Abstract
Due to complex 3D human atrial structure, atrial fibrillation (AF) mapping with multielectrode arrays (MEA) mostly represents surface activation. Therefore, MEA may not properly visualize patient specific AF mechanisms, which impairs ablation outcomes. Conversely, near-infrared optical mapping (NIOM) visualizes subsurface intramural activation and can efficiently reveal reentrant drivers responsible for AF maintenance. Delay between surface activation seen by MEA electrograms (EGMs) vs subsurface activation seen by NIOM optical action potentials (OAPs) occurs due to dyssynchrony between myocardium layers, especially during AF. Coronary perfused explanted human atria (n=7) were mapped with NIOM (0.3-0.9mm 2 resolution) and 64-electrode MEA (3mm 2 resolution). Unipolar EGMs were analyzed for the steepest negative deflection. The delay between [-dV/dtmax] of unipolar EGMs and corresponding optical action potentials (OAPs) was compared in 500ms and 300ms pacing and AF. Subsequent structural analysis was done by 9.4T MRI (154-180μm 3 resolution) with gadolinium enhancement and histology. Delay between EGM and OAP local activation times rate-dependently and heterogeneously increased from 6±3 ms and 10±4 ms during 500ms and 300ms pacing to 15±11 ms (with maximum delay 47±18 ms) during pacing induced AF (average cycle length 124±65ms). Large local OAP-EGM delay, seen during AF, correlates with higher fibrosis percentage and fiber twist (p<0.05). NIOM identified reentrant drivers maintaining AF, which were incorrectly visualized as multiple breakthroughs in 68% of MEA maps (n=22). Higher frequency leads to an increased activation discrepancy between EGM and NIOM caused by increased dyssynchrony in regions of higher fibrosis percentage and fiber twist, which may prevent MEA from proper identification of AF drivers in diseased fibrotic human atria. Reannotation of EGM activation based on NIOM may be required for correct AF mechanisms visualization.
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