Atrial fibrillation (AF) is a very common arrhythmia, which increases in prevalence in patients older than 60 years.1 ,2 Over time, it tends to become persistent or chronic, even if no underlying structural heart disease is present.1 ,2 Evidence that AF promotes AF emerges from the fact that the success rate of electrical cardioversion and the maintenance of sinus rhythm are highly dependent on the duration of the previous AF episode.3 ,4 A possible explanation for these epidemiological and clinical observations, apart from the progressive change caused by underlying cardiovascular disease, is the concept of electrical remodelling of the atria: AF itself causes progressive electrophysiological and structural changes to the atria, which promote the initiation or perpetuation of AF.5

The phenomenon of “AF begetting more AF” was first described in a goat model. Atrial electrical remodelling induced by AF seemed to develop quickly, to be progressive, and to be completely reversible within one week after restoration of sinus rhythm.5 To date, many reports have confirmed the presence of atrial electrical remodelling after short and long term AF or rapid atrial pacing in animal models.6-12 In humans, the time course of appearance and reversal of atrial electrical remodelling resembles that seen in goats and dogs.13-21

The mechanism behind this phenomenon has not yet been clarified. There are some indications that intracellular calcium overload plays an important role. In both animal and human models, verapamil administered during rapid atrial pacing or short episodes of artificially induced AF reduces atrial electrical remodelling.7 ,9 ,12 ,14 ,16 By contrast, pretreatment with verapamil results in a shortening of refractory periods in humans and animals with long lasting AF.11 ,18 ,22 ,23 Only two studies have found …