Nagao T, Hamamoto M, Kanda A, Tsuganesawa T, Ueda M, Kobayashi K, Miyazaki T, Terashi A
Department of Neurology, Tokyo Metropolitan Tama Geriatric Hospital, Japan.
Stroke. 1995 Aug;26(8):1365-8. doi: 10.1161/01.str.26.8.1365.
It is generally accepted that the coagulation system is activated in ischemic stroke and that platelet activation is involved in the pathogenesis of this disease. However, little is known about how and to what extent platelet activity participates in coagulation system enhancement. We evaluated the hemostatic condition, especially with regard to platelet function and the coagulation system, within 3 days of onset of acute stroke. The study participants were limited to elderly patients with cardioembolic stroke due to nonvalvular atrial fibrillation.
Seventeen elderly patients with acute cardioembolic stroke due to nonvalvular atrial fibrillation were investigated. Within 3 days of stroke onset, beta-thromboglobulin (BTG), platelet factor 4 (PF4), thrombin-antithrombin III complex (TAT), and D-dimer from arterial blood were carefully evaluated in these patients. Blood samples from 19 healthy age- and sex-matched control subjects were also examined.
The two studied markers of platelet activity did not change in the patients or the control subjects, and the between-group differences between the stroke and control groups were not statistically significant (BTG, 43.8 versus 31.9 ng/mL; PF4, 9.06 versus 5.78 ng/mL; respectively). In contrast, the two studied coagulation-system indicators were markedly elevated in the patients compared with the control subjects (TAT, 13.8 versus 3.5 ng/mL, P < .01; D-dimer, 366.3 versus 147.2 ng/mL, P < .01; respectively).
Platelet function was not enhanced in the acute stage of cardioembolic stroke with nonvalvular atrial fibrillation. This result indicates that enhancement of the coagulation system in cardioembolic stroke is not the result of platelet hyperfunction, ie, "platelet-fibrin" thrombi, but rather of "stasis-related" thrombi formation.
普遍认为凝血系统在缺血性卒中时被激活，且血小板活化参与该疾病的发病机制。然而，关于血小板活性如何以及在多大程度上参与凝血系统增强，人们所知甚少。我们评估了急性卒中发病3天内的止血状况，尤其是血小板功能和凝血系统。研究参与者仅限于因非瓣膜性心房颤动导致心源性栓塞性卒中的老年患者。
对17例因非瓣膜性心房颤动导致急性心源性栓塞性卒中的老年患者进行了研究。在卒中发病3天内，仔细评估了这些患者动脉血中的β-血小板球蛋白（BTG）、血小板因子4（PF4）、凝血酶-抗凝血酶III复合物（TAT）和D-二聚体。还检查了19名年龄和性别匹配的健康对照者的血样。
所研究的两种血小板活性标志物在患者和对照者中均未改变，卒中组与对照组之间的组间差异无统计学意义（BTG分别为43.8对31.9 ng/mL；PF4分别为9.06对5.78 ng/mL）。相比之下，与对照者相比，所研究的两种凝血系统指标在患者中显著升高（TAT分别为13.8对3.5 ng/mL，P <.01；D-二聚体分别为366.3对147.2 ng/mL，P <.01）。
非瓣膜性心房颤动的心源性栓塞性卒中急性期血小板功能未增强。这一结果表明，心源性栓塞性卒中时凝血系统的增强不是血小板功能亢进的结果，即“血小板-纤维蛋白”血栓，而是“淤滞相关”血栓形成的结果。
