Anticoagulants in Stroke Treatment

Introduction

Anticoagulants continue to play a central role in the prevention of stroke. Unlike thrombolytics, anticoagulants do not degrade clot; rather, they prevent thrombus formation and propagation by reduction of fibrin formation. Anticoagulants act on different steps of the intrinsic and extrinsic coagulation pathways. Unfractionated heparin, low-molecular-weight heparins (LMWHs) and heparinoids are parenteral anticoagulants of rapid onset that act by indirect inhibition of thrombin and factor Xa via antithrombin. Warfarin (coumadin), the most commonly used oral vitamin K antagonist (VKA), inhibits the conversion of oxidized vitamin K epoxide into its reduced form, vitamin K. It diminishes the K-dependent γ-carboxylation of clotting factors II, VII, IX, and X, as well as the naturally occurring endogenous anticoagulant proteins C and S; the full antithrombotic effect of warfarin is not achieved for several days. During the past few years, a number of new oral anticoagulants (NOAC) have been added to the standard anticoagulant armamentarium. These novel anticoagulants selectively target thrombin (factor IIa) or factor Xa, have much more rapid onset (hours), better therapeutic window, and less drug and food interactions than VKAs ( Fig. 167.1 ).