Increased thrombin–antithrombin III complex during an episode of paroxysmal atrial fibrillation

Coagulation Activity is Increased in the Left Atria of Patients With Paroxysmal Atrial Fibrillation During the Non-Paroxysmal Period Comparison With Chronic Atrial Fibrillation

“…10,18,19 Yamaji et al speculated that the development of hypercoagulability is related to enlargement of the left atrium, 19 which results in the secretion of atrionatriuretic hormone and increased hematocrit. Iga et al hypothesized that a sudden loss of the atrial booster function causes stagnation of blood in both atria and activates the coagulation system.…”

“…Iga et al hypothesized that a sudden loss of the atrial booster function causes stagnation of blood in both atria and activates the coagulation system. 18 However, those previous studies were conducted using peripheral blood samples and the samples were obtained during the paroxysmal period, and it was therefore unclear whether the LA plays a role in the hypercoagulability in patients with pAF during the non-paroxysmal period.…”

“…9,[13][14][15][16] Risk stratification using coagulation or fibrinolytic markers would be useful for preventing thrombosis in patients with AF, 17 and some studies have evaluated the levels of coagulation markers in the peripheral blood of patients with pAF during a paroxysm. 10,18,19 However, few studies have evaluated the risk of thromboembolism in the non-paroxysmal period (eg, during sinus rhythm) in patients with pAF. Furthermore, no studies have evaluated LA thrombotic activity in those patients.…”

Denser plasma clot formation and impaired fibrinolysis in paroxysmal and persistent atrial fibrillation while on sinus rhythm: Association with thrombin generation, endothelial injury and platelet activation

“…Elevated plasma fibrinogen, von Willebrand factor (vWF), and soluble P-selectin have been shown to be linked to thromboembolic events in AF patients [6,7]. An increase in thrombin generation (TG) in circulating venous blood is observed during or shortly after PAF episodes [8]. Patients with permanent AF and stroke or AF alone present higher TG than those on sinus rhythm without stroke [9].…”

Evaluación de la anticoagulación con rivaroxaban, en pacientes con fibrilación auricular no valvular de reciente diagnóstico

“…La FA confiere un estado protrombótico o de hipercoagulabilidad, con alteraciones de la hemostasia, trombosis, activación de plaquetas y disfunción endotelial 22 . Se ha asociado a niveles elevados de marcadores procoagulantes, tales como GT y complejos TAT [23][24] , los que persisten elevados incluso en pacientes que están en tratamiento anticoagulante oral 25 . Los niveles plasmáticos elevados de fragmentos 1+2 de protrombina y los complejos TAT, reflejan la GT in vivo y sus niveles han sido asociados a mayor riesgo de accidente cerebrovascular [26][27] .…”