Discussion:
Although rate dependent block is believed to increase the likelihood of recurrent arrhythmia for CTI dependent atrial flutter, it is unlikely to be the culprit for our patient’s recurrence of atrial fibrillation. Specifically, the inability to conduct at faster cycle lengths would suggest that automaticity, or tightly coupled premature atrial contractions, would not likely reach the left atrium and thus not trigger arrhythmia. Nonetheless, we did re-isolate the vein.
To our knowledge, this is the first report of chronic rate dependent exit block (i.e. Rate dependent exit block discovered 7 years after circumferential PV antral isolation). The most probable explanation is phase 3 block or tachycardia induced block secondary to the ablation. Normal cells are characterized by a more negative resting potential, larger action potential amplitude, and fast depolarization sodium current. Diseased cells have a less negative resting potential, smaller action potential amplitude of shorter duration, and a much slower depolarizing current that could still be carried by a sodium current with depressed kinetics6. The injured tissue has not completely repolarized, and thus cannot generate an action potential at short cycle lengths (i.e. there is a long effective refractory period).
While it is possible this reconnection in the LSPV was the etiology of arrhythmia recurrence, as we were not able to provoke triggers, it is not our hypothesis as the etiology for the recurrent arrhythmia. The electrophysiologic observation is interesting and may have more significant implications in the acute setting. We have seen the use of adenosine in PV isolation as well as the importance of entrance and exit block. We now observe rate dependent block of a pulmonary vein. We believe that, as with CTI ablation, rate independent pulmonary vein isolation should be confirmed.
Figure 1: Capture of LA at paced CL of 1000 ms from inside the LSPV