[Electrophysiological remodeling induced by atrial fibrillation. An experimental curiosity or major factor in atrial fibrillation in man?].
Atrial fibrillation usually progresses from a paroxysmal to a permanent arrhythmia, even in the absence of underlying cardiac disease. The treatment is more difficult when the arrhythmia is chronic. This progression may be explained by the aggravation of underlying cardiac disease with time. Another explanation is that the arrhythmia induces functional and structural changes of the atrial tissues (remodelling) which promote the perpetuation of the arrhythmia and which make treatment less effective. Although the electrophysiological changes predisposing to atrial fibrillation have been known for over 15 years, it was only in 1995 that experimental studies showed the presence of atrial electrophysiological remodelling induced by the arrhythmia. This process of long term adaptation of the atrial myocytes to the tachycardia comprises marked changes of the parameters which sustain the arrhythmia: changes in refractory period (decreased duration, inadaptation to the heart rate, increased dispersion), reduced conduction speed and sinus dysfunction. Atrial remodelling also affects the contractile function by the structural changes. The calcium currents play a major role in its development. This mechanism has not yet been completely defined in the clinical setting and its importance in sustaining the arrhythmia has not been clearly evaluated. Atrial fibrillation remains one of the most difficult arrhythmias to treat. A better understanding of cellular mechanisms of remodelling could open up new therapeutic approaches to limit the natural history of the arrhythmia with progression to chronicity and structural changes responsible for the degradation of atrial contractility.
Piot
O
O
Service de cardiologie A, hôpital Broussais, Paris.
Paziaud
O
O
Digeos
S
S
Copie
X
X
Lavergne
T
T
Guize
L
L
Le Heuzey
J Y
JY
D001281:Atrial Fibrillation / Q000150:complications* / Q000473:pathology; D018450:Disease Progression; D006325:Heart Atria / Q000473:pathology*; D006339:Heart Rate; D006801:Humans; D009200:Myocardial Contraction; D020257:Ventricular Remodeling