Key result
Recent evidence indicates that atrial fibrillation has a significant heritable component, with specific genetic variants in ion-channel and nonion-channel genes contributing to its pathogenesis.
This review highlights the growing evidence that atrial fibrillation has a significant genetic and heritable component, which may influence therapeutic response and future management.
May inform future AF risk models; leaves open whether variants guide therapy or outcomes.
PURPOSE OF REVIEW: Atrial fibrillation is traditionally regarded as a sporadic, nongenetic disorder. Nevertheless, recent growing evidence points to an important heritable basis for atrial fibrillation, with significant genetic determinants. This paper reviews recent progress in understanding the role of genetic contributors to the pathogenesis of atrial fibrillation and its familial susceptibility. RECENT FINDINGS: Population-based studies have demonstrated a significant heritable component in atrial fibrillation, with specific contributors including single-gene mutations and single-nucleotide polymorphisms. Variants in both ion-channel and nonion-channel genes have been identified as potential atrial fibrillation-risk determinants. In addition, studies have pointed to interesting combined roles of genetic and environmental factors in atrial fibrillation pathogenesis, providing insights into gene-environment interactions. Clinical studies suggest that individual genetic profiles may determine the therapeutic response of atrial fibrillation. SUMMARY: Rapidly evolving work indicates that there are important genetic determinants of atrial fibrillation, and suggests that understanding these determinants will help us both to appreciate better the underlying pathophysiology and to provide new approaches in diagnosis, prevention and treatment of this common cardiac condition.
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Andalib et al. (2008) conducted a review in Atrial fibrillation. Genetic determinants was evaluated. Recent evidence indicates that atrial fibrillation has a significant heritable component, with specific genetic variants in ion-channel and nonion-channel genes contributing to its pathogenesis.
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