Learn why most AF patients, other than those at very low stroke risk, should receive anticoagulants.
The coagulation cascade (Figure 19) refers to a series of enzymatic reactions that begins when damage to the endothelium of a blood vessel exposes circulating platelets to collagen in the wall and plasma factor VII/VIIa to extravascular tissue factor. Other proteins (including von Willebrand factor) help platelets bind to the damaged vessel wall. The complex between tissue factor VIIa – the ‘extrinsic pathway’ – activates the coagulation cascade.39
Thrombus development depends on additional platelets and amplification of the coagulation cascade by the intrinsic pathway, which includes factors VIII and IX. Platelets amplify the coagulation cascade by providing a surface that stimulates thrombosis.39 Thrombin (factor II) promotes platelet activation. In turn, platelet activation facilitates further thrombin generation. Thrombin also activates multiple factors in the coagulation cascade, including production of fibrinogen from fibrin, which stabilises the thrombus.39,40
Anticoagulants act on critical steps in the cascade to prevent thrombus formation. This Learning Zone introduces the two classes of anticoagulants used in AF management: vitamin K antagonists and DOACs. The ESC/EHRA guidelines recommend that most AF patients, other than those at very low stroke risk, should receive anticoagulants.5 Another section in this Learning Zone, outlines the detailed European guidelines and American recommendations regarding anticoagulation in AF patients.Learn about warfarin in the next section
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