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 journal › SCORING: Review article › Research
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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 -