The atrioventricular (AV) node is the specialized conduction system, which electrically connects the atria and the ventricles. Under critical fast atrial rates, as observed during atrial tachyarrhythmias, the AV node filters atrial beats, producing a variety of abnormal AV conduction rhythms. Among these, Wenckebach rhythms are characterized by a progressive prolongation of the AV conduction time leading to a blocked beat, which repeatedly occurs when the atrial cycle length becomes shorter than the node functional refractory period (1). Despite the significant clinical importance of the phenomenon, the mechanisms and nodal determinants underlying AV nodal Wenckebach periodicity remain elusive (2,3). To investigate the dynamical features of Wenckebach rhythms in humans at spontaneous high atrial rates, we analyzed 29 episodes of spontaneous or pacing-induced atrial flutter (AFL) (4), covering a wide range of high atrial rates (cycle lengths from 145 to 270 ms). Atrial electrograms and ECG signals were recorded in patients during an electrophysiological study after light sedation with diazepam (10 mg i.m.). Wenckebach patterns of n:m order (i.e., repeating cycles of n atrial and m ventricular activations) were identified by application of firing sequence (5) and surrogate data analysis to atrial and ventricular activation series. In order to disclose the role of different nodal properties in the generation of Wenckebach patterns, data analysis was complemented with computer simulations by a difference-equation AV model, including recovery and dual pathway properties. Wenckebach rhythmicity in AFL patients was characterized by: i) the presence of n:m rhythms with decreasing conduction ratios (m/n=0.34±0.12 to 0.23±0.06, p<0.01) at shorter atrial cycle lengths (AA=236.3±32.4 to 172.6±17.8 ms, p<0.01), ii) the ordering of rhythms at changing atrial cycle length according to the Farey sequence, with (n+N):(m+M) rhythms between n:m and N:M rhythms, iii) the appearance of high-order alternating Wenckebach rhythms (type A), such as 6:2, 10:2 and 12:2, associated with large ventricular oscillations (amplitudes of 407.7±150.4 ms) in five episodes. Simulations showed that a single pathway AV model, described by a monotonically decreasing recovery curve, predicted the existence and Farey sequence ordering of different Wenckebach patterns, with the exception of higher-order alternating Wenckebach rhythms (type A). The latter rhythms were, instead, predicted by the dual pathway model and originated from an alternate propagation of the impulse in the two pathways. These results support the idea of an intimate connection between nodal recovery and dual pathway physiology in the generation of AV Wenckebach patterns at high atrial rates in the intact human AV node (2,3).