Brush up on Your Oral Anticoagulation: A Brief Q & A


Three questions on 3 topics that are central to optimal use of OAC for patients with atrial fibrillation.

Q1. What do current guidelines recommend regarding initiation of oral anticoagulation in patients with non-valvular atrial fibrillation (AF)?

Answer: According to the ACC/AHA/HRS 2014 atrial fibrillation guidelines, the decision to start anticoagulation should be based on a discussion of risk-benefit ratio with the patient; this includes assessment of absolute and relative risks of stroke and bleeding and consideration of the patient’s values and personal preference. The CHA2DS2-Vasc risk stratification calculator is recommended to identify risk of stroke. The decision to initiate anticoagulation should be independent of the type of atrial fibrillation (paroxysmal, persistent, permanent) and applies to all atrial flutter. Any patient with a CHA2DS2-Vasc score ≥2 should be treated with oral anticoagulation as he/she is considered at moderate to high risk for thromboembolism (Class I).

Treatment can be individualized (aspirin or oral anticoagulant) for those with CHA2DS2-Vasc score=1 (Class IIb) and omitted for CHA2DS2-Vasc score=0. Patients should be reevaulated periodically to reassess stroke and bleeding risk and anticoagulation adjusted accordingly.

Please click here for Question #2 - OAC, AF, and PCI.


Q2. In patients with AF undergoing percutaneous coronary intervention (PCI), what is the recommended strategy for anticoagulation?Answer: It is recommended that warfarin be interrupted prior to the arterial puncture to minimize the risk of bleeding. The decision to bridge (using low molecular weight or unfractionated heparin) should be individualized based on an individual patient’s risk for thrombosis and bleeding and the anticipated length of time the patient will be without anticoagulation. In addition, bare metal stents (BMS) should be considered over drug eluting stents (DES) in order to minimize the duration of anticoagulant therapy (Class IIb). Once PCI has been completed, clopidogrel once daily and an oral anticoagulant can be used without aspirin for the minimum duration of dual antiplatelet therapy (BMS, 1 month; DES, 1 year).1,2

Please click here for Question #3 - Stats on actual anticoagulation.


Q3. What are the “real world” data on how many patients with AF who meet an indication for anticoagulation are actually treated appropriately? What factors predict treatment?Answer: In an analysis of the PINNACLE (Practice Innovation and Clinical Excellence) registry of outpatients from 2008-2012, of 294,642 patients eligible for anticoagulation (CHA2DS2-Vasc score ≥2), 40.2% were treated with aspirin alone. Clinical factors that emerged after multivariate adjustment associated with selection of aspirin therapy over anticoagulation were: hypertension, dyslipidemia, CAD, prior MI, unstable or stable angina, recent CABG, and peripheral arterial disease. It is likely that patients in these groups were at higher risk for bleeding or had an indication for a second antiplatelet agent, and this drove the provider’s decision making about whether to initiate anticoagulation. Still, it remains startling that more than 1 in 3 patients who met guideline-based indications for anticoagulation did not receive it.


1. January CT, Wann L, Alpert JS, et al. 2014 AHA/ACC/HRS Guideline for the Management of Patients With Atrial Fibrillation: Executive Summary: A Report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines and the Heart Rhythm Society. J Am Coll Cardiol. 2014;64:2246-2280. doi:10.1016/j.jacc.2014.03.021.

2. Dewilde  WJ, Oirbans T, Verheugt FW, et al. Use of clopidogrel with or without aspirin in patients taking oral anticoagulant therapy and undergoing percutaneous coronary intervention: an open-label, randomised, controlled trial. Lancet. 2013;381:1107-1115.

3. Hsu JC, Maddox TM, Kennedy K, et al. Aspirin Instead of Oral Anticoagulant Prescription in Atrial Fibrillation Patients at Risk for Stroke. J Am Coll Cardiol. 2016;67:2913-2923. doi:10.1016/j.jacc.2016.03.581.



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