CrossTalk opposing view: Rotors have not been demonstrated to be the drivers of atrial fibrillation.

Abstract

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 & Abildskov, 1959; 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,2012b,2012c, 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).