Anzej Sasa, Bozic Mojca, Antovic Aleksandra, Peternel Polona, Gaspersic Natasa, Rot Uros, Tratar Gregor, Stegnar Mojca
Department of Vascular Diseases, University Medical Centre, Zaloska 7, 1525 Ljubljana, Slovenia.
Thromb Res. 2007;120(1):39-46. doi: 10.1016/j.thromres.2006.08.005. Epub 2006 Oct 10.
Young subjects with acute cerebral ischaemia - stroke or transient ischaemic attack - form an etiologically heterogeneous and often not clearly explained group of patients. The aim was to investigate possible disturbances in haemostasis and inflammation long after an acute cerebral ischaemic event.
Forty-four consecutive patients referred after having suffered from acute cerebral ischaemia before the age of 45 participated 1 to 9 years (median value 5 years) after the event. At the time of blood sampling 33 (75%) patients were receiving antithrombotic treatment. Forty-six apparently healthy subjects of the same age group served as controls. In all subjects global haemostasis parameters (overall haemostasis, coagulation and fibrinolytic potential), thrombophilia, several markers of haemostasis activation and inflammation were determined.
Patients did not differ from controls in most of the conventional risk factors and the presence of most forms of thrombophilia, although in seven (17.5%) patients the weak presence of lupus anticoagulants was observed. Patients had significantly increased overall haemostasis and coagulation potential, increased soluble P-selectin and D-dimer, decreased overall fibrinolysis potential and increased fibrinogen and C-reactive protein compared to controls. The subgroups of patients receiving antiplatelet treatment, with thrombophilia and recurrent acute cerebral ischaemia, did not differ significantly from the other patients.
In young patients long after acute cerebral ischaemia an imbalance in the haemostatic system and a minor, but significant degree of inflammation was detected. The mechanisms behind haemostatic imbalance seem to be enhanced thrombin generation, platelet activation and depressed fibrinolysis.
患有急性脑缺血（中风或短暂性脑缺血发作）的年轻患者构成了一组病因异质性且往往解释不清的患者群体。本研究旨在调查急性脑缺血事件发生很久之后可能出现的止血和炎症紊乱情况。
44例45岁之前曾患急性脑缺血的连续患者在事件发生后1至9年（中位值5年）参与了研究。在采血时，33例（75%）患者正在接受抗血栓治疗。46例同年龄组的明显健康受试者作为对照。对所有受试者测定了整体止血参数（整体止血、凝血和纤溶潜力）、易栓症、几种止血激活和炎症标志物。
患者在大多数传统危险因素和大多数形式的易栓症方面与对照组无差异，不过在7例（17.5%）患者中观察到存在弱阳性狼疮抗凝物。与对照组相比，患者的整体止血和凝血潜力显著增加，可溶性P选择素和D - 二聚体增加，整体纤溶潜力降低，纤维蛋白原和C反应蛋白增加。接受抗血小板治疗、患有易栓症和复发性急性脑缺血的患者亚组与其他患者无显著差异。
在急性脑缺血很久之后对年轻患者进行检测发现，其止血系统失衡，且存在轻微但显著程度的炎症。止血失衡背后的机制似乎是凝血酶生成增加、血小板激活和纤溶抑制。
