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@ARTICLE{Schmidt:147400,
      author       = {A. F. Schmidt and M. V. Holmes and D. Preiss and D. I.
                      Swerdlow and S. Denaxas and G. Fatemifar and R. Faraway and
                      C. Finan and D. Valentine and Z. Fairhurst-Hunter and F. P.
                      Hartwig and B. L. Horta and E. Hypponen and C. Power and M.
                      Moldovan and E. van Iperen and K. Hovingh and I. Demuth and
                      K. Norman and E. Steinhagen-Thiessen and J. Demuth and L.
                      Bertram and C. M. Lill and S. Coassin and J. Willeit and S.
                      Kiechl and K. Willeit and D. Mason and J. Wright and R.
                      Morris and G. Wanamethee and P. Whincup and Y. Ben-Shlomo
                      and S. McLachlan and J. F. Price and M. Kivimaki and C.
                      Welch and A. Sanchez-Galvez and P. Marques-Vidal and A.
                      Nicolaides and A. G. Panayiotou and N. C. Onland-Moret and
                      Y. T. van der Schouw and G. Matullo and G. Fiorito and S.
                      Guarrera and C. Sacerdote and N. J. Wareham and C.
                      Langenberg and R. A. Scott and J. Luan and M. Bobak and S.
                      Malyutina and A. Pająk and R. Kubinova and A. Tamosiunas
                      and H. Pikhart and N. Grarup and O. Pedersen and T. Hansen
                      and A. Linneberg and T. Jess and J. Cooper and S. E.
                      Humphries and M. Brilliant and T. Kitchner and H. Hakonarson
                      and D. S. Carrell and C. A. McCarty and K. H. Lester and E.
                      B. Larson and D. R. Crosslin and M. de Andrade and D. M.
                      Roden and J. C. Denny and C. Carty and S. Hancock and J.
                      Attia and E. Holliday and R. Scott and P. Schofield and M.
                      O'Donnell and S. Yusuf and M. Chong and G. Pare and P. van
                      der Harst and M. A. Said and R. N. Eppinga and N. Verweij
                      and H. Snieder and T. Christen and D. O. Mook-Kanamori and
                      S. Gustafsson and L. Lind and E. Ingelsson and R. Pazoki and
                      O. Franco and A. Hofman and A. Uitterlinden and A. Dehghan
                      and A. Teumer and S. Baumeister and M. Dörr and M. M. Lerch
                      and U. Völker and H. Völzke and J. Ward and J. P. Pell and
                      T. Meade and I. E. Christophersen and A. H. Maitland-van der
                      Zee and E. V. Baranova and R. Young and I. Ford and A.
                      Campbell and S. Padmanabhan and M. L. Bots and D. E. Grobbee
                      and P. Froguel and D. Thuillier and R. Roussel and A.
                      Bonnefond and B. Cariou and M. Smart and Y. Bao and M.
                      Kumari and A. Mahajan and J. C. Hopewell and S. Seshadri and
                      C. Dale and R. P. E. Costa and P. M. Ridker and D. I.
                      Chasman and A. P. Reiner and M. D. Ritchie and L. A. Lange
                      and A. J. Cornish and S. E. Dobbins and K. Hemminki$^*$ and
                      B. Kinnersley and M. Sanson and K. Labreche and M. Simon and
                      M. Bondy and P. Law and H. Speedy and J. Allan and N. Li and
                      M. Went and N. Weinhold and G. Morgan and P. Sonneveld and
                      B. Nilsson and H. Goldschmidt and A. Sud and A. Engert and
                      M. Hansson and H. Hemingway and F. W. Asselbergs and R. S.
                      Patel and B. J. Keating and N. Sattar and R. Houlston and J.
                      P. Casas and A. D. Hingorani},
      collaboration = {L. C. authors and I. Consortium and M. C. o. t. ISGC},
      title        = {{P}henome-wide association analysis of {LDL}-cholesterol
                      lowering genetic variants in {PCSK}9.},
      journal      = {BMC cardiovascular disorders},
      volume       = {19},
      number       = {1},
      issn         = {1471-2261},
      address      = {London},
      publisher    = {BioMed Central},
      reportid     = {DKFZ-2019-02517},
      pages        = {240},
      year         = {2019},
      abstract     = {We characterised the phenotypic consequence of genetic
                      variation at the PCSK9 locus and compared findings with
                      recent trials of pharmacological inhibitors of
                      PCSK9.Published and individual participant level data
                      (300,000+ participants) were combined to construct a
                      weighted PCSK9 gene-centric score (GS). Seventeen randomized
                      placebo controlled PCSK9 inhibitor trials were included,
                      providing data on 79,578 participants. Results were scaled
                      to a one mmol/L lower LDL-C concentration.The PCSK9 GS
                      (comprising 4 SNPs) associations with plasma lipid and
                      apolipoprotein levels were consistent in direction with
                      treatment effects. The GS odds ratio (OR) for myocardial
                      infarction (MI) was 0.53 $(95\%$ CI 0.42; 0.68), compared to
                      a PCSK9 inhibitor effect of 0.90 $(95\%$ CI 0.86; 0.93). For
                      ischemic stroke ORs were 0.84 $(95\%$ CI 0.57; 1.22) for the
                      GS, compared to 0.85 $(95\%$ CI 0.78; 0.93) in the drug
                      trials. ORs with type 2 diabetes mellitus (T2DM) were 1.29
                      $(95\%$ CI 1.11; 1.50) for the GS, as compared to 1.00
                      $(95\%$ CI 0.96; 1.04) for incident T2DM in PCSK9 inhibitor
                      trials. No genetic associations were observed for cancer,
                      heart failure, atrial fibrillation, chronic obstructive
                      pulmonary disease, or Alzheimer's disease - outcomes for
                      which large-scale trial data were unavailable.Genetic
                      variation at the PCSK9 locus recapitulates the effects of
                      therapeutic inhibition of PCSK9 on major blood lipid
                      fractions and MI. While indicating an increased risk of
                      T2DM, no other possible safety concerns were shown; although
                      precision was moderate.},
      cin          = {C020},
      ddc          = {610},
      cid          = {I:(DE-He78)C020-20160331},
      pnm          = {323 - Metabolic Dysfunction as Risk Factor (POF3-323)},
      pid          = {G:(DE-HGF)POF3-323},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:31664920},
      doi          = {10.1186/s12872-019-1187-z},
      url          = {https://inrepo02.dkfz.de/record/147400},
}