Genetics of atrial fibrillation-practical applications for clinical management: if not now, when and how?

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Genetics of atrial fibrillation-practical applications for clinical management: if not now, when and how? / Kany, Shinwan; Reissmann, Bruno; Metzner, Andreas; Kirchhof, Paulus; Darbar, Dawood; Schnabel, Renate B.

In: CARDIOVASC RES, Vol. 117, No. 7, 16.06.2021, p. 1718-1731.

Research output: SCORING: Contribution to journalSCORING: Review articleResearch

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@article{106e28c71fc440048dfb4639b3f48218,
title = "Genetics of atrial fibrillation-practical applications for clinical management: if not now, when and how?",
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.",
keywords = "Animals, Anti-Arrhythmia Agents/therapeutic use, Atrial Fibrillation/diagnosis, Catheter Ablation, Clinical Decision-Making, Genetic Predisposition to Disease, Genetic Variation, Genomics, Humans, Phenotype, Precision Medicine, Predictive Value of Tests, Prognosis, Risk Assessment, Risk Factors",
author = "Shinwan Kany and Bruno Reissmann and Andreas Metzner and Paulus Kirchhof and Dawood Darbar and Schnabel, {Renate B}",
note = "Published on behalf of the European Society of Cardiology. All rights reserved. {\textcopyright} The Author(s) 2021. For permissions, please email: journals.permissions@oup.com.",
year = "2021",
month = jun,
day = "16",
doi = "10.1093/cvr/cvab153",
language = "English",
volume = "117",
pages = "1718--1731",
journal = "CARDIOVASC RES",
issn = "0008-6363",
publisher = "Oxford University Press",
number = "7",

}

RIS

TY - JOUR

T1 - Genetics of atrial fibrillation-practical applications for clinical management: if not now, when and how?

AU - Kany, Shinwan

AU - Reissmann, Bruno

AU - Metzner, Andreas

AU - Kirchhof, Paulus

AU - Darbar, Dawood

AU - Schnabel, Renate B

N1 - Published on behalf of the European Society of Cardiology. All rights reserved. © The Author(s) 2021. For permissions, please email: journals.permissions@oup.com.

PY - 2021/6/16

Y1 - 2021/6/16

N2 - 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.

AB - 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.

KW - Animals

KW - Anti-Arrhythmia Agents/therapeutic use

KW - Atrial Fibrillation/diagnosis

KW - Catheter Ablation

KW - Clinical Decision-Making

KW - Genetic Predisposition to Disease

KW - Genetic Variation

KW - Genomics

KW - Humans

KW - Phenotype

KW - Precision Medicine

KW - Predictive Value of Tests

KW - Prognosis

KW - Risk Assessment

KW - Risk Factors

U2 - 10.1093/cvr/cvab153

DO - 10.1093/cvr/cvab153

M3 - SCORING: Review article

C2 - 33982075

VL - 117

SP - 1718

EP - 1731

JO - CARDIOVASC RES

JF - CARDIOVASC RES

SN - 0008-6363

IS - 7

ER -