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  • The results of our initial cross


    The results of our initial cross-sectional analyses assessing the clinical characteristics of the patients participating in ASSAF-K are shown in Table 1. As compared with the “Fushimi AF Registry,” considered a representative Japanese AF registry with an initial registration of 3183 patients [28], the size of ASSAF-K is approximately the same. The Fushimi AF Registry revealed both the underuse and underdosage of warfarin in actual clinical settings. ASSAF-K is expected to show how oral anticoagulants are currently used in the era of NOACs. The mean CHADS2 scores in previous studies in Japan were 2.1 in the RE-LY Japanese dapagliflozin [48], 3.27 in J-ROCKET AF [45], 2.09 in the Fushimi AF Registry, 1.7 in the J-Rhythm Registry [50], and 1.82 in ASSAF-K, indicating a relatively lower thrombotic risk among the participants. Thus, ASSAF-K is expected to reveal changes in risks and benefits associated with the launching of NOACs in Japan.
    Sources of funding
    Conflict of interest
    Introduction Anticoagulation therapy for patients with atrial fibrillation (AF) is essential for prophylaxis against ischemic stroke and systemic embolism [1,2]. There has been a rapid shift in anticoagulants used for this purpose, from conventional anticoagulants, vitamin K antagonists (VKA) to novel oral anticoagulants (NOACs) [3]. NOACs include the direct thrombin inhibitor, dabigatran, and factor Xa (FXa) inhibitors, rivaroxaban and apixaban. Recently published randomized clinical trials have supported the efficacy and safety of NOACs compared with the VKA, warfarin [4–6]. Warfarin acts as an anticoagulant by inhibiting the production of the vitamin K-dependent coagulation factors II, VII, IX, and X. In contrast, NOACs selectively and reversibly target thrombin or FXa. Additionally, NOACs have a rapid onset and short half-lives. This causes fluctuations in their effects between peak and trough phases compared with warfarin, which develops a constant anticoagulation effect throughout the entire day [7]. The aforementioned clinical trials have demonstrated a similar incidence of stroke and systemic embolism despite the unique pharmacological features of NOACs [4–6]. Meanwhile, Protein C/Protein S (PC/PS) and AT III have additional antithrombotic effects as physiological anticoagulation factors. However, little is known about whether NOAC use has influence on trends in these physiological anticoagulant factors. Therefore, the purpose of the study is to reveal the trends in physiological inhibitors such as AT III, PC or PS, and markers of thrombus formation in patients receiving NOACs compared with those using warfarin.
    Blood sampling
    Funding sources
    Conflicts of interest
    Introduction Owing to recent advances in transplant immunology and surgical improvements, heart transplantation appears to be a prevailing alternative for end-stage heart disorders. Early postoperative atrial rhythm disturbances occur in approximately 10–20% of heart transplant patients [1,2]. However, they become significantly less common during the late follow-up period after heart transplantation. While macro-reentrant atrial tachyarrhythmia arises from surgical anastomosis lines, focal atrial tachyarrhythmias can be seen in the late postoperative period [3]. The most common arrhythmias encountered after heart transplantation are ventricular or atrial premature complexes, sinus or junctional bradycardia, atrial fibrillation, and atrial flutter, which have varying clinical significance, depending on associated or causative conditions. Allograft rejection, transplant coronary artery disease, altered anatomy, or autonomic nervous system changes have been suggested to be responsible for posttransplant arrhythmia [4]. Atrial electromechanical coupling (PA) and atrial electromechanical delay (AEMD) measured by Doppler tissue imaging (DTI) were found to be significantly longer in patients with paroxysmal atrial fibrillation (AF) [5–7]. AEMD has also been demonstrated to be longer in many diseases that affect heart tissue [8–14].