High Density Epicardial Mapping of the Pulmonary Vein–LA Junction in Humans: Insights into Mechanisms of Pulmonary Vein Arrhythmogenesis

Abstract

Introduction: The electrophysiological characteristics of the PV–LA junction was assessed using high-density epicardial mapping. Methods: Seventeen patients undergoing cardiac surgery were studied. A 128-point epicardial plaque was positioned at the RSPV covering three regions: LA, PV–LA Junction (Jn) and RSPV. Isochronal maps were created during: 1. SR, 2. Atrial pacing (AP), 3. Programmed-stimulation (PES) 10 ms above ERP. Conduction slowing/block (CS/CB) was defined by a CV of 10–20 cm s−1 and <10 cm s−1. Results: A region of isochronal crowding representing CS/CB developed in the centre of the plaque at the PV–LA Jn in 84% of maps. Three patterns of activation were seen. Pattern 1 (five patients) Uniform SR activation without CS/CB. AP and PES caused one to two lines of isochronal crowding (CS/CB) at the PV–LA Jn. Pattern 2 (three patients) CS/CB occurred at the PV–LA Jn in SR. Atrial pacing and PES caused an increase in CS/CB at the PV/LA Jn with widely split double potentials (DP) and fractionated signals (FS). Pattern 3 (nine patients) a single incomplete line of CS at the PV–LA Jn in SR. With AP and PES multiple lines (≥3) of CS/CB developed at the PV–LA Jn with evidence of circuitous activation and a marked increase in DP and FS. FS/DP were present at the PV–LA Jn in 10 ± 11% SR, 21 ± 11% AP and 31 ± 16% PES (p < 0.001). Conclusion: In patients undergoing cardiac surgery, functional conduction delay occurs at the PV–LA junction rather than within the PV muscle sleeve. Atrial pacing and premature stimulation results in decremental conduction and circuitous activation patterns at the PV–LA junction, creating the substrate for re-entry.