The following are key points to remember about this American Heart Association (AHA) Scientific Statement on Management of Patients on Non–Vitamin K Antagonist Oral Anticoagulants in the Acute Care and Periprocedural Setting:

1. Non–vitamin K antagonist oral anticoagulants (NOACs; also known as direct oral anticoagulants) are widely available as alternatives or first-line therapies for stroke prevention in atrial fibrillation and venous thromboembolism.
2. NOACs work through direct inhibition of either thrombin (dabigatran) or factor Xa (rivaroxaban, apixaban, and edoxaban). They each have a rapid onset of action, a shorter half-life, and more predictable pharmacokinetics as compared to warfarin.
3. Although not recommended routinely, laboratory monitoring is possible for the NOACs. A normal partial thromboplastin time (PTT) or thrombin time most likely excludes therapeutic levels of dabigatran. Undetectable anti-Xa activity level likely excludes clinically relevant concentrations of rivaroxaban, apixaban, and edoxaban.
4. Hospitals should adopt anticoagulation reversal protocols with multidisciplinary representation.
5. The anticoagulant effect of dabigatran is rapidly reversed with idarucizumab (Praxbind) given as two consecutive intravenous infusions of 2.5 g each. Prothrombin complex concentrates (PCCs) and hemodialysis may also be effective, especially if implemented within a few hours of oral ingestion.
6. Rivaroxaban, apixaban, and edoxaban do not have a drug-specific reversal agent currently available. Current management options include use of four-factor PCCs or fresh frozen plasma.
7. In the setting of intracranial hemorrhage and concurrent NOAC use, reversal attempts should be made as above. Additionally, rapid control of blood pressure to <140 mm Hg systolic is recommended. It is unclear if/when a NOAC can be re-introduced following an intracranial hemorrhage.
8. In patients who suffer an acute ischemic stroke while taking a NOAC, it is recommended to avoid use of recombinant tissue-type plasminogen activator unless sensitive laboratory tests are normal or a patient has not taken a NOAC in >48 hours. In general, it is advised to withhold resuming any OAC for 1-2 weeks following a stroke in patients with atrial fibrillation (shorter time for patients suffering transient ischemic attacks or smaller, nondisabling strokes).
9. In patients undergoing a low bleeding risk procedure (e.g., minor dental, minor dermatologic, ophthalmologic, or endoscopic without biopsy) while taking NOACs, it is advised to not interrupt the NOAC for the procedure.
10. In patients undergoing moderate-high bleeding risk procedures, it is recommended to stop a NOAC based on the creatinine clearance (unique for each NOAC subclass). Given the short half-life of NOACs, no bridging heparin is necessary for these patients.
11. For patients on chronic NOAC therapy who experience an acute coronary syndrome and require urgent cardiac catheterization, appropriate dual antiplatelet therapy (DAPT) and heparin should be started upstream and the NOAC discontinued as the patient is being scheduled for urgent catheterization.
12. In patients with atrial fibrillation who undergo coronary stenting, clinicians should weigh the benefits and risk when determining the length of triple therapy (OAC plus DAPT). Use of proton pump inhibitors and avoidance of nonsteroidal anti-inflammatory medications are advised during this period.
13. For patients undergoing cardioversion or catheter ablation for atrial fibrillation, either 3-4 weeks of uninterrupted NOAC therapy or a transesophageal echocardiogram without evidence of left atrial appendage thrombus is advised. NOAC therapy can either be continued or interrupted for catheter ablation procedures.

Keywords: Acute Coronary Syndrome, Anticoagulants, Arrhythmias, Cardiac, Atrial Appendage, Atrial Fibrillation, Blood Coagulation Factors, Blood Pressure, Cardiac Catheterization, Cardiac Surgical Procedures, Catheter Ablation, Creatinine, Echocardiography, Transesophageal, Factor Xa, Heparin, Infusions, Intravenous, Intracranial Hemorrhages, Ischemic Attack, Transient, Perioperative Care, Platelet Aggregation Inhibitors, Proton Pump Inhibitors, Primary Prevention, Risk Assessment, Stents, Stroke, Thrombin Time, Thrombosis, Venous Thromboembolism

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