Avtor/Urednik		Anžej, Saša; Božič, Mojca; Antovič, Aleksandra; Peternel, Polona; Gašperšič, Nataša; Rot, Uroš; Tratar, Gregor; Stegnar, Mojca
Naslov		Evidence of hypercoagulability and inflammation in young patients long after acute cerebral ischaemia
Tip		članek
Vir		Thromb Res
Vol. in št.		Letnik 120, št. 1
Leto izdaje		2007
Obseg		str. 39-46
Jezik		eng
Abstrakt		Introduction: 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. Materials and methods: 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. Results: 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. Conclusions: 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.
Deskriptorji		ACUTE DISEASE ADULT BLOOD COAGULATION DISORDERS BLOOD COAGULATION TESTS CASE-CONTROL STUDIES HEMOSTASIS INFLAMMATION INFLAMMATION MEDIATORS TIME FACTORS