BACKGROUND: A hypercoagulable state is often associated with an acute stroke in cerebrovascular disease (CVD). However, in Binswanger disease (BD), no information is available on the coagulation-fibrinolysis pathway except for the presence of high plasma fibrinogen levels. OBJECTIVE: To determine the association of BD and coagulation-fibrinolysis pathway activation. PATIENTS AND METHODS: We examined the levels of fibrinogen, thrombin-antithrombin complex, prothrombin fragment(1+2), and cross-linked D-dimer in 17 patients with BD, 24 neurologic patients without CVD, and 26 patients with lacunar infarction in either the acute or chronic stage. RESULTS: As compared with the non-CVD and lacunar infarction groups, the patients with BD had significantly elevated levels of thrombin-antithrombin complex (P<.001), prothrombin fragment(1+2) (P<.05), and cross-linked D-dimer (P<.01). There was also a significant increase in fibrinogen levels compared with the non-CVD group (P<.05). In the BD group, 8 patients in stable condition (ie, those without obvious neurologic deficits in the past 3 months) showed normal levels or a mild increase in their fibrinogen, thrombin-antithrombin complex, prothrombin fragment(1+2), or cross-linked D-dimer levels. In contrast, 9 patients with BD with a subacute aggravation of their focal or subcortical cerebral functions (deteriorating group) showed a significant increase in their thrombin-antithrombin complex levels compared with the stable patients (P<.01). Similarly, the fibrinogen, prothrombin fragment(1+2), and cross-linked D-dimer levels were elevated in the deteriorating patients, but this trend did not reach statistical significance. CONCLUSIONS: These results indicate that the coagulation-fibrinolysis pathway is activated in patients with BD with a subacute aggravation. Coagulation activation may result in the formation of microthrombi and microcirculatory disturbances in the brains of these patients, and thus promote further biological and neurologic insults.
BACKGROUND: A hypercoagulable state is often associated with an acute stroke in cerebrovascular disease (CVD). However, in Binswanger disease (BD), no information is available on the coagulation-fibrinolysis pathway except for the presence of high plasma fibrinogen levels. OBJECTIVE: To determine the association of BD and coagulation-fibrinolysis pathway activation. PATIENTS AND METHODS: We examined the levels of fibrinogen, thrombin-antithrombin complex, prothrombin fragment(1+2), and cross-linked D-dimer in 17 patients with BD, 24 neurologic patients without CVD, and 26 patients with lacunar infarction in either the acute or chronic stage. RESULTS: As compared with the non-CVD and lacunar infarction groups, the patients with BD had significantly elevated levels of thrombin-antithrombin complex (P<.001), prothrombin fragment(1+2) (P<.05), and cross-linked D-dimer (P<.01). There was also a significant increase in fibrinogen levels compared with the non-CVD group (P<.05). In the BD group, 8 patients in stable condition (ie, those without obvious neurologic deficits in the past 3 months) showed normal levels or a mild increase in their fibrinogen, thrombin-antithrombin complex, prothrombin fragment(1+2), or cross-linked D-dimer levels. In contrast, 9 patients with BD with a subacute aggravation of their focal or subcortical cerebral functions (deteriorating group) showed a significant increase in their thrombin-antithrombin complex levels compared with the stable patients (P<.01). Similarly, the fibrinogen, prothrombin fragment(1+2), and cross-linked D-dimer levels were elevated in the deteriorating patients, but this trend did not reach statistical significance. CONCLUSIONS: These results indicate that the coagulation-fibrinolysis pathway is activated in patients with BD with a subacute aggravation. Coagulation activation may result in the formation of microthrombi and microcirculatory disturbances in the brains of these patients, and thus promote further biological and neurologic insults.
Authors: Francesco Arba; Benedetta Piccardi; Vanessa Palumbo; Betti Giusti; Patrizia Nencini; Anna Maria Gori; Alice Sereni; Mascia Nesi; Giovanni Pracucci; Giorgio Bono; Paolo Bovi; Enrico Fainardi; Domenico Consoli; Antonia Nucera; Francesca Massaro; Giovanni Orlandi; Francesco Perini; Rossana Tassi; Maria Sessa; Danilo Toni; Rosanna Abbate; Domenico Inzitari Journal: Transl Stroke Res Date: 2018-04-23 Impact factor: 6.829
Authors: Mihail V Pokrovskiy; Mihail V Korokin; Svetlana A Tsepeleva; Tatyana G Pokrovskaya; Vladimir V Gureev; Elena A Konovalova; Oleg S Gudyrev; Vladimir I Kochkarov; Liliya V Korokina; Eleonora N Dudina; Anna V Babko; Elena G Terehova Journal: Int J Hypertens Date: 2011-06-15 Impact factor: 2.420
Authors: Brittney L Blevins; Harry V Vinters; Seth Love; Donna M Wilcock; Lea T Grinberg; Julie A Schneider; Rajesh N Kalaria; Yuriko Katsumata; Brian T Gold; Danny J J Wang; Samantha J Ma; Lincoln M P Shade; David W Fardo; Anika M S Hartz; Gregory A Jicha; Karin B Nelson; Shino D Magaki; Frederick A Schmitt; Merilee A Teylan; Eseosa T Ighodaro; Panhavuth Phe; Erin L Abner; Matthew D Cykowski; Linda J Van Eldik; Peter T Nelson Journal: Acta Neuropathol Date: 2020-10-24 Impact factor: 17.088