Chew P H, Brinker J A
Division of Cardiology, Francis Scott Key Medical Center, Baltimore, MD 21224.
Pacing Clin Electrophysiol. 1990 Jun;13(6):808-11. doi: 10.1111/j.1540-8159.1990.tb02107.x.
An 81-year-old man was treated for high degree AV block and syncope with an AV universal (DDD) pacemaker. Bipolar active fixation atrial and ventricular leads were used. Intermittent oversensing from the ventricular lead was detected on Holter monitoring following implantation. This resulted in inappropriate inhibition of ventricular pacing. Ventricular electrogram showed spurious signals between 5 mV and 15 mV in magnitude coincident with ventricular lead inhibition. Treatment consisted of reprogramming the device to the VVT mode. Six weeks after implantation normal pacemaker function in the DDD mode was demonstrated on Holter monitoring and inappropriate pacer inhibition could not be demonstrated. We postulate that electrode 'chatter' between the cathodal ring electrode and the helix of the ventricular lead resulted in artifactual potentials sufficient to inhibit pacing. We hypothesize that fibrosis and fixation of the ventricular lead tip over a period of weeks eliminated these electromechanical artifacts and resulted in the oversensing problem being self-limited. Physicians should be aware of electrode 'chatter' as a cause of pacemaker oversensing.
一名81岁男性因高度房室传导阻滞和晕厥接受了房室通用（DDD）起搏器治疗。使用了双极主动固定心房和心室导线。植入后动态心电图监测发现心室导线间歇性感知过度。这导致心室起搏被不适当抑制。心室电图显示在心室导线抑制时出现幅度在5 mV至15 mV之间的伪信号。治疗方法是将设备重新编程为VVT模式。植入六周后，动态心电图监测显示DDD模式下起搏器功能正常，未发现不适当的起搏器抑制。我们推测阴极环形电极与心室导线螺旋之间的电极“颤动”导致了足以抑制起搏的伪电位。我们假设数周内心室导线尖端的纤维化和固定消除了这些机电伪像，导致感知过度问题自限。医生应意识到电极“颤动”是起搏器感知过度的一个原因。
