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[Atrial fibrillation: molecular biology bases]
Wilhelm Haverkamp1, Richard Ammer, Paulus Kirchhof
1Medizinische Klinik, Poliklinik C (Kardiologie und Angiologie), Universitätsklinikum Münster, Institut für Arterioskleroseforschung, Westfälischen Wilhelms-Universität Münster. w.haverkamp@uni-muenster.de
Background:
Atrial fibrillation is the most frequent form of sustained arrhythmia. In most cases the arrhythmia is acquired, in rarer cases it may occur as a familial disease with a autosomal dominant pattern of inheritance. Recent advances in molecular biology and genetics have had a major impact on our understanding of the mechanisms responsible for the initiation, maintenance and chronification of the arrhythmia. Recently, the chromosomal locus for familial atrial fibrillation has been mapped to chromosome 10q22-q23, however, so far the causative gene has not been identified.
Atrial Remodeling:
Atrial fibrillation itself modifies atrial electrical properties in a way that promotes the occurrence and maintenance of the arrhythmia, in other words "atrial fibrillation begets atrial fibrillation". The principle stimulus for atrial remodeling is the rapid atrial rate.
Perspectives:
It is hoped that the results of future studies will not only further improve our understanding of the mechanisms underlying atrial fibrillation but may also help to develop new therapeutic strategies.