Overview of warfarin
Warfarin inhibits the production of functional vitamin K–dependent coagulation factors II, VII, IX and X, and the anticoagulant proteins C and S. When starting warfarin, there is a delay in achieving therapeutic anticoagulation because it takes several days for circulating coagulation factors to decrease. Additionally, the rapid fall in protein C and S levels causes an initial increase in prothrombotic potential. Therefore, when starting warfarin for an indication that requires immediate anticoagulant effect (eg treatment of acute venous thromboembolism), concurrent therapy with a parenteral anticoagulant is needed until warfarin achieves a therapeutic effect. In patients at high thromboembolic event risk (eg mechanical heart valves, antiphospholipid syndrome), consider concurrent therapy with a parenteral anticoagulant at the start of warfarin treatment (until the international normalised ratio [INR] is therapeutic), as well as during treatment if the INR becomes subtherapeutic (eg if interruption of warfarin treatment is needed for a procedure or a bleed).
When immediate anticoagulant effect is not required (eg stroke prevention for patients with permanent atrial fibrillation), start warfarin without concurrent parenteral therapy.
Phenindione is another vitamin K antagonist. It is occasionally used for patients that are intolerant of warfarin1.