**3. Objectives of anticoagulant therapy**

Anticoagulant therapy is recommended in patients with AF with risk factors for systemic em‐ bolism. The choice of treatment is based on the absolute risk of stroke, the risk of bleeding and the risk/benefit ratios for each patient [14]. The recent development of NOACs, with innova‐ tive mechanisms of action of therapeutic targets in the coagulation could change the current standard anticoagulant drug treatment [15]. The NOACs are orally administered drugs that di‐ rectly inhibit the coagulation steps defined by decreasing or inhibiting thrombin generation of the final enzyme, thrombin. Thrombin (factor IIa) is the end effector of the coagulation cascade that catalyzes the formation of fibrin from plasma fibrinogen. Is the most potent physiological agonist of platelet activation, so it is considered a key therapeutic target in the development of NOACs. The Factor Xa acts as a point of convergence of the intrinsic and extrinsic pathways of coagulation and catalyzes the conversion of prothrombin to thrombin [16,17]. A single mole‐ cule of factor Xa can generate more than 1.000 molecule of thrombin, as a consequence the in‐ hibition of factor Xa can block this process by reducing the activation of coagulation and platelet thrombin mediated. Whether the coagulation cascade is inhibited at the level of throm‐ bin and factor Xa, or even above the sequence, the net result is a decreased activity of thrombin.

The NOACs are characterized by specific inhibition of one of the two key factors in the coag‐ ulation system, factor Xa and thrombin. Dabigatran, MCC977 and AZD0837 acts by directly inhibiting thrombin thus interfere with the first phase (initial phase) and late (amplification / propagation phase) the model based on the coagulation system. Rivaroxaban, apixaban, edoxaban, betrixaban, eribaxaban, LY517717, YM150, TAK-442 and bind to either factor Xa or factor Xa without bound in the prothrombinase complex thus blocking the conversion of prothrombin to thrombin in the early stage (stage start) and end (amplification / propaga‐ tion phase) the model based on the coagulation system.
