Supplementary Table 9, column 'Edoxaban', row 'eGFR category', '95 mL/min' (page 15). The cell should be coloured green instead of yellow. It should also read "60 mg"instead of "60 mg (use with caution in 'supranormal' renal function)."In the above-indicated cell, a footnote has also been added to state: "Edoxaban should be used in patients with high creatinine clearance only after a careful evaluation of the individual thromboembolic and bleeding risk."Supplementary Table 9, column 'Edoxaban', row 'Dose reduction in selected patients' (page 16). The cell should read "Edoxaban 60 mg reduced to 30 mg once daily if any of the following: creatinine clearance 15-50 mL/min, body weight <60 kg, concomitant use of dronedarone, erythromycin, ciclosporine or ketokonazole"instead of "Edoxaban 60 mg reduced to 30 mg once daily, and edoxaban 30 mg reduced to 15mg once daily, if any of the following: creatinine clearance of 30-50 mL/min, body weight <60 kg, concomitant us of verapamil or quinidine or dronedarone."

/pdf/2020-esc-guidelines-for-the-diagnosis-and-management-of-38dpic1xu8.pdf

2020 ESC Guidelines for the diagnosis and management of atrial fibrillation developed in collaboration with the European Association for Cardio-Thoracic Surgery (EACTS).

A correction has been published: European Heart Journal, ehaa895, https://doi.org/10.1093/eurheartj/ehaa895

2020 ESC Guidelines for the management of acute coronary syndromes in patients presenting without persistent ST-segment elevation

2019 AHA/ACC/HRS Focused Update of the 2014 AHA/ACC/HRS Guideline for the Management of Patients With Atrial Fibrillation: A Report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines and the Heart Rhythm Society

Writing Group Members* Craig T. January, MD, PhD, FACC (Chair), L. Samuel Wann, MD, MACC, FAHA (Vice Chair), Hugh Calkins, MD, FACC, FAHA, FHRS,* Lin Y. Chen, MD, MS, FACC, FAHA, FHRS, Joaquin E. Cigarroa, MD, FACC, Joseph C. Cleveland Jr., MD, FACC,*,x Patrick T. Ellinor, MD, PhD,* Michael D. Ezekowitz, MBChB, DPhil, FACC, FAHA,*,k Michael E. Field, MD, FACC, FAHA, FHRS,k Karen L. Furie, MD, MPH, FAHA,k Paul A. Heidenreich, MD, FACC, FAHA,{ Katherine T. Murray, MD, FACC, FAHA, FHRS,k Julie B. Shea, MS, RNCS, FHRS,*,k Cynthia M. Tracy, MD, FAHA,k Clyde W. Yancy, MD, MACC, FAHAk

2019 AHA/ACC/HRS Focused Update of the 2014 AHA/ACC/HRS Guideline for the Management of Patients With Atrial Fibrillation: A Report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines and the Heart Rhythm Society in Collaboration With the Society of Thoracic Surgeons

The current manuscript is the second update of the original Practical Guide, published in 2013 [Heidbuchel et al. European Heart Rhythm Association Practical Guide on the use of new oral anticoagulants in patients with non-valvular atrial fibrillation. Europace 2013;15:625-651; Heidbuchel et al. Updated European Heart Rhythm Association Practical Guide on the use of non-vitamin K antagonist anticoagulants in patients with non-valvular atrial fibrillation. Europace 2015;17:1467-1507]. Non-vitamin K antagonist oral anticoagulants (NOACs) are an alternative for vitamin K antagonists (VKAs) to prevent stroke in patients with atrial fibrillation (AF) and have emerged as the preferred choice, particularly in patients newly started on anticoagulation. Both physicians and patients are becoming more accustomed to the use of these drugs in clinical practice. However, many unresolved questions on how to optimally use these agents in specific clinical situations remain. The European Heart Rhythm Association (EHRA) set out to coordinate a unified way of informing physicians on the use of the different NOACs. A writing group identified 20 topics of concrete clinical scenarios for which practical answers were formulated, based on available evidence. The 20 topics are as follows i.e., (1) Eligibility for NOACs; (2) Practical start-up and follow-up scheme for patients on NOACs; (3) Ensuring adherence to prescribed oral anticoagulant intake; (4) Switching between anticoagulant regimens; (5) Pharmacokinetics and drug-drug interactions of NOACs; (6) NOACs in patients with chronic kidney or advanced liver disease; (7) How to measure the anticoagulant effect of NOACs; (8) NOAC plasma level measurement: rare indications, precautions, and potential pitfalls; (9) How to deal with dosing errors; (10) What to do if there is a (suspected) overdose without bleeding, or a clotting test is indicating a potential risk of bleeding; (11) Management of bleeding under NOAC therapy; (12) Patients undergoing a planned invasive procedure, surgery or ablation; (13) Patients requiring an urgent surgical intervention; (14) Patients with AF and coronary artery disease; (15) Avoiding confusion with NOAC dosing across indications; (16) Cardioversion in a NOAC-treated patient; (17) AF patients presenting with acute stroke while on NOACs; (18) NOACs in special situations; (19) Anticoagulation in AF patients with a malignancy; and (20) Optimizing dose adjustments of VKA. Additional information and downloads of the text and anticoagulation cards in different languages can be found on an EHRA website (www.NOACforAF.eu).

/pdf/the-2018-european-heart-rhythm-association-practical-guide-4iood3iocz.pdf

The 2018 European Heart Rhythm Association Practical Guide on the use of non-vitamin K antagonist oral anticoagulants in patients with atrial fibrillation.

