Abstract

Persistent AF (perAF) may be maintained by reentrant drivers within arrhythmogenic fibrotic substrates. Conventional multielectrode mapping (MEM) and delayed enhancement (DE) magnetic resonance imaging (MRI) are suffering to identify drivers and their substrates and require rigorous validation. Define AF driving mechanism in vivo and ex vivo using near-infrared optical mapping (NIOM) in a perAF canine model and correlate driver locations with fibrosis architecture detected by histology validated 3D DE MRI. Canines (n=5) were imaged via DE MRI prior to perAF (induced by rapid atrial pacing) and after 4 months of self-sustained perAF. Atria were mapped with NIOM and MEM in vivo and ex vivo (Figure). Regional histology sections validated chamber-specific fibrosis thresholds on DE MRI. In all animals, AF was maintained by 2 localized temporally competing reentrant drivers in the left atrium (LA) visualized both in vivo and ex vivo. Ex vivo targeted ablation terminated or converted AF to slower tachycardia. MEM and NIOM showed comparable AF cycle length in vivo and ex vivo with driver regions faster than LA non-drivers and right atria (p<0.05). Histology validated DE MRI showed AF induced heterogeneous biatrial fibrosis upregulation, with higher fibrotic content in driver regions. In canine perAF model, integration of in vivo to ex vivo NIOM, MEM and DE MRI revealed that localized AF reentrant drivers within fibrotic substrates maintain AF. The higher imaging acuity of in vivo NIOM and histology validated DE MRI could allow to define fingerprints of arrhythmogenic fibrotic driver hubs for patient-specific targeted AF ablation.

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