High-density epicardial mapping of the pulmonary vein–left atrial junction in humans: Insights into mechanisms of pulmonary vein arrhythmogenesis

Background The pulmonary veins (PVs) and the PV–LA (left atrium) junction are established sources of triggers initiating atrial fibrillation. In addition, they have been implicated in the maintenance of arrhythmia. Objective To undertake high-density electrophysiological characterization of the right superior PV–LA junction in humans. Methods Mapping was performed in 18 patients without a history of atrial fibrillation undergoing cardiac surgery. A high-density epicardial plaque was positioned at the anterior right superior pulmonary vein covering 3 regions: LA, PV–LA junction, and the PV. Isochronal maps were created during (1) sinus rhythm (SR); (2) LA pacing (LA-Pace); (3) PV pacing (PV-Pace); (4) LA programmed electrical stimulation (LA-PES); and (5) PV programmed electrical stimulation (PV-PES). Regional differences in conduction slowing/conduction block (CS/CB) and the prevalence of fractionated signals (FS) and double potentials (DPs) were assessed. Results A region of isochronal crowding representing CS/CB developed at the PV–LA junction in 84% of the maps. Three distinct activation patterns were seen. Pattern 1: Uniform SR activation without CS/CB. LA-Pace and PES caused 1 to 2 lines of isochronal crowding (CS/CB) at the PV–LA junction. Pattern 2: CS/CB occurred at the PV–LA junction in SR. LA/PV-Pace and LA/PV-PES caused an increase in CS/CB at the PV–LA junction with widely split DPs and FS. Pattern 3: A single incomplete line of CS at the PV–LA junction in SR. With LA/PV pacing and LA/PV-PES, multiple lines (≥3) of CS/CB developed at the PV–LA junction with evidence of circuitous activation and a marked increase in DPs and FS. Conclusion High-density epicardial mapping of the right superior pulmonary vein demonstrates marked functional conduction delay and circuitous activation patterns at the PV–LA junction, creating the substrate for reentry.