Genome and atrial fibrillation

Abstract

Atrial fibrillation (AF), the most common type of arrhythmia, can cause several adverse effects, such as stroke, heart failure, and cognitive dysfunction, also in addition to reducing quality of life and increasing mortality. Evidence suggests that AF is caused by a combination of genetic and clinical predispositions. In line with this, genetic studies on AF have progressed significantly through linkage studies, genome-wide association studies, use of polygenic risk scores, and studies on rare coding variations, gradually elucidating the relationship between genes and the pathogenesis and prognosis of AF. This article will review current trends in genetic analysis concerning AF.

DNA Methylation and Telomeres—Their Impact on the Occurrence of Atrial Fibrillation during Cardiac Aging

“…Several theories include ion-flow disruption, structural remodeling, and electrical remodeling [9,[20][21][22]. The formation of ectopic foci of excitation and, thus, the knotting of reentry loops, the intensity of proliferation, differentiation, and the remodeling of the extracellular matrix, as well as the efficiency of flow through ion channels, are associated with changes in gene expression [23][24][25][26]. Some changes in gene expression related to signaling pathways, fibroblast activity, and electrical conductivity, or associated with the development of inflammation in AF patients, have been identified [27][28][29][30][31][32][33].…”