Conti J B, Curtis A B, Hill J A, Raymenants E R
University of Florida College of Medicine, Division of Cardiology, Gainesville 32610-0277.
Clin Cardiol. 1994 Jan;17(1):47-8. doi: 10.1002/clc.4960170111.
A 30-year-old woman was referred for follow-up right- and left-heart catheterization 4 years after cardiac transplantation. She had an implanted epicardial pacemaker for bradycardia; this was programmed to the DDD mode. At the time of her catheterization, as a pigtail catheter was pulled back across the aortic valve, runs of premature ventricular complexes occurred and tachycardia with ventricular pacing spikes and ventricular capture was initiated at a rate of 126 beats/min. Adenosine 6 mg was given intravenously through a femoral venous sheath and within 20 s the tachycardia broke. The tachycardia was consistent with pacemaker-mediated tachycardia (PMT), a circus movement tachycardia occurring when ventricular pacing causes retrograde atrial depolarization followed by triggering of ventricular pacing. With reprogramming of the pacemaker to an AV delay of 160 ms and a postventricular atrial refractory period of 300 ms, no further episodes of PMT have occurred. This case illustrates that intravenous adenosine can effectively terminate PMT by causing ventriculoatrial block, thus interrupting the reentrant circuit by eliminating retrograde atrial activation.
一名30岁女性在心脏移植4年后因需要进行右心和左心导管检查的随访而前来就诊。她因心动过缓植入了心外膜起搏器,该起搏器设置为DDD模式。在进行导管检查时,当猪尾导管从主动脉瓣回撤时,出现了室性早搏,随后以126次/分钟的频率启动了伴有心室起搏尖峰和心室夺获的心动过速。通过股静脉鞘管静脉注射了6毫克腺苷,20秒内心动过速终止。该心动过速符合起搏器介导的心动过速(PMT),即心室起搏导致逆行心房去极化,随后触发心室起搏时发生的一种折返性心动过速。将起搏器重新编程为房室延迟160毫秒和心室后心房不应期300毫秒后,未再发生PMT发作。该病例表明,静脉注射腺苷可通过导致房室传导阻滞有效终止PMT,从而通过消除逆行心房激动中断折返环路。