Abstract

The prevalence and economic burden of atrial fibrillation (AF) are predicted to more than double over the next few decades. In addition to anticoagulation and treatment of concomitant cardiovascular conditions, early and standardized rhythm control therapy reduces cardiovascular outcomes as compared with a rate control approach, favouring the restoration, and maintenance of sinus rhythm safely. Current therapies for rhythm control of AF include antiarrhythmic drugs (AADs) and catheter ablation (CA). However, response in an individual patient is highly variable with some remaining free of AF for long periods on antiarrhythmic therapy, while others require repeat AF ablation within weeks. The limited success of rhythm control therapy for AF is in part related to incomplete understanding of the pathophysiological mechanisms and our inability to predict responses in individual patients. Thus, a major knowledge gap is predicting which patients with AF are likely to respond to rhythm control approach. Over the last decade, tremendous progress has been made in defining the genetic architecture of AF with the identification of rare mutations in cardiac ion channels, signalling molecules, and myocardial structural proteins associated with familial (early-onset) AF. Conversely, genome-wide association studies have identified common variants at over 100 genetic loci and the development of polygenic risk scores has identified high-risk individuals. Although retrospective studies suggest that response to AADs and CA is modulated in part by common genetic variation, the development of a comprehensive clinical and genetic risk score may enable the translation of genetic data to the bedside care of AF patients. Given the economic impact of the AF epidemic, even small changes in therapeutic efficacy may lead to substantial improvements for patients and health care systems.

Highlights

  • Retrospective studies suggest that response to antiarrhythmic drugs (AADs) and catheter ablation (CA) is modulated in part by common genetic variation, the development of a comprehensive clinical and genetic risk score may enable the translation of genetic data to the bedside care of atrial fibrillation (AF) patients

  • More than 30 million people around the world were affected by atrial fibrillation (AF) in 2010.1 The lifetime risk of developing AF in people of European descent older than 40 years one in three and AF is associated with significant morbidity and increased mortality.[2]

  • We review whether the increased knowledge on common genetic variation associated with AF can improve our management of the arrhythmia and how and when this may be best accomplished

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Summary

Introduction

More than 30 million people around the world were affected by atrial fibrillation (AF) in 2010.1 The lifetime risk of developing AF in people of European descent older than 40 years one in three and AF is associated with significant morbidity and increased mortality.[2]. Genetic approaches to AF have revealed that susceptibility to AF development and response to therapy is modulated in part by the underlying genetic substrate, the impact of these discoveries on the bedside care of patients has been limited. In this monograph, we review whether the increased knowledge on common genetic variation associated with AF can improve our management of the arrhythmia and how and when this may be best accomplished

Genetic basis of AF
Genetic risk scores
Catheter ablation therapy
Antiarrhythmic therapy
Clinical predictors of response to AADs for AF
Ablation therapy
Current value of genetics in clinical application
Future perspective on clinical applications of AF genetics
Results
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