Novel Anticoagulants for Stroke Prevention in Patients with Atrial Fibrillation

Abstract

Atrial fibrillation (AF) is the most common cardiac arrhythmia that can potentially result in stroke. Vitamin K antagonists (VKA) like warfarin were for many decades the only oral anticoagulants available for stroke prevention in patients with non-valvular atrial fibrillation (AF) at high risk of stroke. Recently, new oral anticoagulants (NOACS) have been introduced that act via direct inhibition of thrombin (dabigatran) or activated factor X (edoxaban, rivaroxaban and apixaban). Unlike VKAs, these anticoagulants do not require routine INR monitoring and posses favorable pharmacological properties. NOACs act rapidly, and have a stable and predictable dose-related anticoagulant effect with few clinically relevant drug-drug interactions. Phase III trials comparing these agents to warfarin for stroke prevention in patients with non-valvular AF demonstrated that they are at least as efficacious and safe as warfarin. Evolution of clinical guidelines to incorporate the new anticoagulants for stroke prevention in non-valvular AF may result in a reduction in the incidence of AF-related strokes. Safe and effective use of these new drugs in clinical practice requires understanding of their distinct pharmacological properties.

Adherence is an optimal factor for maximizing the effective and safe use of oral anticoagulants in patients with atrial fibrillation

“…For selecting OACs, direct oral anticoagulants (DOACs) are preferred over vitamin K antagonists, mostly warfarin, as DOACs result in a lower risk of bleeding and are less affected by time in the therapeutic range (TTR) while securing similar effectiveness when compared with warfarin 7 , 8 . Nevertheless, patients with AF taking anticoagulants need to be carefully observed owing to the increased risk of bleeding 9 – 11 .…”

Profilaxis farmacológica para la prevención de la enfermedad tromboembólica en paciente con enfermedad cerebrovascular

“…Inhibidores del factor XA Los inhibidores del factor Xa se unen directamente al sitio activo del factor Xa, bloqueando así la actividad del factor de coagulación (22) . El Rivaroxaban se administra vía oral, y produce una inhibición reversible, tiene una vida media estimada de 8-10 horas.…”

“…Y Edoxaban cuenta con una vida media de 9-11 horas, además un tercio es eliminado vía renal. (23) Rivaroxaban es un sustrato para la P-glucoproteína, por lo tanto, la administración conjunta con otros inhibidores de P-glucoproteina y CYP3A4 (por ejemplo, ketoconazol) da como resultado una mayor concentraciones farmacológicas de rivaroxaban y por ello, estaría contraindicado su uso (22) .…”

Coagulation and anticoagulation in idiopathic pulmonary fibrosis

“…The direct factor Xa inhibitors, apixaban and rivaroxaban, have efficacy in preventing stroke and other systemic emboli in patients with atrial fibrillation, and in the treatment of VTE [47][48][49]. Factor Xa facilitates the production of thrombin from prothrombin and is increased in fibrotic lung tissue [50].…”