Discussions
Even today, we may encounter patients with varying degrees of transient
increase in the pacing threshold after pacemaker implantation. Uehara et
al5 demonstrated an acute and transient, but not
persistent, rise in the capture threshold (TRACT) in 6% of patients
undergoing dual-chamber pacemaker implantation, which most likely
occurred when the damaged atrial myocardium was associated with SSS.
Their colleagues also reported three similar TRACT cases of
bradycardia-dependent nature in which the involvement of a phase 4 block
was suggested2. However, to the best of our knowledge,
this is the first report in which the potential role of phase 4
depolarization in bradycardia-dependent increase in the pacing threshold
was evaluated using ATP.
The resting membrane potential in the normal atrial myocardium is
usually at a steady negative level (about -80 mV), whereas in the
damaged atrial myocardium, it is expected to be decreased (becomes less
negative), such as in canine PV myocytes injured by RF application. As
the resting membrane potential decreases, the voltage-dependent
inactivation Na+ channel gradually closes and inward
Na+ current is reduced to a level at which action
potential cannot occur against external stimulations. On the other hand,
as described above, ATP could hyperpolarize damaged cardiomyocytes and
subsequently facilitate depolarization. Accordingly, we hypothesized
that the bradycardia-dependent increase in the pacing threshold observed
in the early phase after pacemaker implantation was associated with
phase 4 depolarization in the damaged myocardium, cause by factors such
as inflammation and edema due to lead-contact and could be improved by
the administration of ATP, which increases the resting membrane
potential and activates sufficient Na+ current (Figure
3). Indeed, Blazek et al6 suggested that
pacemaker-lead implantation-induced myocardial micro-damage, either with
an active or passive fixation lead, could be monitored by using the
high-sensitive troponin T level as an index.
Although further investigations are required, many cases of
bradycardia-dependent increase in the pacing threshold early after
pacemaker implantation could be due to phase 4 depolarization and ATP
could be useful for investigating the mechanism.