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.