Alterations of atrial Ca2+ handling as cause and consequence of atrial fibrillation

Maura Greiser, W. Jonathan Lederer, Ulrich Schotten*

*Corresponding author for this work

Research output: Contribution to journalArticleAcademicpeer-review

54 Citations (Web of Science)

Abstract

Atrial fibrillation (AF) is the most prevalent sustained arrhythmia. As the most important risk factor for embolic stroke, AF is associated with a high morbidity and mortality. Despite decades of research, successful (pharmacological and interventional) 'ablation' of the arrhythmia remains challenging. AF is characterized by a diverse aetiology, including heart failure, hypertension, and valvular disease. Based on this understanding, new treatment strategies that are specifically tailored to the underlying pathophysiology of a certain 'type' of AF are being developed. One important aspect of AF pathophysiology is altered intracellular Ca2+ handling. Due to the increase in the atrial activation rate and the subsequent initial [Ca2+](i) overload, AF induces 'remodelling' of intracellular Ca2+ handling. Current research focuses on unravelling the contribution of altered intracellular Ca2+ handling to different types of AF. More specifically, changes in intracellular Ca2+ homeostasis preceding the onset of AF, in conditions which predispose to AF (e.g. heart failure), appear to be different from changes in Ca2+ handling developing after the onset of AF. Here we review and critique altered intracellular Ca2+ handling and its contribution to three specific aspects of AF pathophysiology, (i) excitation-transcription coupling and Ca2+- dependent signalling pathways, (ii) atrial contractile dysfunction, and (iii) arrhythmogenicity.
Original languageEnglish
Pages (from-to)722-733
JournalCardiovascular Research
Volume89
Issue number4
DOIs
Publication statusPublished - Mar 2011

Keywords

  • Atrial fibrillation
  • Calcium handling
  • Contractile remodelling arrhythmogenesis
  • Excitation-transcription coupling

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