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PVI's Inconvenient Truths: Lights Out for Dormant Reconnection?

The advent of pulmonary vein isolation (PVI) as an effective therapy for atrial fibrillation (AF) was accompanied by the inconvenient realization that durable, long-term PVI is difficult to achieve. PV reconnection was found by several groups to be a common feature in patients with recurrent AF after ablation.1-3 Re-isolation could render many of such patients free of arrhythmia. Small studies suggest that subjects without recurrence appear to have fewer reconnected veins than those with ongoing AF. As a result, PVI, originally devised to isolate known and potential pulmonary vein sources of AF while limiting the risks associated with direct trigger ablation, became the “cornerstone” of AF ablation.4 Although clinical predictors of ablation success such as LA volume and scar burden, AF duration, and the presence of comorbidities have helped identify optimal and suboptimal ablation candidates, intraoperative predictors of ablation success have been more elusive. Isoproterenol infusion and burst pacing have varying ability to identify non-PV triggers of AF post-PVI; however, neither have allowed for dependable prediction of either acute or chronic PV reconnection, the most important cause of AF recurrence.5,6 Regardless of the ablation approach—segmental or some form of circumferential isolation—PV reconnection appears to result from small gaps in the lesion set rather than large sectors of incomplete ablation. Anatomic, substrate, and technical factors may each contribute to the inability to create transmural lesions at all targeted locations. A means of reliably identifying and treating the sites of future ablation gaps during the initial procedure would be an invaluable tool to improve the long-term efficacy and durability of PVI. A potential breakthrough emerged when 2 groups separately described that adenosine, infused after PVI, could transiently unmask incompletely isolated veins, dubbed dormant reconnection, or re-conduction. Arentz et al.7 found that immediately post-PVI, adenosine exposed transient reconnection in 34% of left and 13% of right superior PVs. Examining all PVs after PVI, Tritto et al.8 similarly found transient (and a small degree of permanent) reconnection with adenosine in 35% of PVs. As with chronically reconnected PVs, Tritto and others studying this phenomenon found that re-isolation