Hope R R, Scherlag B J, El-Sherif N, Lazzara R
Am J Cardiol. 1977 Nov;40(5):733-8. doi: 10.1016/0002-9149(77)90189-8.
Twenty dogs were studied 3 to 9 days after myocardial infarction. None had ventricular arrhythmias during sinus rhythm, and ventricular automaticity (as revealed by sinus nodal crush procedure or vagal stimulation, or both) was within the normal range. With regular atrial pacing or pacing with long-short cycle sequences it was possible to induce ventricular arrhythmias in all animals. Quadrigeminal and pentageminal rhythms (19 of 20 dogs) and trigeminal (17 of 20) and bigeminal ventricular rhythms (8 of 20) were observed. These rhythms which were manifest or partially or entirely concealed were always associated with delayed and fractionated electrical activity within the "infarcted" subepicardium. Continuous electrical activity (electrical activity that bridged the interval between two or more successive beats) was recorded from the infarct zone. Such activity either was manifest as ventricular arrhythmia during atrial pacing or remained concealed until atrial pacing was stopped and then was manifest as ventricular tachycardia.
对20只狗在心肌梗死后3至9天进行了研究。在窦性心律期间，无一出现室性心律失常，并且室性自律性（通过窦房结挤压术或迷走神经刺激，或两者同时进行所揭示）在正常范围内。通过规则的心房起搏或长短周期序列起搏，在所有动物中都有可能诱发室性心律失常。观察到了四联律和五联律（20只狗中有19只）以及三联律（20只狗中有17只）和二联律室性心律（20只狗中有8只）。这些明显的或部分或完全隐匿的心律总是与“梗死”心外膜下延迟和碎裂的电活动相关。从梗死区域记录到了持续的电活动（连接两个或更多连续搏动之间间隔的电活动）。这种活动要么在心房起搏期间表现为室性心律失常，要么一直隐匿，直到心房起搏停止，然后表现为室性心动过速。
