P984Proof of endo-epicardial asynchrony of the left atrial wall in humans

Abstract

Abstract Funding Acknowledgements Prof. Dr. NMS de Groot is supported by funding grants from CVON-AFFIP (914728), NWO-Vidi (91717339), Biosense Webster USA (ICD 783454) and Medical Del Introduction Treatment of atrial fibrillation (AF) is still suboptimal as mechanisms underlying AF initiation and persistence are incompletely understood. Endo-Epicardial asynchrony (EEA) plays an important role in AF persistence and has so far only been demonstrated in the right atrium (RA). Purpose To investigate whether EEA also exists in the thin walled left atrium (LA) and to measure the maximal degree of EEA between the endo- and epicardial layers during sinus rhythm (SR). Methods Simultaneous endo-epicardial mapping of the LA was performed during SR in 3 male patients (73 ± 1.5 years) with history of paroxysmal AF undergoing cardiac surgery including rhythm surgery and LA appendage amputation. Simultaneous endo-epicardial mapping was performed with a mapping clamp containing two electrode arrays of 8x16 electrodes (diameters: 0.4mm, interelectrode distance: 2mm) positioned exactly opposite to each other. The mapping clamp was introduced through the LA appendage with its tip towards the superior pulmonary vein. Local endo-epicardial activation time differences were determined by selecting the median time delay within the exact opposite electrode and its 8 surrounding electrodes. The asynchrony map consisted of the maximum of 2 medians from direct opposite electrodes. EEA was defined as time differences ≥15ms. Conduction delay (CD) and conduction block (CB) were defined as differences in local activation times between neighboring electrodes of respectively ≥7 and ≥12ms. Results A total of 35 SR beats were analyzed. Mean total activation time of the whole endo-epicardial LA tissue was 42.4 ± 9.5ms and did not differ between both layers (epicardium: 31.2 ± 9.9ms; endocardium: 37.8 ± 10.3ms; P= 0.62). CD and CB were observed in respectively 3.2% and 6.3% at the epicardium and 3.3% and 3.0% at the endocardium. The lowest amount of CD (5.2%) and CB (0.3%) was observed in the patient who had his first AF episode only 11 days prior to surgery. Also, no EEA was present in this patient. In two patients with paroxysmal AF >6 months, the prevalence of EEA was respectively 2.7% and 41.4% and the degree of EEA ranged from 15 to 44ms. Interestingly, the patient with the highest degree of EEA was diagnosed with paroxysmal AF for almost 5 years (Figure 1). Conclusion Our data provides evidence for the existence of EEA in the human left atrium which appears to be already present during SR. Knowledge of EEA and the ability to stage AF based on the degree of EEA is essential for individualized and staged future therapy for AF. Abstract Figure 1. The maximal degree of endo-epi