title: Prevalent platelet dysfunction in patients with aortic valve disease.
abstract: OBJECTIVE
  In patients with heart valve disease, the valve leaflets display a gapped, rough endothelial lining often covered with calcified areas. As a consequence, blood flow is disturbed and a stimulation of components of the hemostasis system is assumed. The possible mechanisms of this process are, however, unclear at present.
  
  
  METHODS
  Platelet function was studied in 660 patients considered for isolated coronary artery bypass graft (CABG) surgery, and in 421 patients considered for single aortic valve replacement (AVR). Platelet function was monitored preoperatively using the platelet function analyzer device (PFA-100). The test results were reported as closure time of the membrane hole at the end of a capillary tube. The von Willebrand factor antigen, and its collagen-binding activity, were also determined among subgroups of 40 AVR and 50 CABG candidates.
  
  
  RESULTS
  Platelet dysfunction was displayed by only 22% of CAD patients, but by 83% of AVR candidates. The mean PFA closure time in AVR patients was considerably higher than in CAD patients (231 +/- 59 s versus 153 +/- 60 s, respectively; p < 0.01). The mean platelet volume, platelet distribution width and von Willebrand factor collagen binding and antigen levels did not differ between the patient groups.
  
  
  CONCLUSIONS
  It is assumed that, due to disturbed flow and shear exposition, following an initial activation, the platelets are partially degranulated, shed microparticles, and might become involved in the pathogenesis of microvascular dysfunction and thrombotic events in patients with aortic valve disease.
authors.affiliation: Institute for Laboratory and Transfusion Medicine, Heart and Diabetes Center North Rhine Westfalia, University Hospital of the Ruhr, University Bochum, Bad Oeynhausen, Germany. wprohaska@hdz-nrw.de
authors.forename: Wolfgang
authors.initials: W
authors.lastname: Prohaska
authors.forename: Armin
authors.initials: A
authors.lastname: Zittermann
authors.forename: Jan U
authors.initials: JU
authors.lastname: Lüth
authors.forename: Kazuo
authors.initials: K
authors.lastname: Inoue
authors.forename: Wilhelm
authors.initials: W
authors.lastname: Köster-Eiserfunke
authors.forename: Detlev
authors.initials: D
authors.lastname: Baller
authors.forename: Reiner
authors.initials: R
authors.lastname: Körfer
authors.forename: Knut
authors.initials: K
authors.lastname: Kleesiek
mesh_terms: D000368:Aged; D000941:Antigens / Q000097:blood; D001024:Aortic Valve Stenosis / Q000097:blood* / Q000601:surgery*; D001791:Blood Platelet Disorders / Q000097:blood*; D015331:Cohort Studies; D001026:Coronary Artery Bypass; D005260:Female; D006350:Heart Valve Prosthesis; D006801:Humans; D008297:Male; D008875:Middle Aged; D015539:Platelet Activation / Q000502:physiology; D010979:Platelet Function Tests; D010980:Platelet Membrane Glycoproteins / Q000378:metabolism; D012189:Retrospective Studies; D014842:von Willebrand Diseases / Q000097:blood / Q000175:diagnosis; D014841:von Willebrand Factor / Q000276:immunology
chemical_list: D000941:Antigens; D010980:Platelet Membrane Glycoproteins; C029417:Von Willebrand antigen; D014841:von Willebrand Factor; C028254:von Willebrand factor receptor