Poredoš Pavel
Department of Vascular Diseases, Ljubljana University Medical Centre, Ljubljana, Slovenia -
Int Angiol. 2017 Aug;36(4):295-298. doi: 10.23736/S0392-9590.17.03820-2. Epub 2017 Mar 6.
In the past, arterial and venous thrombosis have been accepted as two completely different diseases. Recently, the thesis of two separate pathogenetic mechanisms of venous and arterial thrombosis has been challenged by accumulation of evidence which suggest that patients with atherothrombosis are at increased risk for venous thrombosis. Pathophysiological studies indicated that etiopathogenetic mechanisms of both diseases are similar and that coagulation and platelet activation participate in both venous and arterial thrombogenesis. Inflammation most probably represents the basic etiopathogenetic mechanism of arterial as well as venous thromboembolic disease, being a common mechanism through which different risk factors trigger thrombus formation in both veins and arteries. Atherothrombosis is accepted as a chronic inflammatory disease and the association between circulating inflammatory markers and venous thromboembolism also indicates an involvement of the inflammatory process in venous thrombosis. During inflammation, there is an increase in the production of procoagulant factors, a down-regulation of the anticoagulant mechanisms and an inhibition of the endogenic fibrinolytic activity. In line with the arguments which support the link between arterial and venous thrombosis is also the recognition that different risk factors are common in both diseases, such as age, metabolic syndrome, hypercholesterolemia and thrombophilia. A relation was also found between subjects with preclinical or clinical atherosclerotic disease and venous thromboembolism. These findings indicate close interrelationship between arterial atherothrombotic and venous thromboembolic disease. It could mean that atherosclerosis may induce venous thrombosis or that these two diseases have common risk factors which promote the development of both diseases.
过去，动脉血栓形成和静脉血栓形成一直被认为是两种完全不同的疾病。最近，静脉和动脉血栓形成的两种独立发病机制的观点受到了越来越多证据的挑战，这些证据表明动脉粥样硬化血栓形成患者发生静脉血栓形成的风险增加。病理生理学研究表明，这两种疾病的病因发病机制相似，凝血和血小板激活参与了静脉和动脉血栓形成过程。炎症很可能是动脉和静脉血栓栓塞性疾病的基本病因发病机制，是不同危险因素在静脉和动脉中触发血栓形成的共同机制。动脉粥样硬化血栓形成被被认为是一种慢性炎症性疾病，循环炎症标志物与静脉血栓栓塞之间的关联也表明炎症过程参与了静脉血栓形成。在炎症过程中，促凝血因子的产生增加，抗凝机制下调，内源性纤维蛋白溶解活性受到抑制。支持动脉和静脉血栓形成之间存在联系的观点还包括认识到这两种疾病有一些共同的危险因素，如年龄、代谢综合征、高胆固醇血症和血栓形成倾向。在患有临床前或临床动脉粥样硬化疾病的受试者与静脉血栓栓塞之间也发现了一种关联。这些发现表明动脉粥样硬化血栓形成疾病和静脉血栓栓塞性疾病之间存在密切的相互关系。这可能意味着动脉粥样硬化可能诱发静脉血栓形成，或者这两种疾病有共同的危险因素促进了这两种疾病的发展。
