Vorhofflimmern: Molekularbiologische Grundlagen

Translated title of the contribution: Atrial fibrillation: molecular biology bases

Wilhelm Haverkamp, Richard Ammer, Paulus Kirchhof, Lars Eckardt, Larissa Fabritz, Günter Breithardt

Research output: Contribution to journalArticlepeer-review

1 Citation (Scopus)

Abstract

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.

Translated title of the contributionAtrial fibrillation: molecular biology bases
Original languageGerman
Pages (from-to)301-5
Number of pages5
JournalHerz
Volume27
Issue number4
DOIs
Publication statusPublished - Jun 2002

Keywords

  • Atrial Fibrillation
  • Chromosome Mapping
  • Chromosomes, Human, Pair 10
  • Connexins
  • Electrocardiography
  • Genes, Dominant
  • Genetic Predisposition to Disease
  • Humans
  • Ion Channels

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