Endocardial-epicardial dissociation (EED) and focal breakthroughs in humans with atrial fibrillation (AF) have been recently demonstrated using activation mapping of short 10-second AF segments. In the current study we used simultaneous endo-epi phase mapping to characterise endo-epi activation patterns on long segments of human persistent AF (PeAF).
Simultaneous intra-operative mapping of endo- and epicardial lateral RA wall was performed in patients with PeAF using two high-density grid catheters (16 electrodes, 3mm spacing). Filtered unipolar and bipolar electrograms (EGM’s) of continuous 2-min AF recordings and electrodes locations were exported for phase analyses. We defined EED as phase difference of ≥20ms between paired endo-epi electrodes. Wavefronts (WF) were classified as rotations, single WF (SWF), focal waves or disorganised activity as per standard criteria. Endo-Epi WF patterns were simultaneously compared on dynamic phase maps. Complex fractionated EGM’s were defined as bipolar EGM’s with ≥5 directional changes occupying at least 70% of sample duration.
Fourteen patients with PeAF undergoing cardiac surgery were included. EED was seen in 50.3% of phase maps with significant temporal heterogeneity. Disorganised activity (Endo:41.3% vs Epi:46.8%, p=0.0194) and SWF (Endo:31.3% vs Epi:28.1%, p=0.129) were the dominant patterns. Transient rotations (Endo:22% vs Epi:19.2%, p=0.169; mean duration: 590±140ms) and non-sustained focal waves (Endo:1.2% vs Epi:1.6%, p=0.669) were also observed. Apparent transmural migration of rotational activations (n=6) from the epi- to the endocardium was seen in 2 patients. EGM fractionation was significantly higher in the epicardium than endocardium (61.2% vs 51.6%, p<0.0001).
Simultaneous endo-epi phase mapping of prolonged human PeAF recordings shows significant EED marked temporal heterogeneity, discordant and transitioning WF patterns and complex fractionations. No sustained focal activity was observed. Such complex 3D-interactions provide insight into why endocardial mapping alone may not fully characterise the AF mechanism and why endocardial ablation may not be sufficient.