Figure legends
Figure 1. A: Continuous ECG of lead Ⅱ shows 2:1 wide QRS complexes
accompanied by ventricular pacing following the loss of atrial capture.
The pacemaker mode was DDD 60-110 bpm with a paced AV interval of 350
ms, 3.5 V at a 0.4 ms setting of atrial pacing output. B: Intracardiac
EGM strips during 2:1 atrial pacing failure. The middle portion
indicates the atrial EGM channel; the bottom indicates the ventricular
EGM channel. Because intrinsic atrial beats (indicated as PAC) were
observed after atrial pacing failure, but they were within the
post-ventricular atrial refractory period (PVARP), the pacemaker timing
cycle was not reset. A shorter coupling period (510 ms and 725 ms) of
atrial pacing, followed by the intrinsic atrial beat could capture the
atrial myocardium. A longer coupling period (1000 ms was the lower rate
interval) of atrial pacing could not capture the atrial myocardium.
Figure 2. A: Pacing threshold during atrial pacing is plotted against
each pacing rate. Larger output was required as a lower pacing rate. B:
Intracardiac EGM immediately after ATP 20 mg injection. Although the
first, second, fourth and fifth pacing could not capture the atrial
myocardium, the sixth, seventh, eighth, and ninth pacing could all
capture the atrial myocardium with 2.5 V at 0.4 ms where the threshold
before ATP injection was 3.5 V at 0.4 ms at 50 bpm, without changing the
pacing rate.
Figure 3. A proposed mechanism of ATP-induced transient improvement of
rate-dependent pacing failure. A. The resting membrane potential in the
normal atrial myocardium is steady negative and most of Na+ channels are
available for generating action potential (D: blue point). B.
Bradycardia-dependent pacing failure with myocardial injury after pacing
lead implantation can be explained by gradual depolarization during
phase 4, in a similar manner to rate-dependent phase 4 block. When
pacing with a shorter coupling interval (510 ms) from the preceding
depolarization, the Na+ channel fraction is available
enough to capture (D: yellow point). On the other hand, when pacing with
a longer coupling interval (1000 ms), a large fraction of the
Na+ channels is inactivated (D: red point), resulting
in pacing failure. C. Bolus ATP injection induces hyperpolarization
during phase 4 by increasing inward rectifier K+current (IKAdo). Consequently, Na+channel availability is restored (D: red point to yellow point) and the
myocardium is captured by pacing with a longer coupling interval.