Stott D J, Spilg E, Campbell A M, Rumley A, Mansoor M A, Lowe G D
Academic Section of Geriatric Medicine, University of Glasgow, Glasgow Royal Infirmary, Glasgow, UK.
Blood Coagul Fibrinolysis. 2001 Dec;12(8):651-7. doi: 10.1097/00001721-200112000-00006.
Abnormalities of coagulation and fibrinolysis may play an important role in the pathogenesis of ischaemic stroke and vascular dementia. We aimed to determine whether haemostatic function is altered in acute recent-onset or chronic ischaemic cerebrovascular disease. We studied consecutive patients with ischaemic stroke (n = 74) and vascular dementia (n = 42) compared with healthy controls (n = 40) in a case-control study. The ischaemic stroke group was assessed twice, 3-10 days after the acute stroke and at 1-3 months. Fibrinogen, fibrin D-dimer (marker of fibrin turnover) and von Willebrand factor (vWF) (marker of endothelial disturbance) were elevated acutely (P < 0.0001) and in the convalescent phase after ischaemic stroke (P < 0.0001, P < 0.0001, and P < 0.01 respectively, compared with controls). Similar results were seen in the vascular dementia group. Stepwise multivariate regression analyses showed that cerebrovascular disease correlated independently with fibrinogen (P < 0.001) and fibrin D-dimer levels (P < 0.001), while vWF correlated independently with electrocardiograph evidence of ischaemic heart disease (P = 0.004). Changes between acute and convalescent phases in ischaemic stroke were slightly inconsistent. However, in the acute stage there were tendencies for fibrinogen, D-dimer and vWF to be increased, and factor VIII was significantly higher. Abnormalities of haemostasis, including increased fibrin turnover and endothelial disturbance, are found in both acute and chronic cerebral ischaemia. Many of these patients have co-existent ischaemic heart disease and this may contribute to some of these changes. Acute ischaemic stroke is associated with transient changes in haemostatic factors; however, most abnormalities persist into the convalescent phase, and are also demonstrable in subjects with vascular dementia.
凝血和纤维蛋白溶解异常可能在缺血性中风和血管性痴呆的发病机制中起重要作用。我们旨在确定在急性近期发病或慢性缺血性脑血管疾病中止血功能是否发生改变。在一项病例对照研究中，我们研究了连续的缺血性中风患者（n = 74）和血管性痴呆患者（n = 42），并与健康对照者（n = 40）进行比较。缺血性中风组在急性中风后3 - 10天和1 - 3个月时进行了两次评估。纤维蛋白原、纤维蛋白D - 二聚体（纤维蛋白周转标志物）和血管性血友病因子（vWF）（内皮功能紊乱标志物）在急性缺血性中风时升高（P < 0.0001），在缺血性中风后的恢复期也升高（与对照组相比，分别为P < 0.0001、P < 0.0001和P < 0.01）。血管性痴呆组也出现了类似结果。逐步多元回归分析表明，脑血管疾病与纤维蛋白原（P < 0.001）和纤维蛋白D - 二聚体水平（P < 0.001）独立相关，而vWF与缺血性心脏病的心电图证据独立相关（P = 0.004）。缺血性中风急性期和恢复期之间的变化略有不一致。然而，在急性期，纤维蛋白原、D - 二聚体和vWF有升高趋势，且因子VIII显著升高。在急性和慢性脑缺血中均发现止血异常，包括纤维蛋白周转增加和内皮功能紊乱。这些患者中有许多同时患有缺血性心脏病，这可能是导致其中一些变化的原因。急性缺血性中风与止血因子的短暂变化有关；然而，大多数异常持续到恢复期，并且在血管性痴呆患者中也可检测到。
