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Mode of action of heparin and related drugs.

There are three main classes of antithrombotic drugs: Platelet inhibitors, oral anticoagulants, and drugs such as heparin that inhibit activated clotting factors. Oral anticoagulants and heparins are roughly equally effective in preventing venous thrombosis. However, these two families of drugs are essentially different in their mode of action. They each have numerous properties in addition to their anticoagulant action, but for neither of the two has it been demonstrated that it is indeed the anticoagulant action that is responsible for the antithrombotic effect. Yet, the anticoagulant action is the only action that they have in common. Therefore we consider it more likely than not that the anticoagulant property bears some direct relationship to the therapeutic effect. Despite active research on platelet aggregation inhibitors for over 25 years, it is now generally acknowledged that these substances make less effective antithrombotic agents than anticoagulants do.1 It must even be considered a possibility that antiplatelet drugs act via an activation on platelet-induced thrombin formation.' We will therefore discuss the mode of action of heparins and other thrombin scavengers in terms of inhibition of the coagulation process. Neither oral anticoagulants nor heparins are ideal drugs. Oral anticoagulant treatment requires laboratory control and constant expert supervision. Heparin needs frequent administration by injection and side effects are common. Both drugs have a relatively narrow therapeutic window, that is, the gap between the effective dose and the dose that will cause bleeding, is not very wide. This explains why at this moment much active research is spent in finding more efficient antithrombotics. In this article we will discuss those drugs, such as heparin, that are known to scavenge active clotting