Platelet Adhesion Mediated by von Willebrand Factor at High Shear Rates Is Associated with Premature Coronary Artery Disease
Sergey Okhota,
Sergey Kozlov,
Yuliya Avtaeva,
Ivan Melnikov,
Olga Saburova,
Konstantin Guria,
Evgeny Matroze,
Zufar Gabbasov
Affiliations
Sergey Okhota
Department of Problems of Atherosclerosis, National Medical Research Centre of Cardiology Named after Academician E.I. Chazov of the Ministry of Health of the Russian Federation, 121552 Moscow, Russia
Sergey Kozlov
Department of Problems of Atherosclerosis, National Medical Research Centre of Cardiology Named after Academician E.I. Chazov of the Ministry of Health of the Russian Federation, 121552 Moscow, Russia
Yuliya Avtaeva
Laboratory of Cell Hemostasis, National Medical Research Centre of Cardiology Named after Academician E.I. Chazov of the Ministry of Health of the Russian Federation, 121552 Moscow, Russia
Ivan Melnikov
Laboratory of Cell Hemostasis, National Medical Research Centre of Cardiology Named after Academician E.I. Chazov of the Ministry of Health of the Russian Federation, 121552 Moscow, Russia
Olga Saburova
Laboratory of Cell Hemostasis, National Medical Research Centre of Cardiology Named after Academician E.I. Chazov of the Ministry of Health of the Russian Federation, 121552 Moscow, Russia
Konstantin Guria
Laboratory of Cell Hemostasis, National Medical Research Centre of Cardiology Named after Academician E.I. Chazov of the Ministry of Health of the Russian Federation, 121552 Moscow, Russia
Evgeny Matroze
Laboratory of Cell Hemostasis, National Medical Research Centre of Cardiology Named after Academician E.I. Chazov of the Ministry of Health of the Russian Federation, 121552 Moscow, Russia
Zufar Gabbasov
Laboratory of Cell Hemostasis, National Medical Research Centre of Cardiology Named after Academician E.I. Chazov of the Ministry of Health of the Russian Federation, 121552 Moscow, Russia
This study investigated von Willebrand factor (VWF)-mediated platelet adhesion at high shear rates in patients with premature coronary artery disease (CAD). The study included 84 patients with stable premature CAD and 64 patients without CAD. Whole blood samples were perfused through a microfluidic cell over a collagen-coated surface at a shear rate of 1300 s−1. Measurements were performed before and after the inhibition of VWF-specific platelet GPIb receptors with an anti-GPIb monoclonal antibody (mAb). Platelet adhesion decreased by 77.0% (55.9; 84.7) in patients with premature CAD and by 29.6% (0.0; 59.7) in control patients after the inhibition of VWF–platelet interaction with anti-GPIb mAb (p p < 0.001). The optimal cut-off level value of GPIb-mediated platelet adhesion was 62.8%, with 70.2% sensitivity and 81.2% specificity for CAD. The plasma levels of VWF or antiplatelet therapy did not affect the GPIb-mediated component of platelet adhesion. Thus, the GPIb-mediated component of platelet adhesion was more pronounced in patients with premature CAD. This may indicate the possible role of excessive VWF–platelet interactions in the development of premature CAD.