BackgroundIdarucizumab, a monoclonal antibody fragment, was developed to reverse the anticoagulant effect of dabigatran. MethodsWe performed a multicenter, prospective, open-label study to determine whether 5 g of intravenous idarucizumab would be able to reverse the anticoagulant effect of dabigatran in patients who had uncontrolled bleeding (group A) or were about to undergo an urgent procedure (group B). The primary end point was the maximum percentage reversal of the anticoagulant effect of dabigatran within 4 hours after the administration of idarucizumab, on the basis of the diluted thrombin time or ecarin clotting time. Secondary end points included the restoration of hemostasis and safety measures. ResultsA total of 503 patients were enrolled: 301 in group A, and 202 in group B. The median maximum percentage reversal of dabigatran was 100% (95% confidence interval, 100 to 100), on the basis of either the diluted thrombin time or the ecarin clotting time. In group A, 137 patients (45.5%) presented ...

/pdf/idarucizumab-for-dabigatran-reversal-full-cohort-analysis-21jjzaudcu.pdf

Idarucizumab for Dabigatran Reversal — Full Cohort Analysis

Haemophilia B Leyden is characterized by severe factor IX deficiency during childhood with partial resolution at puberty or following the administration of anabolic steroids. The disorder has recently been associated with point mutations in the putative factor IX promoter region, which contains an imperfect direct repeat spanning a possible start site of transcription. We have identified a T to C transition at position +8 in the promoter region of a patient with the haemophilia B Leyden phenotype. A mutation at this site has not been previously reported and occurs within the repeat consensus sequence in the transcribed but untranslated portion of the gene. There is no family history of haemophilia and sequence analysis of his mother and other family members indicates that the mutation has arisen de novo in this patient. This observation provides further support for a causal relationship between point mutations in the presumptive promoter region of the factor IX gene and the Leyden phenotype.

Haemophilia B Leyden arising de novo by point mutation in the putative factor IX promoter region.

The absolute polycythaemias (also known as the erythrocytoses) are a heterogeneous group of disorders defined by an absolute increase in red cell mass (Prchal & Prchal, 1999), calculated using predictive formulae based on body surface area rather than weight (Pearson et al, 1995). Historically, these have been divided into three categories: primary (chiefly polycythaemia rubra vera ± PV), secondary (when excessive erythroid proliferation is driven by a discernible cause) and a third group in which no cause is identifiable ± the idiopathic erythrocytoses (IE) (Messinezy et al, 1994; Messinezy & Pearson, 1999). The distinction between primary and secondary has been whether or not erythropoiesis is erythropoietin-driven. Measurement of serum erythropoietin (EPO) levels has been useful in distinguishing myeloproliferative polycythaemia (PV), treatment and prognosis of which differ from the secondary disorders (Messinezy et al, 1995; Pearson, 2001). Increasingly, however, our ability to define underlying cellular and molecular defects reveals heterogeneity within the primary group, some of which have more in common with the secondary polycythaemias, and may permit a reclassification along more clinically relevant lines. Likewise, the idiopathic group is steadily being depleted as mechanisms are identified. This process has shown that disorders previously regarded as IE are also heterogeneous, including some cases of evolving PV and various secondary erythrocytoses. In practical terms, it is important to diagnose PV and life threatening secondary causes, such as renal carcinoma. Early recognition and treatment of evolving PV can prevent serious or fatal vascular events, and prognosis can be determined. Identification of secondary causes avoids inappropriate myelosuppressive treatment, now recognized as having a leukaemogenic risk (Fruchtman et al, 1997; Sterkers et al, 1998). This review will explore our progress in understanding the molecular and pathological mechanisms involved in the development of polycythaemia, illustrating how this has allowed reclassification of many hitherto idiopathic erythrocytoses, and will discuss the remaining diagnostic difficulties.

Idiopathic erythrocytosis--a declining entity.

BACKGROUND
Rivaroxaban is used increasingly as an oral anticoagulant, however a specific reversal agent is not currently available in the Australasian setting. There is also variation across international consensus guidelines regarding advice on the use of non-specific haemostatic agents for management of bleeding.


METHODS
A retrospective cohort analysis was performed of patients prescribed rivaroxaban who presented to four metropolitan hospital Emergency Departments between 01/08/2018 and 31/05/2021 with major bleeding as defined by the International Society on Thrombosis and Haemostasis.


RESULTS
112 patients were identified accounting for 115 major bleeding presentations. Upper gastrointestinal (34%) and intracranial (31%) bleeding sites were most common. Procedural intervention was required in 44% of patients. Haemostatic management involved tranexamic acid in 26%, prothrombin complex concentrate in 55% (dose range 1000-6000 IU or 10-65 IU/kg), vitamin K in 16% and fresh frozen plasma in 1%. Rivaroxaban was discontinued permanently following 56 events (49%), switched to another anticoagulant in 24 (21%) and withheld in 30 (26%) from 2 days to 3 months (median 8.5 days). All-cause mortality at 90 days after bleeding was 17% (19 patients) and the incidence of combined venous and arterial thrombotic events was 10%.


CONCLUSIONS
There is considerable heterogeneity in the acute clinical management of patients presenting with rivaroxaban-related major bleeding. The use of PCC and dosage administered is inconsistent. Tranexamic acid was utilised in only around one quarter of all cases. Evidence-based guidance for treating rivaroxaban-related bleeding would improve the management of these patients and potentially improve clinical outcomes. This article is protected by copyright. All rights reserved.

Gordon A. Royle

Papers

Idarucizumab for Dabigatran Reversal — Full Cohort Analysis

Haemophilia B Leyden arising de novo by point mutation in the putative factor IX promoter region.

Idiopathic erythrocytosis--a declining entity.

Real world decision making in the management of patients presenting with major bleeding on rivaroxaban: The Auckland regional experience.