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No evidence of a causal association of type 2 diabetes and glucose metabolism with atrial fibrillation
Stanford Univ, Sch Med, Dept Med, Div Endocrinol, Stanford, CA USA.
Stanford Univ, Falk Cardiovasc Res Ctr, Div Cardiovasc Med, Dept Med,Sch Med, 300 Pasteur Dr,CV 273, Stanford, CA 94305 USA.
Stanford Univ, Dept Bioengn, Stanford, CA 94305 USA.
Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences, Molecular epidemiology. Uppsala University, Science for Life Laboratory, SciLifeLab.ORCID iD: 0000-0001-5894-0351
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2019 (English)In: Diabetologia, ISSN 0012-186X, E-ISSN 1432-0428, Vol. 62, no 5, p. 800-804Article in journal (Refereed) Published
Abstract [en]

Aims/hypothesis

Several epidemiological studies have shown an increased risk of atrial fibrillation in individuals with type 2 diabetes or milder forms of dysglycaemia. We aimed to assess whether this relation is causal using a Mendelian randomisation approach.

Methods

Two-sample Mendelian randomisation was used to obtain estimates of the influence of type 2 diabetes, fasting blood glucose (FBG), and HbA(1c) on the risk of atrial fibrillation. Instrumental variables were constructed using available summary statistics from meta-analyses of genome-wide association studies (GWAS) for type 2 diabetes and associated phenotypes. Pleiotropic SNPs were excluded from the analyses. The most recent GWAS meta-analysis summary statistics for atrial fibrillation, which included over 1 million individuals (approximately 60,000 individuals with atrial fibrillation) was used for outcome analysis.

Results

Neither type 2 diabetes (OR 1.01 [95% CI 0.98, 1.03]; p=0.37), nor FBG (OR 0.95 [95% CI 0.82, 1.09] per mmol/l; p=0.49) or HbA(1c) (OR 1.01 [95% CI, 0.85, 1.17] per mmol/mol [%]; p=0.88) were associated with atrial fibrillation in Mendelian randomisation analyses. We had >80% statistical power to detect ORs of 1.08, 1.06 and 1.09 or larger for type 2 diabetes, FBG and HbA(1c), respectively, for associations with atrial fibrillation.

Conclusions/interpretation

This Mendelian randomisation analysis does not support a causal role of clinical significance between genetically programmed type 2 diabetes, FBG or HbA(1c) and development of atrial fibrillation. These data suggest that drug treatment to reduce dysglycaemia is unlikely to be an effective strategy for atrial fibrillation prevention.

Place, publisher, year, edition, pages
SPRINGER , 2019. Vol. 62, no 5, p. 800-804
Keywords [en]
Atrial fibrillation, Genome-wide association, Mendelian randomisation, Type 2 diabetes
National Category
Endocrinology and Diabetes
Identifiers
URN: urn:nbn:se:uu:diva-382548DOI: 10.1007/s00125-019-4836-yISI: 000463795300008PubMedID: 30810766OAI: oai:DiVA.org:uu-382548DiVA, id: diva2:1314932
Available from: 2019-05-10 Created: 2019-05-10 Last updated: 2019-05-10Bibliographically approved

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