Vilahur Gemma, Fuster Valentin
Research Institute, Hospital de la Santa Creu i Sant Pau, IIB-Sant Pau, Carrer Sant Quintí 77-79, Barcelona 08041, Spain.
CiberCV, Institute Carlos III, Madrid 28029, Spain.
Eur Heart J. 2025 Feb 3;46(5):413-423. doi: 10.1093/eurheartj/ehae776.
Haemostasis refers to the physiological process aimed at repairing vessel injury and preventing bleeding. It involves four interlinked stages culminating in the formation of a platelet-fibrin haemostatic plug that is eventually dissolved once the vessel heals. In contrast, arterial thrombosis is a pathological condition resulting from atheroma exposure, triggering the formation of a platelet-rich thrombus that may obstruct blood flow, leading to the clinical manifestations of ischaemic cardiovascular disease. The following review will provide a comprehensive overview of the finely regulated endogenous antithrombotic mechanisms responsible for maintaining the haemostatic balance and preventing intravascular thrombosis. Thereafter, it will further detail the different stages and mechanisms governing the intricate interplay between the vessel, platelets, and the coagulation cascade in haemostasis, highlighting the most recent advances in platelet biology and function, to further elucidate the differential traits and players contributing to pathological arterial thrombus growth. The review will also delve into the impact of emerging cardiovascular risk factors on tilting the haemostatic balance towards a pro-thrombotic state, thereby increasing the patient's vulnerability to thrombotic events. Finally, it will underscore the importance of early screening for subclinical atherosclerosis through advanced imaging technologies capable of quantifying plaque burden and metabolic activity since they may set the stage for an increased thrombotic risk. Implementing proactive interventions to halt atherosclerosis progression or inducing its regression at early stages is crucial for preserving haemostasis and reducing the likelihood of ischaemic atherothrombotic disease.
止血是指旨在修复血管损伤和防止出血的生理过程。它涉及四个相互关联的阶段，最终形成血小板 - 纤维蛋白止血栓，一旦血管愈合，该止血栓最终会溶解。相比之下，动脉血栓形成是一种病理状态，由动脉粥样硬化斑块暴露引发，导致富含血小板的血栓形成，可能阻塞血流，从而引发缺血性心血管疾病的临床表现。以下综述将全面概述负责维持止血平衡和预防血管内血栓形成的精细调节的内源性抗血栓机制。此后，它将进一步详细阐述止血过程中血管、血小板和凝血级联之间复杂相互作用的不同阶段和机制，突出血小板生物学和功能的最新进展，以进一步阐明促成病理性动脉血栓生长的差异特征和因素。该综述还将深入探讨新兴心血管危险因素对使止血平衡向促血栓形成状态倾斜的影响，从而增加患者发生血栓事件的易感性。最后，它将强调通过能够量化斑块负荷和代谢活性的先进成像技术早期筛查亚临床动脉粥样硬化的重要性，因为它们可能为增加的血栓形成风险奠定基础。实施积极干预措施以阻止动脉粥样硬化进展或在早期诱导其消退对于维持止血和降低缺血性动脉粥样硬化血栓形成疾病的可能性至关重要。
