Anticoagulants

Anticoagulants reduce the formation or activity of fibrin so that an existing clot is less likely to enlarge and new clots are less likely to form. They do not dissolve a clot that is already present; thrombolytics are the drugs that actively break down selected clots. Antiplatelet drugs act mainly on platelet aggregation, so they are not interchangeable with anticoagulants. The clinical balance is narrow. Too little anticoagulant effect permits venous thromboembolism, embolic stroke, or clot extension. Too much effect, or a normal dose given to a newly vulnerable patient, can produce gastrointestinal, retroperitoneal, intracranial, or other major bleeding. The drug class predicts the monitoring strategy: - Unfractionated heparin and low-molecular-weight heparin enhance antithrombin activity. - Warfarin reduces production of vitamin K–dependent clotting factors II, VII, IX, X and the anticoagulant proteins C and S. - Apixaban, rivaroxaban, and edoxaban inhibit factor Xa directly; fondaparinux inhibits factor Xa indirectly through antithrombin. - Dabigatran inhibits thrombin directly. The first question is therefore not “Is this a blood thinner?” It is “Which haemostatic pathway is being altered, for what reason, and is...