% IMPORTANT: The following is UTF-8 encoded.  This means that in the presence
% of non-ASCII characters, it will not work with BibTeX 0.99 or older.
% Instead, you should use an up-to-date BibTeX implementation like “bibtex8” or
% “biber”.

@ARTICLE{Patel:143353,
      author       = {R. S. Patel and A. F. Schmidt and V. Tragante and R. O.
                      McCubrey and M. V. Holmes and L. J. Howe and K. Direk and A.
                      Åkerblom and K. Leander and S. S. Virani and K. A. Kaminski
                      and J. D. Muehlschlegel and M.-P. Dubé and H. Allayee and
                      P. Almgren and M. Alver and E. V. Baranova and H. Behlouli
                      and B. Boeckx and P. S. Braund and L. P. Breitling and G.
                      Delgado and N. E. Duarte and L. Dufresne and N. Eriksson and
                      L. Foco and C. M. Gijsberts and Y. Gong and J. Hartiala and
                      M. Heydarpour and J. A. Hubacek and M. Kleber and D. Kofink
                      and P. Kuukasjärvi and V.-V. Lee and A. Leiherer and P. A.
                      Lenzini and D. Levin and L.-P. Lyytikäinen and N.
                      Martinelli and U. Mons$^*$ and C. P. Nelson and K. Nikus and
                      A. P. Pilbrow and R. Ploski and Y. V. Sun and M. W. T. Tanck
                      and W. H. W. Tang and S. Trompet and S. W. van der Laan and
                      J. Van Setten and R. O. Vilmundarson and C. Viviani Anselmi
                      and E. Vlachopoulou and E. Boerwinkle and C. Briguori and J.
                      F. Carlquist and K. F. Carruthers and G. Casu and J.
                      Deanfield and P. Deloukas and F. Dudbridge and N.
                      Fitzpatrick and B. Gigante and S. James and M.-L. Lokki and
                      P. A. Lotufo and N. Marziliano and I. R. Mordi and J. B.
                      Muhlestein and C. Newton-Cheh and J. Pitha and C. H. Saely
                      and A. Samman-Tahhan and P. B. Sandesara and A. Teren and A.
                      Timmis and F. Van de Werf and E. Wauters and A. A. M. Wilde
                      and I. Ford and D. J. Stott and A. Algra and M. G. Andreassi
                      and D. Ardissino and B. J. Arsenault and C. M. Ballantyne
                      and T. O. Bergmeijer and C. R. Bezzina and S. C. Body and P.
                      Bogaty and G. J. de Borst and H. Brenner$^*$ and R.
                      Burkhardt and C. Carpeggiani and G. Condorelli and R. M.
                      Cooper-DeHoff and S. Cresci and U. de Faire and R. N.
                      Doughty and H. Drexel and J. C. Engert and K. A. A. Fox and
                      D. Girelli and E. Hagström and S. L. Hazen and C. Held and
                      H. Hemingway and I. E. Hoefer and G. K. Hovingh and J. A.
                      Johnson and P. A. de Jong and J. W. Jukema and M. P. Kaczor
                      and M. Kähönen and J. Kettner and M. Kiliszek and O. H.
                      Klungel and B. Lagerqvist and D. Lambrechts and J. O.
                      Laurikka and T. Lehtimäki and D. Lindholm and B. K.
                      Mahmoodi and A. H. Maitland-van der Zee and R. McPherson and
                      O. Melander and A. Metspalu and W. Pepinski and O. Olivieri
                      and G. Opolski and C. N. Palmer and G. Pasterkamp and C. J.
                      Pepine and A. C. Pereira and L. Pilote and A. A. Quyyumi and
                      A. M. Richards and M. Sanak and M. Scholz and A. Siegbahn
                      and J. Sinisalo and J. G. Smith and J. A. Spertus and A. F.
                      R. Stewart and W. Szczeklik and A. Szpakowicz and J. M. Ten
                      Berg and G. Thanassoulis and J. Thiery and Y. van der Graaf
                      and F. L. J. Visseren and J. Waltenberger and P. Van der
                      Harst and J.-C. Tardif and N. Sattar and C. C. Lang and G.
                      Paré and J. M. Brophy and J. L. Anderson and W. März and
                      L. Wallentin and V. A. Cameron and B. D. Horne and N. J.
                      Samani and A. D. Hingorani and F. W. Asselbergs},
      title        = {{A}ssociation of {C}hromosome 9p21 with {S}ubsequent
                      {C}oronary {H}eart {D}isease {E}vents: {A} {GENIUS}-{CHD}
                      {S}tudy of {I}ndividual {P}articipant {D}ata.},
      journal      = {Circulation Genomic and precision medicine [...]},
      volume       = {12},
      number       = {4},
      issn         = {2574-8300},
      address      = {Philadelphia, Pa.},
      publisher    = {Lippincott, Williams $\&$ Wilkins},
      reportid     = {DKFZ-2019-00941},
      pages        = {e002471},
      year         = {2019},
      abstract     = {Genetic variation at chromosome 9p21 is a recognized risk
                      factor for coronary heart disease (CHD). However, its effect
                      on disease progression and subsequent events is unclear,
                      raising questions about its value for stratification of
                      residual risk.A variant at chromosome 9p21 (rs1333049) was
                      tested for association with subsequent events during
                      follow-up in 103,357 Europeans with established CHD at
                      baseline from the GENIUS-CHD Consortium $(73.1\%$ male, mean
                      age 62.9 years). The primary outcome, subsequent CHD death
                      or myocardial infarction (CHD death/MI), occurred in 13,040
                      of the 93,115 participants with available outcome data.
                      Effect estimates were compared to case/control risk obtained
                      from CARDIoGRAMPlusC4D including 47,222 CHD cases and
                      122,264 controls free of CHD.Meta-analyses revealed no
                      significant association between chromosome 9p21 and the
                      primary outcome of CHD death/MI among those with established
                      CHD at baseline (GENIUS-CHD OR 1.02; $95\%$ CI 0.99-1.05).
                      This contrasted with a strong association in
                      CARDIoGRAMPlusC4D OR 1.20; $95\%$ CI 1.18-1.22; p for
                      interaction Conclusions: In contrast to studies comparing
                      individuals with CHD to disease free controls, we found no
                      clear association between genetic variation at chromosome
                      9p21 and risk of subsequent acute CHD events when all
                      individuals had CHD at baseline. However, the association
                      with subsequent revascularization may support the postulated
                      mechanism of chromosome 9p21 for promoting atheroma
                      development.},
      cin          = {C070 / C120},
      ddc          = {610},
      cid          = {I:(DE-He78)C070-20160331 / I:(DE-He78)C120-20160331},
      pnm          = {323 - Metabolic Dysfunction as Risk Factor (POF3-323)},
      pid          = {G:(DE-HGF)POF3-323},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:30897348},
      doi          = {10.1161/CIRCGEN.119.002471},
      url          = {https://inrepo02.dkfz.de/record/143353},
}