Background
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.
Objective
To evaluate electrophysiology in-vivo and morphology of the A-PV junction.
Methods
We performed percutaneous endocardial electrophysiological studies and histological preparations of the right pulmonary vein (PV) in healthy sheep.
Results
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).
Conclusion
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.
Article info
Identification
Copyright
© 2021 Published by Elsevier Inc.
