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

Abstract

<h4>Background</h4>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.<h4>Objective</h4>To undertake high-density electrophysiological characterization of the right superior PV-LA junction in humans.<h4>Methods</h4>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.<h4>Results</h4>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.<h4>Conclusion</h4>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.