title: [Hemostatic abnormalities in ischemic stroke].
abstract: The authors studied whether haemostatic abnormalities connected with the development of cerebral circulatory disturbances can be demonstrated in young stroke patients in whom Doppler and angiographic examination failed to reveal deviations indicative of stroke. They determined the in vivo activation of the coagulation system (TAT, F 1 + 2), the degree of secondary fibrinolysis (D-dimer), the plasma levels of the markers of fibrinolysis, with special regard to inhibitors: plasminogen activator inhibitor (PAI-1), alpha 2 antiplasmin (alpha 2 AP), alpha 2 macroglobulin (alpha 2 M), the frequency of pathologic serum lipoprotein (a)-Lp(a)-values and the association of PAI-1 and Lp(a) with the fibrinolytic system. They conclude that in the acute phase of the disease, the TAT and F 1 + 2 values were significantly elevated compared to the control, without change in the D-dimer value. The results suggest that in the tested period increased thrombin generation dominated and it significantly surpassed plasmin activity since the D-dimer values of that period did not indicate substantial increase in secondary fibrinolysis. The results of the study were separately analyzed in acute, chronic TIA and stroke groups. In the TIA and acute group the F 1 + 2 values, while in stroke the TAT values were more elevated. The in vitro fibrinolytic capacity of the patients significantly decreased compared to controls, showing significant correlation with the Lp(a) level, but not with the PAI value. Examination of the marker molecules renders possible to assess the degree of hypercoaguability and of endogenous lysis. Their knowledge is held important for judging the progression of the disease and the therapeutic consequences.
authors.affiliation: Debreceni Orvostudományi Egyetem Neurológiai Klinika, Klinikai Biokémiai és Molekuláris Patológiai Intézet.
authors.forename: M
authors.initials: M
authors.lastname: Misz
authors.forename: L
authors.initials: L
authors.lastname: Oláh
authors.forename: J
authors.initials: J
authors.lastname: Kappelmayer
authors.forename: G
authors.initials: G
authors.lastname: Blaskó
authors.forename: M
authors.initials: M
authors.lastname: Udvardy
authors.forename: I
authors.initials: I
authors.lastname: Fekete
authors.forename: T
authors.initials: T
authors.lastname: Csépány
authors.forename: E
authors.initials: E
authors.lastname: Ajzner
authors.forename: L
authors.initials: L
authors.lastname: Csiba
mesh_terms: D000328:Adult; D000933:Antifibrinolytic Agents / Q000627:therapeutic use*; D001778:Blood Coagulation Disorders / Q000188:drug therapy / Q000209:etiology; D002545:Brain Ischemia / Q000150:complications / Q000188:drug therapy / Q000209:etiology*; D002561:Cerebrovascular Disorders / Q000188:drug therapy / Q000209:etiology*; D005260:Female; D006487:Hemostasis; D006801:Humans; D008297:Male; D008875:Middle Aged; D009422:Nervous System Diseases / Q000209:etiology
chemical_list: D000933:Antifibrinolytic Agents