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Despite extensive research, it is still not clear how atrial fibrillation (AF) perpetuates itself. Experimental studies have shown that various mechanisms may sustain this ‘eternal’ arrhythmia (Lewis et al. 1921; Moe Moe, 1962; Allessie et al. 1977, 1985; Konings et al. 1994; Mandapati et al. 2000; Jalife et al. 2002; Waldo, 2003). Roughly, they can be divided into focal (repetitive ectopic discharges) and reentrant mechanisms (mother-wave, rotor, multiple wavelets). Recently, we introduced a third mechanism, independent of focal or reentrant activity (the double layer hypothesis; Allessie et al. 2010; de Groot et al. 2010; Eckstein et al. 2011). Using high-resolution optical mapping in isolated sheep hearts subjected to high concentrations of acetylcholine, Jalife and co-workers clearly demonstrated that pacing-induced AF was due to the presence of a very rapid rotor (15–20 Hz) in the left atrium (Mandapati et al. 2000; Jalife et al. 2002). However, although it is unquestionable that under experimental conditions a single rapid rotor can serve as a ‘driver’ of AF, the question still remains whether this is also the operative mechanism in patients with longlasting persistent AF. Based on a series of clinical studies, in which the electrical activity of the atria was mapped by two basket catheters, Narayan et al. (2012a,b,c, 2013) postulated that human AF is due to the presence of a stable rotor that serves as a ‘driver’ to sustain AF. Ablation of the centre of these rotors abruptly terminated or consistently slowed AF in the vast majority of cases, and substantially improved long-term freedom from AF compared to conventional ablation alone (Narayan et al. 2012b). High resolution mapping of AF has been performed in patients during open-chest surgery, by positioning a regular array of 128–256 electrodes (spatial resolution 10 min (equating to thousands of cycles)’ (Narayan et al. 2012b), in none of their studies do they actually show that the maps were reproducible over a prolonged period of time. Given the large size of the rotors (in the latest two examples they occupied the whole posterior or anterior wall of the left atrium; Narayan et al. 2013), even in the case of some spatial precession, one would expect predominantly regular and monomorphic electrograms in the area of stable repetitive circular activation. However all recordings from the rotor area presented in the publications of Narayan et al. are highly irregular and polymorphic (Narayan et al. 2012a,b,c, 2013). Only a few electrograms are given to support the presence of a rotor and in no case were local activation times assigned to them. Many electrograms are of poor quality and represent either far-field or injury potentials (Fig. 1 of Narayan et al. 2012b). In the most recent publication, only two or three bipolar electrograms at the rotor path were given (Narayan et al. 2013). Magnification of these electrograms reveals that the two electrograms recorded from opposite limbs of a rotor in the anterior wall of the left atrium (LA) (their Fig. 2; A54 and H65) were not in anti-phase, whereas the three electrograms along a rotor in the posterior LA (their Fig. 3; D45, F45 and E12) did not bear any fixed time relationships. Thus, in none of the maps of the publications of Narayan et al. (2012a,b,c, 2013) are the pathways of repetitive circular activation documented by a sufficient number of electrograms recorded around the rotor path. In the absence of convincing evidence that human AF is driven by a single rotor, it is puzzling how we should interpret the CONFIRM study, in which ‘rotor ablation’ almost doubled the long-term success rate of AF-ablation (Narayan et al. 2012b). In itself, this observation does not prove that human AF is driven by a single rapid source, and the reported clinical success needs to be confirmed by other centres, especially in patients with longstanding persistent AF. It also remains to be seen to what extent body surface mapping might improve the long-term efficacy of AF-ablation (Haissaguerre et al. 2013). At present, the mechanisms responsible for perpetuation of human AF remain unclear. Low-resolution mapping studies claiming that a stable rotor is the main ‘driving force’ behind AF need to be validated by high-resolution mapping. On the other hand, the hypothesis that the substrate of AF is primarily based on endo-epicardial dissociation requires additional proof by simultaneous endo-epicardial mapping in patients with AF. Understanding the mechanisms operative in the perpetuation of human AF is essential for the development of more effective strategies to modify the substrate of AF in order to restore and maintain sinus rhythm (Allessie 592/15/3167 Natasja M. S. de Groot was trained as cardiologist-electrophysiologist at the Leiden University Medical Center and Cardiovascular Research Institute in Maastricht. She received her PhD from Leiden University on the basis of a dissertation entitled ‘Mapping and ablation of atrial tachyarrhythmias; from signal to substrate’. Currently, she works as an associate professor at the Erasmus Medical Center and she is head of the Translational Electrophysiology Research Unit. Her research focuses on mapping studies of atrial fibrillation, the mechanism of post-operative atrial fibrillation, dysrhythmias in patients with congenital heart disease and the development of electro-anatomical mapping techniques. Please note: The publisher is not responsible for the content or functionality of any supporting information supplied by the authors. Any queries (other than missing content) should be directed to the corresponding author for the article. None declared.
Allessie et al. (Fri,) studied this question.