Malfatto G, Rosen T S, Rosen M R
Department of Pharmacology, Columbia University College of Physicians and Surgeons, New York, NY 10032.
Circulation. 1988 May;77(5):1139-48. doi: 10.1161/01.cir.77.5.1139.
Although triggered activity has been identified in isolated atrial tissue with the use of cellular electrophysiologic techniques, there has been no identification of triggered atrial arrhythmias in situ. Moreover, it is unclear whether triggered rhythms of different causes and sites of origin in the heart exhibit uniform responses to pacing that might aid in their identification. We therefore studied arrhythmias induced by overdrive pacing in three canine preparations, and based the analysis of our results on guidelines derived from microelectrode studies. We studied ventricular tachycardias induced by ouabain or by anterior wall myocardial infarction and atrial (coronary sinus) arrhythmias induced by the infusion of epinephrine into the great cardiac vein. In the ouabain and postinfarction preparations, right ventricular epicardial pacing induced ventricular premature beats or tachycardias whose recovery intervals after cessation of pacing shortened and showed overdrive acceleration as pacing rate increased. The first postpacing beat displayed progressive fusion with the paced beats but transient entrainment could not be induced. In the coronary sinus, the recovery intervals of impulses induced by epinephrine and pacing decreased as the drive rate increased, and inducibility of the paced rhythms increased at faster drive rates. Thus, the recovery intervals of triggered activity induced in the coronary sinus are phenomenologically similar to those of infarct- and digitalis-induced triggered rhythms. This is the first demonstration of consistent behavior in response to pacing of diverse types of triggered activity. Considered in light of the failure to induce transient entrainment, the results emphasize the potential utility of pacing in clinical identification of triggered rhythms and their differentiation from reentry.
尽管利用细胞电生理技术在离体心房组织中已识别出触发活动，但尚未在原位识别出触发型房性心律失常。此外，尚不清楚心脏中不同病因和起源部位的触发节律对起搏是否表现出有助于其识别的一致反应。因此，我们在三种犬类标本中研究了超速起搏诱发的心律失常，并根据微电极研究得出的指南对结果进行分析。我们研究了由哇巴因或前壁心肌梗死诱发的室性心动过速以及通过向心大静脉注入肾上腺素诱发的心房（冠状窦）心律失常。在哇巴因和心肌梗死后的标本中，右心室心外膜起搏诱发室性早搏或心动过速，起搏停止后的恢复间期缩短，并随着起搏频率增加呈现超速加速。起搏后第一个搏动与起搏搏动逐渐融合，但无法诱发短暂拖带。在冠状窦，随着驱动频率增加，由肾上腺素和起搏诱发的冲动的恢复间期缩短，且起搏频率越快，起搏节律的诱发率越高。因此，在冠状窦诱发的触发活动的恢复间期在现象学上与梗死和洋地黄诱发的触发节律相似。这是首次证明不同类型触发活动对起搏的反应具有一致性。鉴于未能诱发短暂拖带，这些结果强调了起搏在临床识别触发节律及其与折返鉴别中的潜在效用。
