Ablative pulmonary vein isolation (PVI) is ineffective in atrial fibrillation (AF) prevention in 40% of AF patients. The role of the atrial-pulmonary vein (A-PV) junction in arrhythmogenesis is poorly understood since incomplete PVI can be curative. We aimed to test the hypothesis that the A-PV junction constitutes a structural and functional arrhythmogenic substrate.
To evaluate electrophysiology in-vivo and morphology of the A-PV junction.
We performed percutaneous endocardial electrophysiological studies and histological preparations of the right pulmonary vein (PV) in healthy sheep.
The proximal PV wall contained more myocytes than distal PV and a higher percentage of collagen and fat tissue than both distal PV and left atrial walls. Local fractionated electrograms occurred in both distal and proximal PV, however a large local activation in the unipolar electrograms (>0.75mV) was more often present in the proximal than distal PV (86% vs. 50% of electrograms, respectively, p=0.017). While proximal PV premature stimulation caused atrial arrhythmias in 10/14 sheep (1-147 premature atrial complexes (PACs) per run), distal PV premature stimulation was less arrhythmogenic (1-6 PACs per run in 2/14 sheep, p=0.004 vs. proximal). The refractory period was shorter in the proximal than distal PV (170±50 (mean±SD) vs. 244±57ms, p<0.001). The diastolic stimulation threshold was higher in proximal than distal PV (0.8±0.3 vs. 0.4±0.2mA, p=0.004).
Atrial arrhythmias were induced by premature stimulation in the proximal PV but not in the distal PV. The structural and functional properties of the A-PV junction differ from those of the distal PV and favor re-entrant arrhythmias. Ablative therapy guided by electrogram morphology should focus on this substrate.
© 2021 Published by Elsevier Inc.