Platelets assume the driving seat when it comes to arterial thrombosis. Subsequent to plaque rupture, they adhere to exposed subendothelial agonists, such as collagen and von Willebrand factor (vWF), in order to produce an initial platelet plug. The subendothelial ligands activate platelets, which change in shape and secrete thromboxane A2 (TXA2) and ADP. TXA2 activates platelets further and ADP amplifies and sustains activation through platelet P2Y12 receptors, leading to further expansion of the platelet-rich thrombus (Take home figure). Thrombin is also generated at the site of arterial injury, with activated platelets as well as tissue factor playing dominant roles in this, but pre-clinical data suggest that thrombin may play a greater role in stabilization of the core of the arterial thrombus rather than its expansion. As a result, preventative therapy following acute coronary syndrome (ACS) consists of dual antiplatelet therapy (DAPT) with aspirin and a P2Y12 inhibitor. 3,4

中文翻译：

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左心室血栓患者抗栓治疗的挑战

当涉及到动脉血栓形成时，血小板占据主导地位。斑块破裂后，它们粘附在暴露的内皮下激动剂上，如胶原蛋白和血管性血友病因子 (vWF)，以产生初始血小板栓。内皮下配体激活血小板，血小板改变形状并分泌血栓素 A2 (TXA2) 和 ADP。TXA2 进一步激活血小板，ADP 通过血小板 P2Y12 受体放大并维持激活，导致富含血小板的血栓进一步扩张（带回家图）。凝血酶也在动脉损伤部位产生，活化的血小板和组织因子在这方面起主导作用，但临床前数据表明，凝血酶可能在稳定动脉血栓的核心方面发挥更大的作用，而不是其扩张。因此，急性冠脉综合征 (ACS) 后的预防性治疗包括阿司匹林和 P2Y12 抑制剂的双重抗血小板治疗 (DAPT)。3,4