Department of Cardiology, Deutsches Herzzentrum München, Technische Universität München, Munich, Germany.
AdvanceCOR GmbH, Martinsried, Germany.
Thromb Haemost. 2024 Apr;124(4):297-306. doi: 10.1055/s-0043-1772221. Epub 2023 Aug 17.
Glycoprotein VI (GPVI) is the major platelet-specific collagen receptor. GPVI shedding with generation of soluble GPVI (sGPVI) is an endogenous feedback mechanism preventing platelet overstimulation. sGPVI has not been investigated in patients with chronic coronary syndrome (CCS) undergoing percutaneous coronary intervention (PCI), especially regarding its potential value as a predictor of ischemic and bleeding risk.
Baseline plasma sGPVI levels were available in 318 patients with CCS undergoing PCI. Platelet function was assessed by measuring both adenosine diphosphate (ADP) and collagen-induced platelet aggregation. Co-primary endpoints were a composite of death or myocardial injury at 48 hours after PCI, and Bleeding Academic Research Consortium (BARC) type 1 to 5 bleeding at 30 days.
There was no significant correlation between sGPVI and platelet function at baseline or at 48 hours after PCI and loading with antiplatelet drugs. Baseline plasma sGPVI levels were not associated with the ischemic risk: the incidence of the ischemic endpoint was 25.0% in the lower, 22.9% in the middle, and 26.7% in the upper sGPVI tertile ( = 0.82). There was a significant nonlinear relationship between sGPVI and the risk of bleeding: the incidence of the bleeding endpoint was 11.8% in the lower, 12.6% in the middle, and 26.4% in the upper sGPVI tertile ( = 0.006).
In patients with CCS undergoing PCI, plasma levels of sGPVI did not correlate with ADP- or collagen-induced platelet aggregation. Patients with higher baseline levels of sGPVI may carry an increased risk of bleeding at 30 days after PCI but no excess risk of ischemic events.
糖蛋白 VI(GPVI)是血小板特异性胶原受体。GPVI 的脱落及其产生的可溶性 GPVI(sGPVI)是一种内源性反馈机制,可防止血小板过度刺激。在接受经皮冠状动脉介入治疗(PCI)的慢性冠状动脉综合征(CCS)患者中,尚未对 sGPVI 进行研究,特别是关于其作为缺血和出血风险预测因子的潜在价值。
318 例接受 PCI 的 CCS 患者的基线血浆 sGPVI 水平可用。通过测量二磷酸腺苷(ADP)和胶原诱导的血小板聚集来评估血小板功能。主要复合终点为 PCI 后 48 小时内死亡或心肌损伤,以及 30 天内 BARC 1 至 5 型出血。
sGPVI 与基线或 PCI 后 48 小时的血小板功能以及抗血小板药物的负荷之间没有显著相关性。基线血浆 sGPVI 水平与缺血风险无关:较低 sGPVI 三分位组的缺血终点发生率为 25.0%,中等 sGPVI 三分位组为 22.9%,较高 sGPVI 三分位组为 26.7%(=0.82)。sGPVI 与出血风险之间存在显著的非线性关系:较低 sGPVI 三分位组的出血终点发生率为 11.8%,中等 sGPVI 三分位组为 12.6%,较高 sGPVI 三分位组为 26.4%(=0.006)。
在接受 PCI 的 CCS 患者中,sGPVI 的血浆水平与 ADP 或胶原诱导的血小板聚集无关。基线 sGPVI 水平较高的患者在 PCI 后 30 天可能有更高的出血风险,但缺血事件的风险没有增加。