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Arch Mal Coeur Vaiss. 2005 Apr;98(4):308-12.

[Remodelling in atrial fibrillation].

[Article in French]

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Service de cardiologie, hôpital Nord, 13015 Marseille.


It is well known that atrial fibrillation (AF) tends to become permanent with time as illustrated by the fact that it becomes more difficult to maintain sinus rhythm when AF has been present for a long time. Atrial remodelling plays a part in this process and has been studied in experimental models. Atrial remodelling is defined as all the phenomena occurring during AF contributing to its maintenance. The persistence of AF induced by stimulation in the animal depends on the duration and the repetition of the atrial stimulation and it would appear that "AF induces AF". The tendency for AF to persist is associated with a shortening of the effective atrial refractory period with loss of its adaptation to the heart rate. The determining factor of both electrical and structural remodelling is the rapidity of the atrial rhythm of the AF itself. These phenomena lead to a type L calcium cellular overload as shown by its prevention or attenuation by the administration of verapamil, a calcium antagonist. Electrical remodelling is accompanied by a structural remodelling in the experimental model of persistent AF over several weeks. Samples from the two atria examined by electronic microscopy show mitochondrial changes, an accumulation of glycogen, a deficit in myofibrils, a redistribution of the nuclear chromatim and a reduction of sarcoplasmic reticulum with changes in protein structure. This structural remodelling is a reaction of adaptation similar to that observed in hibernating myocardium during ischaemia and aims to prolong cellular viability by decreasing atrial contractility. Another aspect of structural remodelling is the activation of fibroblasts with formation of fibrosis with resulting heterogeneity of the conduction tissue. There is also an increase in converting enzyme and angiotensin II concentrations. Irbesartan, an angiotensin II antagonist, reduced fibroblast growth. This has clinical applications as shown by the reduction in the recurrences of AF after cardioversion when given in association with amiodarone. Persistent AF leads to left atrial dilatation with abnormal atrial contractility. Further studies are necessary to determine the effect of atrial remodelling which might also act on the foci responsible for inducing the AF. Better understanding of atrial remodelling will contribute to the use of new pharmacological agents to prevent AF.

[Indexed for MEDLINE]

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