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In the last 5 years, we have gained an increasing appreciation for the genetic contribution to atrial fibrillation (AF). While Mendelian families with AF have been reported, they have typically been considered rare. Studies from Framingham1 and Iceland2 have demonstrated a genetic basis for AF in the general population. Family members of those with AF have an odds ratios of ∼1.8 for developing the arrhythmia. This risk is considerably greater for younger patients1,2 and those with lone AF.3One approach to identify common genetic determinants of a disease in a population is to perform an association study between a single nucleotide polymorphism (SNP) and the condition of interest. Such a study can be performed using one to many hundreds of thousands of SNPs across the genome. In the case of AF, numerous prior associations have been reported between AF and variants in the cardiac sodium and potassium channels, gap junction proteins, and inflammatory markers, among others. However, the studies to date have generally been underpowered, have not been replicated, and have a low pre-test probability of the SNP actually causing AF.Sinner et al. have described the relationship between the K897T SNP in KCNH2 /HERG and AF in >1200 affected individuals and 2400 controls.4 Based on the well-known relationship between variation in KCNH2 /HERG and ventricular repolarization, the authors hypothesized that this gene may also be … *Corresponding author. Tel: +1 617 726 4959, Fax: +1 617 726 2155. Email: pellinor{at}partners.org

Polymorphisms and atrial fibrillation: sorting the wheat from the chaff