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.