Subendocardial Origin of Ventricular Arrhythmias in 24‐Hour‐Old Experimental Myocardial Infarction
Subendocardial Origin of Ventricular Arrhythmias in 24‐Hour‐Old Experimental Myocardial Infarction
复制标题
24小时实验性心肌梗死中室性心律失常的心内膜下起源
作者：
L. Horowitz;J. Spear;E. Moore
在 12 只麻醉的开胸犬中，在对左冠状动脉前降支进行 Harris 2 阶段结扎后 24 小时，绘制了心室心外膜激活图，并记录了希氏束、左束支和心内膜下浦肯野纤维的电图。所有动物均出现异位心室除极和/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。来自传导系统和心室心肌各个层面的双极记录表明，最早记录的电活动起源于急性心肌梗死后幸存的心内膜下浦肯野纤维。通过记录早期浦肯野活动的电极起搏并将表面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以下假设：急性心肌梗塞后 24-72 小时内发生的室性心律失常起源于在梗塞后幸存的心内膜下浦肯野网络。
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.