抄録
Atrial fibrillation (AF) is the most common sustained arrhythmia and is associated with important morbidity and mortality. AF increases the risk of stroke by a factor of five. Advances in antithrombotic therapy began when traditional anticoagulant agents such as heparin and the vitamin K antagonists (VKAs) like warfarin became commercially available in the 1940s and 1950s. VKAs have well documented limitations, including a delayed onset of action and a poor pharmacokinetic profile, large interindividual dosing differences, a narrow therapeutic index, interactions with dietary vitamin K and a large number of other medications, and the need for constant patient education, patient compliance and frequent follow-up. These limitations make the use of VKAs complex in the clinical setting, creating a burden for patients and healthcare providers. Recent investigation was focused on the identification of small-molecule inhibitors of coagulation enzymes as novel strategy. Two hot targets are the two key serine proteases in the coagulation cascade: thrombin (activated factor IIa), and activated factor X (FXa). The 3 orally active agents in the market are dabigatran (direct thrombin inhibitor, DTI), rivaroxaban (Xa inhibitor), and apixaban (Xa inhibitor). All of them have been shown to be effective in large-scale clinical trials, including RE-LY, ROCKET AF, and AVERROES. It is very clear that we are facing a completely new era of anti-thrombotic therapy in AF.
