Just came across an interesting article with the hypothesis that sustained high heart rate may rewire the heart to cause AF.
heart.bmj.com/content/80/6/...
Atrial fibrillation in the structurally normal human heart: a hypothesis
All the recent clinical and laboratory findings combine to provide a compelling, if somewhat challenging, hypothesis for the initiation and perpetuation of atrial fibrillation in the structurally normal heart, which, if proved, may provide a possible framework for understanding and managing this arrhythmia. That is, atrial fibrillation triggered by an atrial tachyarrhythmia, which may initially be focal, induces atrial remodelling in susceptible individuals leading to a perpetuation of the tendency to fibrillation.3 The reason some patients experience paroxysmal atrial fibrillation and others rapidly progress to having chronic persistent atrial fibrillation may relate to the duration and periodicity of the early arrhythmic episodes and the rate of progression and regression of the atrial remodelling during and between arrhythmic episodes.
According to this hypothesis, once atrial fibrillation is established, the apparently random propagation of multiple simultaneous wavelets of reentrant activity within the atrial myocardial mass11 12would mean that any evidence of an underlying focal or regular tachycardia involving the atria might tend to be lost in the advanced fibrillatory activity and remodelling of the atria. However, patterns of right atrial activation in patients with chronic atrial fibrillation have revealed that atrial activation, even in the chronic phase, is not entirely random and may have a repetitive pattern suggesting some organisation of atrial activation in most cases.13Furthermore, in a proportion of patients in whom atrial fibrillation is terminated by the largely experimental procedure of creating multiple lines of conduction block throughout the atria by linear catheter ablation, when fibrillation ceases a persistent focal atrial tachycardia is revealed.14