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Genomic basis of atrial fibrillation
  1. Aneesh Bapat1,
  2. Christopher D Anderson2,3,
  3. Patrick T Ellinor4,5,
  4. Steven A Lubitz4,5
  1. 1Cardiology Division, Brigham and Women’s Hospital, Boston, Massachusetts, USA
  2. 2Department of Neurology, J. Philip Kistler Stroke Research Center, Massachusetts General Hospital, Boston, Massachusetts, USA
  3. 3Center for Genomic Medicine, Massachusetts General Hospital, Boston, Massachusetts, USA
  4. 4Cardiac Arrhythmia Service and Cardiovascular Research Center, Massachusetts General Hospital, Boston, Massachusetts, USA
  5. 5Program in Medical and Population Genetics, Broad Institute, Cambridge, Massachusetts, USA
  1. Correspondence to Dr   Steven A Lubitz, Massachusetts General Hospital, 55 Fruit Street, GRB 109, Boston, MA 02114, USA; slubitz{at}mgh.harvard.edu

Abstract

Atrial fibrillation (AF) is a prevalent arrhythmia associated with substantial morbidity, mortality and costs. Available management strategies generally have limited efficacy and are associated with potential adverse effects. In part, the limited efficacy of approaches to managing AF reflect an incomplete understanding of the biological mechanisms underlying the arrhythmia, and only a partial understanding of how best to individualise management. Over the last several decades, a greater understanding of genome biology has led to recognition of a widespread genetic susceptibility to AF. Through genome-wide association studies, at least 30 genetic loci have been identified in association with AF, most of which implicate mechanisms not previously appreciated to be involved in the development of AF. We now recognise that AF is a polygenic condition, yet a great deal of work lies ahead to better understand the precise mechanisms by which genomic variation causes AF. Understanding the genetic basis of AF could provide a better understanding of AF mechanisms and cardiovascular biology, inform the management of patients through risk-guided approaches and facilitate the development of novel therapeutics.

  • Atrial Fibrillation
  • Atrial Flutter
  • Genetics
  • Genome Wide Association Studies (gwas)
  • Cardiac Risk Factors And Prevention

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Footnotes

  • Contributors AB and SAL conceived of the manuscript. AB drafted the manuscript. CDA, PTE and SAL critically reviewed and revised the manuscript.

  • Competing interests SAL receives sponsored research support from Bayer HealthCare, Biotronik and Boehringer Ingelheim, and has consulted for St. Jude Medical and Quest Diagnostics. PTE is the PI on a grant from Bayer HealthCare to the Broad Institute focused on the genetics and therapeutics of atrial fibrillation.

  • Provenance and peer review Commissioned; externally peer reviewed.

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