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.