BackgroundNon-vitamin K antagonist oral anticoagulants (NOACs) show a favorable balance between efficacy and safety compared with warfarin for patients with non-valvular atrial fibrillation (NVAF). In “real-world” practice, however, NOAC adherence and persistence among patients are not clear. The aim of this study is to evaluate NOAC and warfarin persistence in Japanese patients with NVAF who newly started these drugs.MethodsWe retrospectively studied 401 patients with NVAF who had newly started NOACs during the first 18 months after our hospital adopted their use (197 dabigatran, 107 rivaroxaban, 102 apixaban) and 200 patients with NVAF who had newly started warfarin during the same period. The endpoint was drug discontinuation for each drug.ResultsDuring the follow-up period (up to a maximum of 24 months), 113 (28%) patients who had newly started NOACs and 33 (17%) patients who had newly started warfarin discontinued the drug. The persistence rates of patients prescribed NOACs was lower than that of patients prescribed warfarin at 3, 6, and 12 months (85% versus 93%, 79% versus 88%, and 70% versus 82%, respectively). One-tenth of patients who had newly started NOACs discontinued the drug by their own decision. Drug adverse events, worsening renal dysfunction, and patient desire were the major causes of NOAC discontinuation.ConclusionsThe rate of persistence of prescribed NOACs was significantly lower than that of warfarin in Japanese patients with NVAF.

on behalf of the J-RHYTHM Registry Investigators* Background--To clarify the influence of hypertension and blood pressure (BP) control on thromboembolism and major hemorrhage in patients with nonvalvular atrial fibrillation, a post hoc analysis of the J-RHYTHM Registry was performed.

yanotic congenital heart disease (CCHD) is associated with an increased risk of stroke and thromboembolism. 1 A recent study using contrast-enhanced computed tomography revealed a high prevalence of pulmonary thrombosis in patients with Eisenmenger syndrome. 2 The precise mechanisms of the increased incidence of thromboembolism in patients with CCHD have not yet been determined, but endothelial dysfunction, hemostatic abnormalities and platelet activation may be underlying factors causing hypercoagulability and thromboembolism. [3][4][5] Platelets interact with endothelial cells, leukocytes and other platelets. 6 Intravascular thrombus formation is enhanced by thrombin, which activates the coagulation cascade, platelets and the formation of neutrophil/platelet conjugates. 6-8 P-selectin is an adhesion molecule found in the secretory granules of platelets and Weibel -Palade bodies of endothelial cells, and is mobilized to the plasma membrane on activation. 6,9,10 P-selectin expressed on platelets may be a direct inducer of pro-coagulant activity associated with vascular and thrombotic diseases. 11 Although P-selectin is likely to play an important role in the thrombus formation, 6,11 there have been only a few studies evaluating Pselectin in CCHD. 4,12,13 Thrombomodulin is expressed mainly on the surface of vascular endothelial cells and prevents blood clotting on the internal surface of vessels. Endothelial thrombomodulin is a key component of the protein C anticoagulant pathway that facilitates the activation of protein C by thrombin. 14 Therefore, thrombomodulin acts as an intrinsic anticoagulant barrier between the blood and the endothelium. The plasma thrombomodulin level was elevated in disseminated intravascular coagulation and atheromatous arterial disease. 15,16 It may initially increase with acute vascular injury but decrease with subsequent downregulation of its production during chronic vessel injury. Several reports have shown that reduced thrombomodulin enhances thrombus formation. 17,18,19 We hypothesized that the decreased expression of protein C and the increased expression of Pselectin on platelets due to a reduced thrombomodulin level may contribute to the formation of thrombi in patients with CCHD. To test this hypothesis, we measured plasma levels of thrombomodulin and protein C, and the expression of Pselectin on platelets in patients with CCHD. The plasma thrombin -antithrombin complex III (TAT) level was also measured to evaluate coaguability. Methods PatientsWe enrolled 35 patients with CCHD. The inclusion criterion was the presence of cyanosis due to right-to-left shunt in patients with congenital heart disease. The demography of the patients is summarized in Table 1. There were 19 men and 16 women, with a mean age of 13±11 years, ranging from 1 to 37 years. Twenty-five patients had undergone palliative operations (Balock-Taussig shunt or bidirectional Glenn). Eight patients underwent definitive operations (Fontan operation in 7 and Rastelli operation in 1), but the Circ J 2007; 71: 948...

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BackgroundIn “real-world” practice, anticoagulant therapy is indicated for patients whose clinical profiles are not addressed in randomized clinical trials. We assessed the effectiveness and safety of dabigatran versus warfarin in “real-world” Japanese patients with non-valvular atrial fibrillation (NVAF).MethodsAmong 613 NVAF patients who initiated dabigatran or warfarin therapy during the period between 2011 and 2013, 362 patients were included in the study after propensity score adjustment. The median follow-up period was 1.3 years. The effectiveness and safety outcomes were thromboembolism and major bleeding, respectively.ResultsThe propensity-matched hazard ratios of thromboembolism and major bleeding with dabigatran were 1.03 (95% CI: 0.12-8.04, p=0.971) and 0.15 (95% CI: 0.01–0.90, p=0.037), respectively.ConclusionsThe ability of dabigatran to prevent thromboembolism is comparable to that of warfarin; however, the major bleeding rate is lower with dabigatran in “real-world” NVAF patients.