Abstract

Atrial fibrillation (AF) is the most common persistent heart rhythm disorder, the prevalence of which increases with age. The progressive prevalence of AF is becoming a serious threat to public health throughout the world, as it is associated with high mortality rates. In the review, we analyzed the literature data on the state of knowledge of the genetic nature of AF. To achieve this goal, a systematic search and subsequent analysis of publications and online resources was carried out. All publications are indexed in PubMed, Medline, e-library, Coogle Scholar. To date, at least 30 loci associated with AF have been identified. At the same time, the research results depend on such factors as ethnicity, concomitant cardiac and extracardiac diseases, inheritance mechanisms, and intergenic interactions. The complexity of etiopathogenesis, the heterogeneity of AF poses the task of researchers to further search for factors that play a leading role in the development of the disease. Significant progress in understanding the genetic basis of AF was achieved with the advent of large-scale genomic GWAS studies, which include genotyping up to a million common variants or single nucleotide polymorphisms. The currently available data on the association of candidate genes with AF in case-control studies are controversial and necessitate more detailed studies on various ethnic groups.

Highlights

  • Atrial fibrillation (AF) is the most common persistent heart rhythm disorder, the prevalence of which increases with age [1]

  • Assessment of the polymorphism of candidate genes associated with AF, depending on ethnicity, would expand the possibility of this disease preventing

  • Significant progress has been achieved in genetic substrate identifying that underlying AF development

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Summary

Introduction

Atrial fibrillation (AF) is the most common persistent heart rhythm disorder, the prevalence of which increases with age [1]. The hypothesis that different forms of AF are based on common molecular mechanisms was made possible by the data on the formation of similar phenotypes of ion channels resulting from electrophysiological remodeling of the myocardium in patients with nonfamilial forms of chronic AF and in individuals with monogenic AF forms [15]. According to studies of AF genetic nature, the occurrence of AF is facilitated by the combined carriage of certain variants of several candidate genes [16,17,18].

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