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冠心病患者血管性血友病因子胶原结合活性及血管性血友病因子介导的血小板黏附

Von Willebrand Factor Collagen-Binding Activity and Von Willebrand Factor-Mediated Platelet Adhesion in Patients with Coronary Artery Disease.

作者信息

Gabbasov Zufar, Okhota Sergey, Avtaeva Yuliya, Saburova Olga, Melnikov Ivan, Shtelmakh Valentina, Bazanovich Sergey, Guria Konstantin, Kozlov Sergey

机构信息

Laboratory of Cell Hemostasis, Chazov National Medical Research Centre of Cardiology of the Ministry of Health of the Russian Federation, 121552 Moscow, Russia.

Department of Problems of Atherosclerosis, Chazov National Medical Research Centre of Cardiology of the Ministry of Health of the Russian Federation, 121552 Moscow, Russia.

出版信息

Biomedicines. 2024 Sep 3;12(9):2007. doi: 10.3390/biomedicines12092007.

Abstract

In this study, we investigated von Willebrand factor (VWF)-related parameters in 30 patients with stable coronary artery disease (CAD) and 50 patients without CAD. In both groups, the following were measured: the VWF antigen level (VWF:Ag); the VWF ristocetin cofactor activity (VWF:RCo); the VWF collagen-binding activity (VWF:CB); and VWF-mediated platelet adhesion. Platelet adhesion was measured in whole blood at a shear rate of 1300 s using a microfluidic chamber with a collagen-coated surface. VWF:Ag and VWF:RCo were found to be the same in both groups of patients. However, VWF:CB was found to be lower in patients with CAD compared with patients without CAD, with values of 106.7% (82.1; 131.6) and 160.4% (112.5; 218.1), respectively ( < 0.001). The decrease in platelet adhesion after GPIb inhibition was more pronounced in patients with CAD compared with patients of the control group, with recorded values of 76.0% (60.6; 82.1) and 29.3% (0.0; 60.4), respectively ( < 0.001). After adjusting for traditional risk factors, the odds ratio for CAD was found to be 0.98 (95% CI, 0.97-0.99; = 0.011) per 1% increase in VWF:CB activity, and 1.06 (95% CI, 1.03-1.09; < 0.001) per 1% decrease in GPIb-mediated platelet adhesion. The findings presented in this paper indicate a possible critical role played by complex VWF-collagen-platelet interactions in the development of CAD.

摘要

在本研究中,我们调查了30例稳定型冠状动脉疾病(CAD)患者和50例无CAD患者的血管性血友病因子(VWF)相关参数。在两组中,均测量了以下指标:VWF抗原水平(VWF:Ag);VWF瑞斯托霉素辅因子活性(VWF:RCo);VWF胶原结合活性(VWF:CB);以及VWF介导的血小板黏附。使用具有胶原包被表面的微流控腔室,在剪切速率为1300 s时于全血中测量血小板黏附。发现两组患者的VWF:Ag和VWF:RCo相同。然而,发现CAD患者的VWF:CB低于无CAD患者,其值分别为106.7%(82.1;131.6)和160.4%(112.5;218.1)(<0.001)。与对照组患者相比,CAD患者中糖蛋白Ib(GPIb)抑制后血小板黏附的降低更为明显,记录值分别为76.0%(60.6;82.1)和29.3%(0.0;60.4)(<0.001)。在调整传统危险因素后,发现VWF:CB活性每增加1%,CAD的比值比为0.98(95%置信区间,0.97 - 0.99;P = 0.011),GPIb介导的血小板黏附每降低1%,CAD的比值比为1.06(95%置信区间,1.03 - 1.09;P < 0.001)。本文呈现的研究结果表明,复杂的VWF - 胶原 - 血小板相互作用在CAD的发生发展中可能起关键作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5e1b/11444127/82f31d086411/biomedicines-12-02007-g001.jpg

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