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Body composition and atrial fibrillation: a Mendelian randomization study
Stanford Univ, Dept Med, Sch Med, Div Cardiovasc Med, 300 Pasteur Dr, Stanford, CA 94305 USA;Stanford Univ, Stanford Cardiovasc Inst, 300 Pasteur Dr, Stanford, CA 94305 USA.
Uppsala University, Science for Life Laboratory, SciLifeLab. Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences, Molecular epidemiology.ORCID iD: 0000-0001-5894-0351
Stanford Univ, Dept Med, Sch Med, Div Cardiovasc Med, 300 Pasteur Dr, Stanford, CA 94305 USA;Stanford Univ, Stanford Cardiovasc Inst, 300 Pasteur Dr, Stanford, CA 94305 USA;Stanford Univ, Stanford Diabet Res Ctr, 300 Pasteur Dr, Stanford, CA 94305 USA.
Stanford Univ, Dept Med, Sch Med, Div Cardiovasc Med, 300 Pasteur Dr, Stanford, CA 94305 USA.
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2019 (English)In: European Heart Journal, ISSN 0195-668X, E-ISSN 1522-9645, Vol. 40, no 16, p. 1277-1282Article in journal (Refereed) Published
Abstract [en]

Aims

Increases in fat-free mass and fat mass have been associated with higher risk of atrial fibrillation (AF) in observational studies. It is not known whether these associations reflect independent causal processes. Our aim was to evaluate independent causal roles of fat-free mass and fat mass on AF.

Methods and results

We conducted a large observational study to estimate the associations between fat-free mass and fat mass on incident AF in the UK Biobank (N = 487 404, N events = 10 365). Genome-wide association analysis was performed to obtain genetic instruments for Mendelian randomization (MR). We evaluated the causal effects of fat-free mass and fat mass on AF with two-sample method by using genetic associations from AFGen consortium as outcome. Finally, we evaluated independent causal effects of fat-free mass and fat mass with multivariate MR. Both fat-free mass and fat mass had observational associations with incident AF [hazard ratio (HR) = 1.77, 95% confidence interval (CI) 1.72-1.83; HR = 1.40, 95% CI 1.37-1.43 per standard deviation increase in fat-free and fat mass, respectively]. The causal effects using the inverse-variance weighted method were 1.55 (95% CI 1.38-1.75) for fat-free mass and 1.30 (95% CI 1.17-1.45) for fat mass. Weighted median, Egger regression, and penalized methods showed similar estimates. The multivariate MR analysis suggested that the causal effects of fat-free and fat mass were independent of each other (causal risk ratios: 1.37, 95% CI 1.06-1.75; 1.28, 95% CI 1.03-1.58).

Conclusion

Genetically programmed increases in fat-free mass and fat mass independently cause an increased risk of AF.

Place, publisher, year, edition, pages
2019. Vol. 40, no 16, p. 1277-1282
Keywords [en]
Fat-free mass, Fat mass, Bioimpedance, Genetics, Atrial fibrillation, Causal effect
National Category
Cardiac and Cardiovascular Systems
Identifiers
URN: urn:nbn:se:uu:diva-396561DOI: 10.1093/eurheartj/ehz003ISI: 000490013700010PubMedID: 30721963OAI: oai:DiVA.org:uu-396561DiVA, id: diva2:1368293
Funder
Knut and Alice Wallenberg Foundation, 2013.0126Available from: 2019-11-06 Created: 2019-11-06 Last updated: 2019-11-06Bibliographically approved

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Gustafsson, StefanIngelsson, Erik

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