Pulmonary vein reentry--properties and size matter: insights from a computational analysis.

BACKGROUND

Pulmonary vein (PV) ablation plays an important role in atrial fibrillation (AF) therapy but suffers from a limited mechanistic understanding of PV arrhythmogenicity. Rapid focal activation has been suggested, but some evidence points to underlying reentry.

OBJECTIVE

This study was performed to evaluate how the electrophysiological properties of PVs may make them a site for reentry and to analyze specifically the roles of PV dimensions and coupling properties.

METHODS

A computer model designed to efficiently reproduce electrophysiological behaviors was fit to action potentials from canine left atria (LA) and PVs. To assess structural and functional arrhythmogenic determinants, an idealized PV of varying length and circumference was attached to LA tissue, and 5 seconds of activity after extrastimulation were simulated.

RESULTS

PV reentrant activity depended critically on vein size and coupling properties. With cumulative removal of transverse and longitudinal connections, sustained (n=23) or nonsustained (n=93) reentries could be observed (687 simulations) for veins 1-3 cm long and 1-2 cm in circumference. The prevalence of sustained reentry increased with PV length (8% for 1 cm vs. 22% and 31% for 2 and 3 cm, respectively; P<.05 for each). The PV circumference did not affect the incidence of sustained reentry (25%, 17%, and 21% for 1-, 1.5-, and 2-cm circumferences; P=NS), but the number of reentrant events increased from 12/201 simulations for PVs with a 1-cm circumference to 48/232 and 56/254 events for PVs with 1.5- and 2-cm circumferences, respectively (P<.05). Sustained reentry cycle lengths were approximately 200-250 ms (16/23), except for the longest PVs.

CONCLUSION

Reentry occurs readily in PVs with realistic properties in the context of specific connection heterogeneities. Reentry properties and incidence depend on PV anisotropy and dimensions but could certainly contribute significantly to PV arrhythmogenesis.