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@ARTICLE{Langnau:168559,
      author       = {C. Langnau and A.-K. Rohlfing and S. Gekeler and M.
                      Günter$^*$ and S. Pöschel and Á. Petersen-Uribe and P.
                      Jaeger and A. Avdiu and T. Harm and K.-P. Kreisselmeier and
                      T. Castor and T. Bakchoul and D. Rath and M. P. Gawaz and S.
                      E. Autenrieth$^*$ and K. A. L. Mueller},
      title        = {{P}latelet {A}ctivation and {P}lasma {L}evels of {F}urin
                      {A}re {A}ssociated {W}ith {P}rognosis of {P}atients {W}ith
                      {C}oronary {A}rtery {D}isease and {COVID}-19.},
      journal      = {Arteriosclerosis, thrombosis, and vascular biology},
      volume       = {41},
      number       = {6},
      issn         = {1524-4636},
      address      = {Stanford, Calif.},
      publisher    = {HighWire},
      reportid     = {DKFZ-2021-00976},
      pages        = {2080-2096},
      year         = {2021},
      note         = {2021 Jun;41(6):2080-2096},
      abstract     = {Patients with coronary artery disease (CAD) are at
                      increased risk for cardiac death and respiratory failure
                      following severe acute respiratory syndrome coronavirus 2
                      (SARS-CoV-2) infection. Platelets are crucially involved in
                      pathogenesis of CAD and might also contribute to
                      pathophysiology of SARS-CoV-2 infection. Approach and
                      Results: We enrolled a cohort of 122 participants from
                      February 2020 to July 2020 including 55 patients with
                      preexisting CAD and acute SARS-CoV-2 infection
                      (CAD-SARS-CoV-2positive), 28 patients with CAD and without
                      SARS-CoV-2 (CAD-SARS-CoV-2negative), and 39 healthy
                      controls. Clinical and cardiac examination of the
                      CAD-SARS-CoV-2positive group included blood sampling,
                      echocardiography, and electrocardiography within 24 hours
                      after hospital admission. Phenotyping of platelets was
                      performed by flow cytometry; plasma levels of chemokines
                      were analyzed by ELISA. Respiratory failure of patients was
                      stratified by the Horovitz index as moderately/severely
                      impaired when Horovitz index <200 mm Hg. The clinical end
                      point was defined as Horovitz index <200 mm Hg with
                      subsequent mechanical ventilation within a follow-up of 60
                      days. CAD-SARS-CoV-2positive patients display a significant
                      enhanced platelet activation and hyper-inflammation early at
                      time of hospital admission. Circulating platelet/leukocyte
                      co-aggregates correlate with plasma levels of
                      cytokines/chemokines like IL (interleukin)-6, CCL2, and
                      CXCL10 as well as activation of platelets is associated with
                      CCL5 and elevation of pulmonary artery pressure.
                      Furthermore, furin is stored and released from activated
                      platelets. High furin plasma levels are associated with poor
                      clinical prognosis in CAD-SARS-CoV-2positive
                      patients.Patients with CAD and SARS-CoV-2 infection exhibit
                      elevated systemic platelet activation and enhanced plasma
                      levels of the subtilisin-like proprotein convertase furin,
                      which may contribute to an unfavorable clinical prognosis.},
      keywords     = {coronary artery disease (Other) / cytokines (Other) / flow
                      cytometry (Other) / furin (Other) / pulmonary artery
                      (Other)},
      cin          = {F171},
      ddc          = {610},
      cid          = {I:(DE-He78)F171-20160331},
      pnm          = {316 - Infektionen, Entzündung und Krebs (POF4-316)},
      pid          = {G:(DE-HGF)POF4-316},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:33910372},
      doi          = {10.1161/ATVBAHA.120.315698},
      url          = {https://inrepo02.dkfz.de/record/168559},
}