Abstract Funding Acknowledgements Type of funding sources: None. Background The ongoing challenge is to generate meaningful data during electrophysiological (EP) studies, integrating the knowledge on atrial fibrillation (AF) progression gained by the EP community in the latest years. At the present time there is a lack of EP protocols: most of the centers perform electroanatomical (EA) ablation to isolate pulmonary veins or, in persistent AF forms, some centers propose the performance of additional lines for atrial compartmentalization. However, none of these approaches take in consideration neither the wavefront propagation nor the analysis of functional phenomena. Purpose To investigate whether zones of delayed conduction (slow conduction, SC) or functional propagation (pivot sites, PS) may play a role in terms of maintenance of paroxysmal (PAF) and persistent (PsAF) AF. Methods Twenty-seven consecutive patients with PAF (14 patients) and PsAF (13 patients) have been enrolled in this study. For each patient, a sinus rhythm activation map and a paced map have been created with a multipolar catheter exploiting the parallel mapping feature. According to these activation maps, we analyzed the wavefront propagation. Abnormal conduction was defined as a delimited zone in which the propagation became suddenly slower (<0.5 m/s, slow conduction corridors) or changed in direction (>90°, pivot sites). At each of these sites, EGMs were collected and analysed in terms of amplitude (mV), location and fractionation. Results In sinus rhythm maps, a total number of 65 pivot sites and slow conduction corridors was identified. In the PAF group 22 PS and SC were found (1,6/pt), whereas those included in the PsAF one showed a significantly higher number: 43 (3,3/pt). The bipolar voltage value reported at abnormal conduction areas amounted to 1,95 ± 0,93 mV and 1,78 ± 0,54 mV for PAF and PsAF patients, respectively, showing a lower value with respect to healthy tissue areas (2,94 ± 4,81 mV). More than four deflections per signal were identified in 57/65 PS and SC zones. In PsAF cases, these areas were mainly found on the posterior wall. A concordance with esophagus location occurred in the 89%. In paced maps, instead, we documented an average value of 38 PS and SC zones (1,5/pt), of which 27 in persistent patients. As for bipolar values, a lower voltage value was reported in PS and SC zones (1,91 ± 0,69 mV for PAF and 1,52 ± 0,36 mV for PsAF) with respect to normal conductive tissue. Fractionation of EGMs was confirmed in almost all cases. Conclusion The main findings of this analysis are: (i) in PsAF patients the number of pivot sites is higher with respect to PAF cases; (ii) In PsAF patients, abnormal conduction phenomena are predominantly localized on the posterior wall, with a strong correlation with esophagus location; (iii) slow conduction zones and pivot sites are characterized by lower voltage amplitude and higher fractionation with respect to normal conduction areas.