Case report
An 82-year-old woman was referred to our hospital for the management of SSS with lightheadedness. She had a history of lone atrial fibrillation (AF), but was not taking any antiarrhythmic drugs. Holter electrocardiography showed a total heart rate (HR) of about 50,000 beats per day (minimum HR was 29 bpm), 8.3 seconds of cardiac arrest was observed at the termination of AF. Consequently, we decided to implant a dual-chamber pacemaker; a passive-fixation lead (INGEVITY MRI, Boston Scientific, USA) and an active-fixation lead (INGEVITY MRI, Boston Scientific, USA) were implanted in the right atrial appendage and right ventricular mid-septum, respectively. The initial atrial pacing threshold was 0.7 V at 0.4 ms at 60 bpm. The sensing threshold and impedance values of the atrial lead were 2.1 mV and 638 Ω, respectively. The pacemaker was programmed to DDD 60-110 bpm with 3.5 V at a 0.4 ms setting of atrial pacing output.
Two days after the implantation, electrocardiographic monitoring showed 2:1 ventricular pacing following atrial pacing spikes, without atrial capture (Figure 1-A). The chest X-ray showed no apparent dislodgement of either the atrial or ventricular leads. Pacemaker interrogation revealed that atrial pacing capture was dependent on the interval of preceding atrial sensing or captured pacing events (Figure 1-B). Therefore, we evaluated the atrial pacing threshold by changing the pacing rate. The atrial pacing threshold was then increased and was inversely correlated with the pacing rate: 4.0 V at 0.4 ms at 50 bpm, 2.7 V at 0.4 ms at 60 bpm, 1.5 V at 0.4 ms at 70 bpm, and 1.0 V at 0.4 ms at 80 bpm (Figure 2-A). Although there was a slight decrease in the atrial pacing threshold when the pulse width extended from 0.4 ms to 1.0 ms, the rate dependency of the pacing threshold remained unchanged. The sensing and impedance values were slightly decreased, but the decrease was not significant, and it was acceptable. (sensing and impedance values were 1.3 mV and 582 Ω, respectively).
The causes of such a bradycardia-dependent increase in the pacing threshold without apparent lead dislodgement are considered as follows: (1) fluctuation in the contact to the myocardium by lead micro-dislodgement1, and (2) phase 4 depolarization and block in the injured myocardium2. We assumed this phenomenon to be associated with phase 4 depolarization in this patient, because the relationship between the pacing threshold and pacing rate indicated a sigmoid curve, which likely is a physiological phenomenon (Figure 2-A). A pause-dependent paroxysmal atrioventricular block mostly occurs in the presence of an injured His-Purkinje system and is known to be responsible for gradual phase 4 depolarization3. On the other hand, Datino et al4 demonstrated that adenosine could hyperpolarize canine pulmonary vein (PV) cardiomyocytes by increasing the inward rectifier K+ current (IKAdo) in which the resting membrane potential decreased by radiofrequency (RF) application and this phenomenon could account for the “dormant conduction” in PV isolation for AF. Therefore, we examined whether the administration of ATP could restore the pacing capture in the damaged atrial myocardium by hyperpolarization during phase 4. An intracardiac electrogram (EGM) immediately after the administration of ATP during atrial pacing under the subthreshold voltage, of 2.5 V at 0.4 ms at 50 bpm (the threshold was 3.5 V at 0.4 ms at 50 bpm), is shown in Figure 2-B. Since ATP administration resulted in 1:1 atrial capture transiently, without a change in the pacing rate, we determined that her bradycardia-dependent increase in the pacing threshold was related with phase 4 depolarization. Some authors have already reported bradycardia-dependent increase in the pacing threshold to improve time-dependently2; hence, we did not replace her atrial lead and changed the pulse width from 0.4 ms to 1.0 ms, avoiding pacing failure.
No improvement in the atrial pacing threshold was observed at the lower pacing rate at seven days after the pacemaker implantation. However, two more weeks later, the atrial pacing threshold was improved as follows: 1.0 V at 0.4 ms at 50 bpm, 0.7 V at 0.4 ms at 60 bpm, and 0.6 V at 0.4 ms at 70 bpm; this has been maintained for over two years. Informed consent was obtained from the patient for the publication of this case report.