Horowitz L N, Spear J F, Moore E N
Circulation. 1976 Jan;53(1):56-63. doi: 10.1161/01.cir.53.1.56.
In 12 anesthetized open-chest dogs, ventricular epicardial activation maps were constructed and electrograms were recorded from the bundle of His, left bundle branch, and subendocardial Purkinje fibers 24 hours following Harris 2-stage ligation of the left anterior descending coronary artery. All animals developed ectopic ventricular depolarizations and/or ventricular tachycardia. The earliest area of epicardial activation was located along the border of the infarct in the left ventricle in all animals. Bipolar recording from various levels of the conduction system and ventricular myocardium revealed that the earliest recorded electrical activity originated in subendocardial Purkinje fibers which had survived the acute myocardial infarction. The origin of these arrhythmias was further studied by pacing through the electrode which had recorded the early Purkinje activity and comparing the surface ECG and activation sequence with that of the spontaneous rhythm. These data tend to support the hypothesis that ventricular arrhythmias occurring 24-72 hours following acute myocardial infarction have their origin in the subendocardial Purkinje network which has survived the infarction.
在12只麻醉开胸犬中,在对左前降支冠状动脉进行哈里斯两阶段结扎24小时后,构建心室心外膜激活图,并从希氏束、左束支和心内膜下浦肯野纤维记录电图。所有动物均出现异位心室去极化和/或室性心动过速。在所有动物中,最早的心外膜激活区域位于左心室梗死边缘。从传导系统和心室心肌的不同水平进行双极记录显示,最早记录到的电活动起源于心内膜下在急性心肌梗死中存活下来的浦肯野纤维。通过记录早期浦肯野活动的电极进行起搏,并将体表心电图和激活序列与自发节律进行比较,进一步研究了这些心律失常的起源。这些数据倾向于支持这样的假设,即急性心肌梗死后24 - 72小时发生的室性心律失常起源于心内膜下在梗死中存活下来的浦肯野网络。