Key result
Genetic factors contribute to the pathogenesis of atrial fibrillation, with 8 loci and 6 genes identified in familial AF, and 3 loci (4q25, 1q21, 16q22) identified in non-familial AF via GWAS.
This review summarizes the genetic underpinnings of familial and non-familial atrial fibrillation, highlighting potential therapeutic gene targets.
Genetic loci in AF warrant no practice change; leaves open validation of therapeutic targets in prospective trials.
Atrial fibrillation (AF) is the most common arrhythmia. Although AF is known to develop during the course of various cardiac pathological conditions, including valvular heart diseases, congestive heart failure, and hypertension, recent clinical data implicate the additional contribution of genetic factors in the pathogenesis of AF. A familial form of AF has been noted, and 8 loci and 6 responsible genes have been identified. In non‐familial AF, genetic risks were originally investigated by the candidate gene approach, and recently by genome‐wide association studies (GWASs). GWASs executed in other countries have identified 3 loci: 4q25 near Pitx2, 1q21 in KCNN3, and 16q22 in ZFHX3. Several AF‐associated SNPs in 4q25 are also associated with the recurrence rate of AF after catheter pulmonary vein isolation. This review will discuss the genetic underpinnings of AF, in both familial AF and non‐familial AF.
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Furukawa et al. (2012) conducted a review in Atrial fibrillation. Genetic factors was evaluated. Genetic factors contribute to the pathogenesis of atrial fibrillation, with 8 loci and 6 genes identified in familial AF, and 3 loci (4q25, 1q21, 16q22) identified in non-familial AF via GWAS.
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