation groups. We conclude that different mechanisms exist for the initiation and maintenance of reperfusion-induced arrhythmias. Further, several features seem to distinguish episodic from fatal arrhythmias following reperfusion.
再灌注性心室颤动的威胁可能会阻碍急性心肌梗死患者进行再灌注治疗的尝试。明确这种心律失常的机制可为设计预防或确定性治疗的新干预措施铺平道路。因此，本研究的目的是探讨再灌注诱导的心室颤动的起始特征，并进一步区分再灌注后的阵发性和持续性室性心律失常。本研究利用来自正常、缺血、再灌注心肌节段及其边界的心内膜双极电图，分析了9例再灌注性心室颤动和5例阵发性快速心律失常。在14例中的11例中，快速心律失常的起始部位位于再灌注心肌；然而，在这些病例中，再灌注心肌均未出现定义为舒张期和/或提示折返的持续性电活动来维持心律失常。14例中有8例观察到舒张期电活动，其出现在缺血心肌的中心或边界。阵发性和持续性心律失常组之间的心率或平均主动脉压均无差异；然而，致命性心律失常的起始搏动比阵发性心律失常的起始搏动明显更早。此外，与阵发性心律失常组相比，持续性心律失常组在快速心律失常期间的周期长度更短、周期长度变化更大以及局部激动差异更大；在心律失常终止前，周期长度增加，局部激动差异逐渐改善。对照组和再灌注性心室颤动组在再灌注前即刻的传导延迟没有特别差异。我们得出结论，再灌注诱导的心律失常的起始和维持存在不同机制。此外，有几个特征似乎可以区分再灌注后的阵发性和致命性心律失常。
