Is there a hypercoagulable phase during initiation of antithrombotic therapy with oral anticoagulants in patients with atrial fibrillation?
BACKGROUND
During commencement of oral anticoagulant therapy (OAT) a theoretical possibility of a transient hypercoagulable state emerges from the difference in plasma half-life between the vitamin K-dependent pro-coagulation factors II and X, and the vitamin K-dependent anticoagulant proteins C and S. In the present study, markers reflecting the activity in the haemostatic system (prothrombin fragment 1+2 [F1+2], D-dimer and soluble fibrin) was assessed during initiation of OAT compared to subcutaneously administered low-molecular weight heparin (LMWH) which does not cause any imbalance between the concentrations of the pro- and anticoagulation proteins.


METHODS
Thirty-three patients with atrial fibrillation were randomly treated either with OAT (warfarin 10, 7.5, and 5 mg for three consecutive days) or LMWH administered in a fixed dose of 200 anti-Xa IU/kg body weight in one subcutaneous injection daily. The biochemical markers were measured at baseline, and after 12, 36 and 60 h of treatment.


CONCLUSIONS
After introducing antithrombotic therapy, none of the biochemical markers increased within the study period in the two treatment groups. The level of F1+2 had declined significantly at 60 h in both groups. The level of soluble fibrin showed a significant decrease within the first 60 h in the OAT group, and no significant changes were seen in the LMWH group. No significant change in the level of D-dimer was seen during the first 60 h of treatment in either group. Taken together, no transient hypercoagulable state could be identified within the first 60 h of commencing OAT in patients with atrial fibrillation.
Zeuthen
Elisabeth L
EL
Department of Internal Medicine and Cardiology, Aarhus Amtssygehus, Aarhus University Hospital, Tage Hansensgade 2, DK-8000 Arhus, Denmark. elz@dadlnet.dk
Lassen
Jens F
JF
Husted
Steen E
SE
D000284:Administration, Oral; D000368:Aged; D001281:Atrial Fibrillation / Q000097:blood* / Q000150:complications; D015415:Biomarkers; D001779:Blood Coagulation Factors / Q000378:metabolism; D017985:Dalteparin / Q000008:administration & dosage / Q000494:pharmacology / Q000627:therapeutic use*; D005260:Female; D005337:Fibrin / Q000032:analysis; D005338:Fibrin Fibrinogen Degradation Products / Q000032:analysis; D005343:Fibrinolytic Agents / Q000008:administration & dosage / Q000494:pharmacology / Q000627:therapeutic use*; D006207:Half-Life; D006801:Humans; D008297:Male; D008875:Middle Aged; D010446:Peptide Fragments / Q000032:analysis; D011516:Prothrombin / Q000032:analysis; D020521:Stroke / Q000517:prevention & control; D019851:Thrombophilia / Q000188:drug therapy / Q000209:etiology*; D013997:Time Factors; D014812:Vitamin K / Q000502:physiology; D014859:Warfarin / Q000008:administration & dosage / Q000494:pharmacology / Q000627:therapeutic use*
D015415:Biomarkers; D001779:Blood Coagulation Factors; D005338:Fibrin Fibrinogen Degradation Products; D005343:Fibrinolytic Agents; D010446:Peptide Fragments; C036309:fibrin fragment D; C045879:prothrombin fragment 1.2; D014812:Vitamin K; D014859:Warfarin; D011516:Prothrombin; D005337:Fibrin; D017985:Dalteparin