Of all known arrhythmia's, atrial fibrillation (AF) is the most often met i
n the clinical setting and it is associated with an increase in mortality r
isk. Several risk factors for AF have been described and several mechanisms
of induction and maintenance have been proposed. Studies in patients with
AF have shown that structural changes occur in the atria, but the relations
hip between the structural remodelling and the chronicity of the arrhythmia
are not well understood. The changes mainly concern adaptive (dedifferenti
ation of cardiomyocytes) and maladaptive (degeneration of cells with replac
ement fibrosis) features. In order to characterise the time course of the s
tructural remodelling the need for animal models which adequately mimic chr
onic atrial fibrillation in humans is felt essential. In this review, the s
tructural changes that are observed during prolonged sustained AF in patien
ts and animal models, are described. Furthermore, the time course and poten
tial mechanisms of structural remodelling are discussed and methods for elu
cidation of the underlying molecular mechanisms an presented. Cardiovasc Pa
thol 2000;9:17-28 (C) 2000 by Elsevier Science Inc.