Abstract

See article by Manios et al. [10] (pages 244–253) in this issue. Mapping of the atrial electrical activation pattern during human Atrial Fibrillation (AF) has provided evidence supporting Moe's hypothesis that AF is based on the continuous propagation of multiple wavelets wandering throughout the atria in the majority of cases [1]. Since the average size of reentry pathways during AF is dependent on atrial wavelength (conduction velocity×refractory period) it is not surprising that different complex atrial activation patterns with different numbers and dimensions of the reentry circuits were found. While long wavelengths are associated with larger and fewer wavefronts, short wavelengths result in a greater number of smaller circuits. A numerical index for quantification of spatial AF organization was proposed and applied to different AF patterns by Botteron and Smith [2]. These authors, by calculating a so-called activation space constant from five bipolar right atrial recordings illustrated that the spatial organisation was smaller in patients with chronic AF, whereas a group of patients with induced AF and no AF history exhibited the highest degree of AF organisation. An intermediate value was observed in patients with paroxysmal AF. From a pathophysiological point of view it can therefore be concluded that AF is not a homogenous arrhythmia. From animal models it is known that atrial effective refractory period (AERP) shortening and the loss of its normal rate adaptation are associated with an increase in AF stability and duration of AF paroxysms leading to the concept that ‘AF begets AF’ [3]. In humans, these findings of this so-called electrical remodeling process were replicated in induced AF [4,5] and confirmed in chronic AF [6,7]. Daoud et al. have … * Tel.: +49-391-671-3203; fax: +49-391-671-3202 andreas.bollmann{at}medizin.uni-magdeburg.de

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