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Low‐dose warfarin decreases coagulability without affecting prothrombin complex activity
Author(s) -
HOLM J.,
BERNTORP E.,
CARLSSON R.,
ERHARDT L.
Publication year - 1993
Publication title -
journal of internal medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.625
H-Index - 160
eISSN - 1365-2796
pISSN - 0954-6820
DOI - 10.1111/j.1365-2796.1993.tb00747.x
Subject(s) - medicine , warfarin , aspirin , factor vii , coagulation , anticoagulant , prothrombin time , protein s , protein c , prothrombin complex concentrate , coagulation cascade , myocardial infarction , thrombin , pharmacology , endocrinology , atrial fibrillation , platelet
. Objectives . To asses the efficacy of a fixed, low dose of warfarin in lowering factor VII coagulant activity (FVII: C) and to investigate the effects on the plasma coagulation cascade. Design . An open pilot study with two dose levels of warfarin: 1.25 and 2.5 mg day −1 during two consecutive 4‐week periods. All subjects received aspirin 75 mg day −1 . Prothrombin fragment 1 + 2 (F (1 + 2) ), protein C, protein S, FVII:C, factor X and P‐prothrombin complex activity (P‐PT) were measured at baseline, at 2‐week intervals and 4 weeks after end of treatment. Coagulation activation peptide F (1 + 2) was used as a marker of thrombin formation [13]. Subjects . Twelve male patients with a history of myocardial infarction. Inclusion was made through a written questionnaire. Results . Warfarin 1.25 mg day −1 lowered FVII:C from 113 U dl −1 to 107 U dl −1 ( P = 0.025) and F (1 + 2) from 1.60 nmol l −1 to 1.27 nmol l −1 ( P = 0.013) but had no effect on protein C or P‐PT. A dose of 2.5 mg day −1 induced further lowering of FVII:C (91 U dl −1 , P = 0.0042), and also of protein C from 116% to 99% ( P = 0.034) and P‐PT from 107% to 81% ( P = 0.0096) mean values. Conclusion . Warfarin 1.25 mg day −1 seems to exert an anticoagulant effect without reduction in PT or the natural anticoagulant protein C and is suggested, in combination with aspirin, to be a safe and simple therapy against arterial thrombotic disease, making regular PT controls unnecessary.