Changes induced by venous occlusion on coagulation and fibrinolysis.

3412 Local intra-arterial fibrinolysis for central venous occlusion

A poor anticoagulant response to activated protein C (APC r&stance) induced hy the ArglGln8g8 mutation of the Factor V gene is, in ssversl countries, the most oommon genetic defect sssootatsd with thmmbophilic disorders. Frequencies of APC resistance between 2050% have teen observed in pstients with deep venous thrombosis, SugQedinQ the importance of the Pmtein C System acttvity. Also, in other...

Inhibition of Fibrinolysis by Coagulation Factor XIII

The inhibitory effect of coagulation factor XIII (FXIII) on fibrinolysis has been studied for at least 50 years. Our insight into the underlying mechanisms has improved considerably, aided in particular by the discovery that activated FXIII cross-links α2-antiplasmin (α2AP) to fibrin. In this review, the most important effects of different cross-linking reactions on fibrinolysis are summarized....

Coagulation and fibrinolysis after injury.

Blood coagulation, fibrinolysis and exercise.

Blood Coagulation, Fibrinolysis and Cellular Haemostasis Introduction

A high plasma concentration of coagulation factor VIII (FVIII) is an important risk factor for venous thromboembolism (VTE) (1-4). In the Leiden Thrombophilia study for example, FVIII levels above 1500 IU/L conferred an almost 5-fold risk for a first episode of deep-vein thrombosis (1). Most importantly, high FVIII is also associated with a very high risk of recurrent venous thromboembolism (4,...