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Mechanisms of atrial fibrillation
  1. Rohan S Wijesurendra,
  2. Barbara Casadei
  1. Division of Cardiovascular Medicine, University of Oxford, Oxford, UK
  1. Correspondence to Dr Rohan S Wijesurendra, Division of Cardiovascular Medicine, University of Oxford, Oxford, UK; rohan.wijesurendra{at}cardiov.ox.ac.uk; Professor Barbara Casadei, Division of Cardiovascular Medicine, University of Oxford, Oxford, UK; barbara.casadei{at}cardiov.ox.ac.uk

Abstract

Atrial fibrillation (AF) is the most common sustained arrhythmia, currently affecting over 33 million individuals worldwide, and its prevalence is expected to more than double over the next 40 years. AF is associated with a twofold increase in premature mortality, and important major adverse cardiovascular events such as heart failure, severe stroke and myocardial infarction. Significant effort has been made over a number of years to define the underlying cellular, molecular and electrophysiological changes that predispose to the induction and maintenance of AF in patients. Progress has been limited by the realisation that AF is a complex arrhythmia that can be the end result of various different pathophysiological processes, with significant heterogeneity between individual patients (and between species). In this focused Review article, we aim to succinctly summarise for the non-specialist the current state of knowledge regarding the mechanisms of AF. We address all aspects of pathophysiology, including the basic electrophysiological and structural changes within the left atrium, the genetics of AF and the links to comorbidities and wider systemic and metabolic perturbations that may be upstream contributors to development of AF. Finally, we outline the translational implications for current and future rhythm control strategies in patients with AF.

  • atrial fibrillation
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Footnotes

  • Contributors RSW drafted the article. BC revised the article critically for important intellectual content. Both authors approved the final version.

  • Funding The authors' research is supported/funded by the British Heart Foundation, the British Heart Foundation Centre of Research Excellence, Oxford, the European Union's Horizon 2020 Research and Innovation Programme, and the NIHR Oxford Biomedical Research Centre.

  • Competing interests RSW has received a speaker fee/honorarium and travel assistance from Biosense Webster and Bayer, and meeting sponsorship/travel assistance from Boston Scientific, Abbott and Sanofi.

  • Patient consent for publication Not required.

  • Provenance and peer review Commissioned; externally peer reviewed.

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