Medizinische Klinik III Kardiologie und Kreislauferkrankungen, Eberhard Karls-Universität Tübingen, Otfried-Muller-Str. 10, 72070 Tübingen, Germany.
Curr Vasc Pharmacol. 2012 Sep;10(5):589-96. doi: 10.2174/157016112801784468.
Platelets and their activation have a pivotal role in the development of atherosclerotic diseases such as acute myocardial infarction (AMI), stroke and peripheral arterial occlusion. Biomarkers of platelet activation are making inroads into clinical studies and may serve as promising agents upstream to established downstream markers of myocardial necrosis such as troponin and creatin kinase. Targeting the degree of platelet activation assessed by the key collagen receptor of platelet activation, glycoprotein VI (GPVI), may have diagnostic and prognostic value for the assessement of high-risk groups of patients with symptomatic coronary artery disease and ischemic stroke and may be worthwhile to help to facilitate clinical decision-making and to rapidly initiate adequate therapy. The concert of platelet count, platelet activation, platelet aggregation and subsequent inflammation has had a significant impact on the clinical outcome in patients with atherosclerotic diseases. For a therapeutical approach to ameliorate prognosis, the use of antiplatelet treatment in particular in AMI patients with low response to clopidogrel has partly been overcome by novel second antiplatelet drugs on top of aspirin such as prasugrel and ticagrelor. Antiplatelet therapy may be adapted according to a GPVI-based platelet activity monitoring along with aggregometry of residual platelet aggregation. Other approaches using protease-activated receptor- 1 antagonists vorapaxar or atopaxar, which inhibit the platelet thrombin receptor, soluble GPVI called Revacept©, which blocks the collagen binding sites at the vascular lesion and anopheline saliva protein derived from the malaria vector mosquito, a platelet adhesion inhibitor independent of a GPVI mechanism, still wait for their breakthrough.
血小板及其激活在动脉粥样硬化疾病（如急性心肌梗死（AMI）、中风和外周动脉闭塞）的发展中起着关键作用。血小板激活的生物标志物正在进入临床研究，并可能作为有前途的药物，作用于心肌坏死的既定下游标志物（如肌钙蛋白和肌酸激酶）之前。通过评估血小板激活的关键胶原受体糖蛋白 VI（GPVI）来靶向血小板激活程度，可能对评估有症状的冠状动脉疾病和缺血性中风高危患者具有诊断和预后价值，并可能有助于帮助临床决策和快速启动适当的治疗。血小板计数、血小板激活、血小板聚集和随后的炎症之间的协同作用对动脉粥样硬化疾病患者的临床结局产生了重大影响。为了改善预后，除了阿司匹林之外，在对氯吡格雷反应不佳的 AMI 患者中使用新型抗血小板药物（如普拉格雷和替卡格雷）部分克服了抗血小板治疗。根据基于 GPVI 的血小板活性监测和残留血小板聚集的聚集度，可以调整抗血小板治疗。其他方法包括使用蛋白酶激活受体-1 拮抗剂 vorapaxar 或 atopaxar，它们抑制血小板血栓素受体，可溶性 GPVI 称为 Revacept©，它阻断血管病变处的胶原结合位点，以及来源于疟疾病媒蚊子的按蚊唾液蛋白，一种独立于 GPVI 机制的血小板黏附抑制剂，仍在等待它们的突破。
