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    • br Monitoring coagulation levels Coagulation levels

    2019-06-27


    Monitoring coagulation levels Coagulation levels can be monitored after warfarin treatment by measuring the prothrombin time (PT). However, monitoring is not needed for novel anticoagulants because these drugs have a much wider therapeutic range than warfarin. Nonetheless, in patients at high risk of major bleeding, the physician may decide to evaluate the coagulation levels. Protocols for measurement of coagulation levels in patients treated with novel anticoagulants that have peak and trough phases in their concentration curves have not been established yet. The concentrations of dabigatran and rivaroxaban are related to activated partial thrombin time (APTT) and PT, respectively [18,19], and major bleeding during treatment with these anticoagulants may be checked by measuring APTT or PT, respectively. Prolonged APTT (more than 80s) in the trough phase is related to major bleeding during treatment with dabigatran [20,21]. The relationship between major bleeding and PT during rivaroxaban treatment has not yet been studied. Ischemic events may be assessed by measuring the plasma levels of molecular markers of the coagulation system, such as prothrombin fragment 1+2, thrombin–antithrombin complex, and soluble fibrin monomer complex (Fig. 7). Further investigation is needed to determine the optimum method for assessing major bleeding and ischemic events during treatment with novel anticoagulants.
    Management of major bleeding Hemorrhagic complications are the most common adverse events associated with both anticoagulants and antiplatelet agents. Patients should be aware of these risks, and physicians should have knowledge on how to manage bleeding complications. It is important to treat the bleeding as promptly and efficiently as possible. For patients with major bleeding during treatment with novel anticoagulants, oral medication should be ceased, bleeding should be stopped by mechanical Pemetrexed or by surgical interventions, and circulating blood volume and blood pressure should be maintained by appropriate intravenous drip infusion [18]. As much as 80% of dabigatran is excreted from the kidney; therefore, intravenous infusion and induction of diuresis can be beneficial when managing major bleeding during dabigatran treatment. For patients with intracranial hemorrhage, treatment to suppress blood pressure should be provided. The Tmax of dabigatran, when taken with food, is 4h. Therefore, it may be important to perform gastric lavage or oral administration of activated charcoal if bleeding occurs within 4h of dabigatran administration. The circulatory system may be supported by supplementation of endogenous procoagulant factors, such as fresh frozen plasma, and factor IX complex (prothrombin complex concentrate [PCC]) containing factors II, VII, IX, and X, or recombinant factor VII. Preclinical studies have reported that PCC and recombinant factor VII inhibit prolongation of bleeding time after administration of dabigatran in rats [22,23]. In a clinical study on healthy volunteers, PCC did not reverse the anticoagulant effects of dabigatran as assessed by measuring APTT, but it did reverse the anticoagulation effects of rivaroxaban [19]. Further studies are needed to verify the effects of PCC, recombinant factor VII, and fresh frozen plasma on bleeding during treatment with new anticoagulants. Hemodialysis to remove dabigatran may be useful. Finally, the development of antibodies that can neutralize dabigatran may offer an important option for patients with severe bleeding [24].
    Conflict of interest
    Introduction
    Hospital studies About a half century ago, the frequency of various arrhythmias detected by electrocardiograms (ECGs) was described by Katz and Pick in part of “Clinical Electrocardiography,” published in 1956 [1]. The authors analyzed the ECGs of 50,000 consecutive patients of the Heart Station at Michael Reese Hospital for over 25 years. AF was seen in 5859 patients, for a frequency of 11.7% (Table 1) [1]. A similar investigation with 8000 consecutive ECGs from Tokyo University in Japan was reported in 1971 [2], in which AF was observed in 538 patients, and the frequency of AF was 6.7%. We also investigated the frequency of arrhythmias and age-related changes in a general hospital in 1983 [3]. Standard ECGs were recorded from 5079 consecutive patients aged 15–93 years. The prevalence of AF was 2.5%, following ventricular premature complex (3.6%), supraventricular premature complex (3.4%), sinus tachycardia (3.2%), and first-degree atrioventricular block (2.7%). In the 1980s, our study showed that the prevalence of AF was higher in men than in women (2.7% and 2.3%, respectively), which was confirmed by later epidemiological surveys in Japan and Western countries. Furthermore, AF was found in 0.58% in subjects younger than 50 years, 2.5% at ages 50–69 years, and 4.7% at 70 years or older, indicating that the prevalence of AF increases linearly with age [3].