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The evolution of direct thrombin inhibitors has significantly improved outcomes in patients with ischemic heart disease. These agents are designed to bind thrombin and block its procoagulant activity. Thrombin is a serine protease which can be activated by 2 different pathways: the coagulation pathway and the platelet activation pathway. Activation of the coagulation pathway occurs in the so-called common pathway and results in the formation of the prothrombinase complex. Thrombin can be activated by this complex via the so-called contact pathway in the presence of factor Xa, factor VIIa, and tissue factor. The platelet activation pathway is initiated by the binding of thrombin to its receptor. Excessively high thrombin concentrations have been suggested to contribute to the development of AF. Although the exact mechanism is unclear, there is evidence that thrombin can lead to the generation of ROS. Hence, thrombin has been implicated in endothelial dysfunction and cardiac arrhythmia in patients with AF. Three thrombin inhibitors have been approved for the treatment of AF: dabigatran, rivaroxaban, and apixaban. The mechanism of action of these agents is similar to that of warfarin. This allows for a lower daily dose of warfarin to be administered in comparison with the warfarin dose required to achieve a similar degree of anticoagulation with warfarin alone. Several trials have shown that these agents are well tolerated and are effective in the prevention of thromboembolism associated with AF, especially if given in combination with ASA. A meta-analysis of 3 randomized, double-blind, placebo-controlled trials has shown that the use of direct thrombin inhibitors to reduce the incidence of stroke in patients with AF is superior to warfarin in terms of major bleeding events, intracranial hemorrhage, and death. A recently published trial has shown that rivaroxaban did not significantly reduce the incidence of stroke or death in comparison with placebo among patients with AF on warfarin. However, more aggressive anticoagulation with rivaroxaban may be indicated in the future when anticoagulation treatment, particularly with warfarin, is not adequate to prevent thromboembolism in patients with AF. More data are needed to establish whether dabigatran can be used to dose warfarin in patients with AF. Trials comparing the direct thrombin inhibitors with warfarin or a vitamin K antagonist are in progress.
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