Electrophysiological remodelling induced by atrial fibrillation an experimental curiosity or a major factor in clinical atrial fibrillation.

Atrial fibrillation usually progresses from a paroxysmal to a permanent arr hythmia, even in the absence of underlying cardiac disease. The treatment i s more difficult when the arrhythmia Is chronic. This progression may be ex plained by the aggravation of underlying cardiac disease with time. Another explanation is that the arrhythmia induces functional and structural chang es of the atrial tissues (remodelling) which promote the perpetuation of th e arrhythmia and which make treatment less effective. Although the electrop hysiological changes predisposing to atrial fibrillation have been known fo r over 15 years, it was only in 1995 that experimental studies showed the p resence of atrial electrophysiological remodelling induced by the arrhythmi a. This process of long term adaptation of the atrial myocytes to the tachycar dia comprises marked changes of the parameters which sustain the arrhythmia : changes in refractory period (decreased duration, inadaptation to the he art rate, increased dispersion), reduced conduction speed and sinus dysfunc tion. Atrial remodelling also affects the contractile function by the struc tural changes. The calcium currents play a major role in its development. T his mechanism has not yet been completely defined in the clinical setting a nd its importance in sustaining the arrhythmia has not been clearly evaluat ed. Atrial fibrillation remains one of the most difficult arrhythmias to tr eat. A better understanding of cellular mechanisms of remodelling could open up new therapeutic approaches to limit the natural history of the arrhythmia w ith progression to chronicity and structural changes responsible for the de gradation of atrial contractility.