Dual Antithrombotic Therapy with Dabigatran after PCI in Atrial Fibrillation

Kevin Lao, Mercer University College of Pharmacy

The 2016 European Society of Cardiology guidelines recommend a short period of triple therapy (oral anticoagulant [OAC], aspirin, clopidogrel) for patients with atrial fibrillation (AFib) undergoing percutaneous coronary intervention (PCI) with a stent placement. [1]

Contrary to the European guidelines, the American Heart Association guidelines state that it may be reasonable to use clopidogrel with OAC without aspirin in AFib patients with CHA2DS2-VASc score ≥ 2 following PCI based on evidence that showed higher rates of bleeding with triple therapy. [2] Additionally, one previous trial has shown that dual therapy (warfarin + clopidogrel [P2Y12 inhibitor]) was associated with lower incidence of bleeding without increased rates of stent thrombosis in PCI patients compared to triple therapy. [3]

With the availability of the new oral anticoagulant (NOAC), some evidence suggests that NOAC, instead of warfarin, with a P2Y12 inhibitor (i.e. clopidogrel) may be an effective thromboprophylaxis in PCI patients. Therefore, the RE-DUAL PCI trial aimed to compare the efficacy and safety of dual therapy composed of dabigatran and P2Y12 inhibitor among patients with AFib undergoing PCI. [4]

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Praxbind® : Clinical Efficacy

Akpan Anani, Mercer University College of Pharmacy

While oral anticoagulants are used for the prevention or treatment of thrombotic events, certain life-threatening scenarios may warrant interventions in which anticoagulant reversal is needed to achieve hemostasis. Consequently, the availability and efficacy of reversal agents can have a large impact on the decision making of healthcare providers in regards to the anticoagulant therapy regimen being utilized by patients. Pradaxa® (dabigatran) is an oral anticoagulant approved in the U.S. in 2010 for the treatment and prevention of different thrombotic events. [1] Conversely, Praxbind® (idarucizumab) is an aptly named humanized monoclonal antibody fragment that binds to dabigatran and reverses its anticoagulant activity. [2] Idarucizumab has been licensed in numerous countries (first approved in the U.S. in 2015) [3] based on preliminary results from the first 90 patients enrolled in the Reversal Effects of Idarucizumab on Active Dabigatran (RE-VERSE AD) trial. [4]

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A Comparison of Stroke and Bleeding Risk Scoring Systems in Atrial Fibrillation

Dakota Thaxton Craft, Mercer University College of Pharmacy

Atrial fibrillation (AF) is a type of supraventricular tachycardia that may lead to blood clots and increase the risk of stroke. [1]  Goals of therapy include rate control or correction of rhythm disturbance and prevention of thromboembolism.  The selection of antithrombotic therapy may be based on the risk of thromboembolism due to stroke as assessed by CHADS2, or the more inclusive CHA2DS2VASC. [2]  Due to increased bleeding risks associated with antithrombotic therapy, it is recommended to stratify bleeding risks by using the HAS-BLED score (hypertension, abnormal renal/liver function, stroke, bleeding history or predisposition, labile INR, elderly > 65 years, drugs/alcohol concomitantly). [3]  The HAS-BLED score is not applicable to all patients due to lack of available information for “labile INR” in naive patients. [4]

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RE-CIRCUITing Anticoagulants for Catheter Ablation

Sandy Liu, Mercer University College of Pharmacy

Catheter ablation of atrial fibrillation is typically performed with uninterrupted anticoagulation with warfarin or interrupted non-vitamin K antagonist (NVKA) oral anticoagulant therapy.  Due to the lack of controlled data, it is unknown whether uninterrupted anticoagulation with a NVKA agent, such as dabigatran, is a safer option than warfarin. [1]

Warfarin is a vitamin K antagonist that competitively inhibits the subunit 1 of the multi-unit vitamin K epoxide reductase (VKOR) complex, thus depleting functional K reserves and reducing synthesis of active clotting factors. [2]  Conversely, dabigatran is a reversible, direct thrombin inhibitor that inhibits both free and fibrin-bound thrombin, thereby preventing thrombin-mediated effects, including cleavage of fibrinogen to fibrin monomers, inhibition of thrombin-induced platelet aggregation and activation of factors V, VIII, XI and XIII. [3]

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