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