The correct answer is: B. Isoproterenol infusion up to 20 mcg/min.

At baseline, all four pulmonary veins (PVs) demonstrated entrance block during sinus rhythm (Figure 1), but exit block had not yet been established. We were unable to observe any spontaneous pulmonary vein firings which would allow us to ascertain the presence of exit block. With isoproterenol infusion to 20 mcg/min, fibrillation originating from the RSPV triggered atrial fibrillation due to the absence of exit block from the vein (Figure 2A). Catheter contact alone resulted in exit block with subsequent termination of AF (Figure 2A). Ablation at a site inferior to the ostium of the RSPV near the anterior carina terminated fibrillation within the RSPV (figure 2B and C). Following ablation, AF resumed within the RSPV, but exit block prevented conduction to the atrium (Figure 3).

Pulmonary vein isolation has been shown to be effective therapy for paroxysmal fibrillation.^(1,2) However, clinical recurrence of AF following ablation is often due to reconnection of previously isolated PVs,^(3,4) and a repeat ablation procedure targeting the reconnected PVs has been shown to improve clinical outcomes.⁽⁴⁾ Since this patient experienced recurrent paroxysms of AF, the likely trigger would be a reconnected PV, and, in this setting, empiric linear ablation and/or CFAE ablation would not be expected to improve the clinical outcome.

Dormant conduction between PVs and the left atrium following ablation predicts recurrence of AF following ablation5. Pharmacologic testing maneuvers with adenosine, isoproterenol, and adenosine + isoproterenol have been used to provoke acute PV-atrial reconnection immediately after ablation.^(5,6,7) Adenosine has shown better efficacy than isoproterenol in unmasking dormant conduction attributed to its superior ability to induce cellular hyperpolarization. Dormant conduction in the acute setting following ablation is attributed to a partially depolarized resting membrane potential with consequent loss of excitability in damaged but not yet dead atrial myocytes.⁽⁸⁾ Following ablation, dormant conduction is typically assessed by demonstration of entrance block (LA to PV) after provocative pharmacologic testing.

In our case, unidirectional conduction block (LA to PV) was present in the RSPV but not immediately discernible with lasso placement in the ostium of the vein during sinus rhythm. Pacing from the lasso catheter positioned within the ostium of the PV could also unmask PV to LA conduction, though capture within the PV is not always reliable. We did not observe spontaneous isolated PV firings in any of the PVs. To demonstrate exit block, pharmacologic testing was necessary to trigger PV firing. In patients with recurrent AF following PVI, isoproterenol infusion up to 20 mcg/min has demonstrated that the majority of AF triggers (54%) originate in previously targeted PVs.⁽⁹⁾ Since many months had elapsed since the initial PVI procedure, dormant conduction would neither have been operative nor have been expected to produce unidirectional conduction block. Therefore, testing with adenosine would not be useful in this case.

Confirmation of bidirectional block of the PV-LA junction has been shown to reduce PV reconnection in the acute setting immediately after ablation.⁽¹⁰⁾ Confirmation of bidirectional block would be expected to improve long term clinical outcomes following PV isolation.

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