Th non-valvular atrial fibrillation [3] and in those with thromboembol…

Th non-valvular atrial fibrillation [3] and in those with thromboembolism after hip and knee replacement surgeries [4]. Thrombin is a key factor in the coagulant process because it converts fibrinogen into fibrin and activates platelets and factors V, VII, VIII, IX and XIII. Following oral administration, dabigatran etexilate is rapidly hydrolyzed into dabigatran and subsequently absorbed from the gastrointestinal tract. Dabigatran inactivates free thrombin and fibrin-bound thrombin in a concentrationdependent manner [5]. The efficacy and safety of dabigatran for the prevention of stroke or systemic embolism in patients with non-valvular atrial fibrillation was shown in the Randomized Evaluation of Long-term Anticoagulation Therapy trial [3]. In that trial, dabigatran administration at 110mg b.i.d. was associated with similar rates of stroke and systemic embolism, but with a lower rate of major bleeding than that associated with warfarin. At 150mg b.i.d., dabigatran was associated with lower rates of stroke and systemic embolism, but similar rates of major bleeding, compared with those of warfarin. Furthermore, the incidence of intra-cranial bleeding was significantly lower during the anti-coagulation therapy with both dabigatran doses compared with those of warfarin. In patients with non-valvular atrial fibrillation, in whom atrial thrombus was identified on transesophageal echocardiography, the atrial thrombus was resolved by four weeks of warfarin administration in approximately 80 to 90 of cases [6,7]. In contrast, the efficacy of the oral anti-coagulant dabigatran in the resolution of previously detected thrombus has not been extensively reported. Vidal et al. [8] reported the first documented case of thrombus resolution following dabigatran administration. In their report, after dabigatran administration (150mg b.i.d.) for eight weeks, a large left atrial appendage thrombus was resolved with no concomitant thromboembolic events. In the present case, on the basis of weekly echocardiographic examinations, the size of the apical aneurysm thrombus gradually decreased. After dabigatran administration for three weeks, the apical aneurysm thrombus disappeared without any thromboembolic events. The absence of clinical events made migration of the thrombus an unlikely explanation for its disappearance. Because plasma levels of fibrinogen and TAT did not increase, systemic coagulation activities did not increase, despite the presence of a left ventricular thrombus. Before andKaku Journal of Medical Case 3-[(Methylamino)methyl]phenol Reports 2013, 7:238 http://www.jmedicalcasereports.com/content/7/1/Page 4 ofABefore treatmentC2 weeks after treatment15?7mm6.8?.0 mm1 week after treatment3 weeks after treatment4 weeks after treatmentBDE10? mmFigure 3 Thrombic progression in apical aneurysm (thrombus indicated by arrows). (A) Prior to anti-coagulation therapy, thrombus size was 15.0mm?7.0mm. (B) One week after initial dabigatran administration (150mg b.i.d.), thrombus size was 10.0mm?.0mm. (C) Two weeks after initial dabigatran administration (150mg b.i.d.), thrombus size was 6.8mm?.0mm. (D) Three weeks after initial dabigatran administration (150mg b.i.d.), thrombus was undetectable. (E) Four weeks after initial dabigatran administration (150mg b.i.d.), thrombus 2-(4-Carbamoylpiperidin-1-yl)acetic acid hydrochloride was still PubMed ID:https://www.ncbi.nlm.nih.gov/pubmed/20618955 undetectable.100 sec 80 60 40 20 0 38.2 76.aPTT 73.3 57.0.4 0.3 0.2 0.1?g/mlD-dimer0.3 0.2 0.after 4 weeksbefore PubMed ID:https://www.ncbi.nlm.nih.gov/pubmed/15127947 treatmentafter 2 weeksbefore treatment after 1 weekafter 3 weeksafter 4 weeksng/mlTAT 1.6.