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Dissociated Pulmonary Vein Potentials: Let Sleeping Dogs Lie

It has been almost 20 years since the discovery that pulmonary vein ectopy is largely responsible for initiation of paroxysmal atrial fibrillation (PAF).1 We have spent the better part of those 20 years seeking effective ways of eliminating pulmonary vein ectopy or its effect on the atrial rhythm. The currently accepted paradigm is that “fencing off” the offending muscle sleeves that run along the pulmonary veins should prevent AF initiation; and perhaps the isolating lesions may also target antral reentrant activity responsible for sustaining AF. What we do not know, however, is the consequence of pulmonary vein ectopy once the veins are isolated—ectopy, or bursts or fibrillation that is, at least for the moment, isolated from the left atrium. An optimistic view may be that the presence of these potentials after ablation is a sign of success—the activity is independent of the left atrium and therefore bursts from that vein will no longer initiate AF. A more realistic view may be that we do not currently have a satisfactory track record of permanently isolating pulmonary veins, and that this ectopy is going to be problematic if and when the ablation lines recover conduction. It would therefore be tempting to target all such ectopy, as a second line of defense, if it were not for our collective wisdom that ablation at or beyond the pulmonary vein ostia, where this activity inevitably arises, can lead to pulmonary vein stenosis with potentially severe consequences. As with any situation where we are inclined to do more but at some risk, what we need is evidence. What prognostic information do these potentials offer? What are the benefits and risks involved in eliminating them? In this issue of the Journal, Buiatti et al.2 seek to define the role of dissociated pulmonary vein activity (DPVA) in recurrence of PAF after pulmonary vein isolation (PVI). They studied 243 patients undergoing PVI for PAF and grouped patients according to presence (n = 65, 27%) or absence (n = 178, 73%) of any DPVA, which they defined as slow (CL 1000 milliseconds) and irregular vein activity. The overall prevalence of DPVA was 12% of veins, on average 1.7 in a DPVA+ patient, and more commonly observed in superior than inferior veins. After a mean 12 months follow-up,