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Sökning: onr:"swepub:oai:DiVA.org:uu-382548" > No evidence of a ca...

  • Harati, HadiStanford Univ, Sch Med, Dept Med, Div Endocrinol, Stanford, CA USA (författare)

No evidence of a causal association of type 2 diabetes and glucose metabolism with atrial fibrillation

  • Artikel/kapitelEngelska2019

Förlag, utgivningsår, omfång ...

  • 2019-02-27
  • SPRINGER,2019
  • printrdacarrier

Nummerbeteckningar

  • LIBRIS-ID:oai:DiVA.org:uu-382548
  • https://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-382548URI
  • https://doi.org/10.1007/s00125-019-4836-yDOI

Kompletterande språkuppgifter

  • Språk:engelska
  • Sammanfattning på:engelska

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  • Ämneskategori:ref swepub-contenttype
  • Ämneskategori:art swepub-publicationtype

Anmärkningar

  • Aims/hypothesisSeveral 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.MethodsTwo-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.ResultsNeither 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/interpretationThis 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.

Ämnesord och genrebeteckningar

Biuppslag (personer, institutioner, konferenser, titlar ...)

  • Zanetti, DanielaStanford Univ, Falk Cardiovasc Res Ctr, Div Cardiovasc Med, Dept Med,Sch Med, 300 Pasteur Dr,CV 273, Stanford, CA 94305 USA (författare)
  • Rao, AbhiramStanford Univ, Dept Bioengn, Stanford, CA 94305 USA (författare)
  • Gustafsson, StefanUppsala universitet,Molekylär epidemiologi,Science for Life Laboratory, SciLifeLab(Swepub:uu)stegu732 (författare)
  • Perez, MarcoStanford Univ, Falk Cardiovasc Res Ctr, Div Cardiovasc Med, Dept Med,Sch Med, 300 Pasteur Dr,CV 273, Stanford, CA 94305 USA (författare)
  • Ingelsson, ErikStanford Univ, Falk Cardiovasc Res Ctr, Div Cardiovasc Med, Dept Med,Sch Med, 300 Pasteur Dr,CV 273, Stanford, CA 94305 USA;Stanford Univ, Stanford Cardiovasc Inst, Stanford, CA 94305 USA;Stanford Univ, Stanford Diabet Res Ctr, Stanford, CA 94305 USA (författare)
  • Knowles, Joshua W.Stanford Univ, Falk Cardiovasc Res Ctr, Div Cardiovasc Med, Dept Med,Sch Med, 300 Pasteur Dr,CV 273, Stanford, CA 94305 USA;Stanford Univ, Stanford Cardiovasc Inst, Stanford, CA 94305 USA;Stanford Univ, Stanford Diabet Res Ctr, Stanford, CA 94305 USA (författare)
  • Stanford Univ, Sch Med, Dept Med, Div Endocrinol, Stanford, CA USAStanford Univ, Falk Cardiovasc Res Ctr, Div Cardiovasc Med, Dept Med,Sch Med, 300 Pasteur Dr,CV 273, Stanford, CA 94305 USA (creator_code:org_t)

Sammanhörande titlar

  • Ingår i:Diabetologia: SPRINGER62:5, s. 800-8040012-186X1432-0428

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