U.O. di Diagnostica Ematochimica, Dipartimento di Patologia e Medicina di Laboratorio, Azienda Ospedaliero-Universitaria di Parma, Via Gramsci, 14, 43126, Parma, Italy.
J Thromb Thrombolysis. 2012 Oct;34(3):367-73. doi: 10.1007/s11239-012-0748-0.
Arterial thrombosis is the leading causes of morbidity and mortality worldwide, whereas venous thrombosis is the most common preventable cause of hospital death. In either case, venous and arterial thrombosis should be considered autonomous entities, with only minor overlaps in terms of risk factors, predisposing conditions and pathogenesis. Besides the widespread perception of embolization originating from low-pressure venous system and triggering ischemic stroke or peripheral arterial occlusion, "paradoxical" thrombosis might also develop or occur within clinical or biological circumstances where the blood should be less predisposed to clot, and wherein this risk is mostly unpredictable or overlooked. In this article we review epidemiological evidence and potential pathogenetic mechanisms of paradoxical thrombosis developing during antithrombotic therapy with vitamin K antagonists and heparin (i.e. heparin-induced thrombocytopenia), or antiplatelet agents such as aspirin, glycoprotein IIb/IIIa inhibitors or clopidogrel, and mostly attributable to direct effect of the agent.
动脉血栓形成是全球发病率和死亡率的主要原因，而静脉血栓形成是医院死亡的最常见可预防原因。在这两种情况下，静脉血栓形成和动脉血栓形成都应被视为独立的实体，只有在危险因素、易患条件和发病机制方面有一些微小的重叠。除了人们普遍认为的源自低压静脉系统的栓塞会引发缺血性中风或外周动脉闭塞之外，“矛盾性”血栓也可能在血液不太容易形成血栓的临床或生物学情况下发展或发生，而这种风险大多是不可预测或被忽视的。在本文中，我们回顾了在使用维生素 K 拮抗剂和肝素（即肝素诱导的血小板减少症）或抗血小板药物（如阿司匹林、糖蛋白 IIb/IIIa 抑制剂或氯吡格雷）进行抗血栓治疗期间发生矛盾性血栓形成的流行病学证据和潜在发病机制，这些主要归因于药物的直接作用。
