Over the past decade, compelling evidence has emerged from population-based studies to suggest that AF is a heritable disease. More recently, we have begun to elucidate the genetic substrate underlying AF. Genome-wide association studies (GWAS) have led to the identification of multiple risk loci that confer increased susceptibility to the arrhythmia. These loci harbor intriguing candidate genes including those encoding ion channels, transcription factors, and signaling molecules. Current efforts are ongoing to functionally validate the role of these genes in disease pathogenesis. In the future, novel genotyping technologies such as exome sequencing and whole-genome sequencing promise to uncover a greater proportion of the heritability underlying AF. In this article we review recent advances in AF genetics research and discuss future developments in the field.
© 2012 Wiley Periodicals, Inc.