Antithrombotic Therapy For Atrial Fibrillation

Publication Date: February 1, 2012
Last Updated: March 14, 2022

Recommendations

STROKE RISK IN ATRIAL FIBRILLATION

For patients with AF, including those with paroxysmal AF, stroke risk should be assessed using a risk factor based approach, rather than an categorisation into low, moderate/high risk strata. We recommend use of the CHA2DS2VASc as a simple clinical based stroke risk score to initially identify ‘low stroke risk’ patients that should not be offered antithrombotic therapy to prevent stroke and reduce mortality. (S-M)
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Subsequent to this initial step, for patients with AF, including those with paroxysmal AF, stroke prevention should be offered to those AF patients with one or more non-sex CHA2DS2VASc stroke risk factors (score of ≥1 in a male or ≥2 in a female). (S-M)
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BLEEDING RISK IN ATRIAL FIBRILLATION

For patients with AF, bleeding risk assessment should be performed in all patients with AF at every patient contact and should initially focus on potentially modifiable bleeding risk factors. (S-L)
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For patients with AF, we recommend use of the HAS-BLED score to address modifiable bleeding risk factors in all AF patients. Those potentially at high risk (HAS-BLED score ≥3) warrant more frequent and regular reviews or follow-up. (S-M)
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In VKA treated patients, we recommend use of the HAS-BLED score for bleeding risk assessment. (W-L)
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ANTITHROMBOTIC THERAPY AND OTHER APPROACHES FOR STROKE PREVENTION

For patients with AF, we recommend against antiplatelet therapy alone (monotherapy or aspirin in combination with clopidogrel) for stroke prevention alone, regardless of stroke risk. (S-M)
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In patients with AF who are eligible for OAC, we recommend NOACs over VKA. (S-M)
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In patients on VKAs with consistently low time in INR therapeutic range (eg. TTR<65%), we recommend considering interventions to improve TTR or switching to NOACs. (S-M)
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In patients with prior unprovoked bleeding, warfarin-associated bleeding, or at high risk of bleeding, we suggest using apixaban, edoxaban, or dabigatran 110 mg (where available) as all demonstrate significantly less major bleeding compared with warfarin. (W-VL)
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ADJUSTED-DOSE ORAL VITAMIN K ANTAGONIST THERAPY

For patients with non-valvular AF, when VKAs are used, we suggest the target should be INR 2.0-3.0, with attention to individual TTR, ideally ≥70%. (U-CBS)
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For patients with AF, we suggest the SAMe-TT2R2score to aid decision making to help identify patients likely to do well on VKA. (U-CBS)
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CARDIOVERSION

For patients with AF of greater than 48 hours or unknown duration undergoing elective electrical or pharmacologic cardioversion, we recommend therapeutic anticoagulation with well-managed VKA (INR 2-3) or a NOAC using dabigatran, rivaroxaban, edoxaban or apixaban for at least 3 weeks before cardioversion or a transesophageal echocardiography (TEE)-guided approach with abbreviated anticoagulation before cardioversion rather than no anticoagulation. (S-M)
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For patients with AF of greater than 48 hours or unknown duration undergoing elective electrical or pharmacologic cardioversion, we recommend therapeutic anticoagulation (with VKA or NOAC) for at least 4 weeks after succesful cardioversion to sinus rhythm rather than no anticoagulation, regardless of the baseline risk of stroke. (S-M)
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In patients in which LAA thrombus is detected on TEE, cardioversion postponed, and OAC continued for another 4-12 weeks, to allow thrombus resolution or endothelisation, we suggest that a decision on whether a repeat TEE is performed should be individualized. (U-CBS)
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For patients with AF of documented duration of 48 hours or less undergoing elective cardioversion (electrical or pharmacologic), we suggest starting anticoagulation at presentation (low-molecular weight heparin or unfractionated heparin at full venous thromboembolism treatment doses) and proceeding to cardioversion rather than delaying cardioversion for 3 weeks of therapeutic anticoagulation or a TEE-guided approach. (W-L)
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For patients with AF and hemodynamic instability undergoing urgent cardioversion (electrical or pharmacologic), after successful cardioversion to sinus rhythm, we recommend therapeutic anticoagulation (with VKA or full adherence to NOAC therapy) for at least 4 weeks rather than no anticoagulation, regardless of baseline stroke risk. (W-L)
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For patients with AF and hemodynamic instability undergoing urgent cardioversion (electrical or pharmacologic), we suggest that therapeutic-dose parenteral anticoagulation be started before cardioversion, if possible, but that initiation of anticoagulation must not delay any emergency intervention. (W-L)
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For patients with AF and hemodynamic instability undergoing urgent cardioversion (electrical or pharmacologic), after successful cardioversion to sinus rhythm, we suggest therapeutic anticoagulation for at least 4 weeks after successful cardioversion to sinus rhythm rather than no anticoagulation, regardless of baseline stroke risk. (W-L)
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For patients with atrial flutter undergoing elective or urgent pharmacologic or electrical cardioversion, we suggest that the same approach to thromboprophylaxis be used as for patients with atrial fibrillation undergoing cardioversion. (U-CBS)
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PATIENTS WITH AF WITH CORONARY ARTERY DISEASE

In AF patients presenting with an ACS and/or undergoing PCI/stenting, we recommend assessment of stroke risk using the CHA2DS2VASc score. (S-M)
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In AF patients presenting with an ACS and/or undergoing PCI/stenting, we suggest attention to modifiable bleeding risk factors at every patient contact, and assessment of bleeding risk using the HAS-BLED score. (W-L)
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In AF patients requiring OAC undergoing elective PCI/stenting, where bleeding risk is low (HAS-BLED 0-2) relative to risk for recurrent ACS and/or stent thrombosis, we suggest triple therapy for one month, followed by dual therapy with OAC plus single antiplatelet (preferably clopidogrel) until 12 months, following which OAC monotherapy can be used. (W-L)
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In AF patients requiring OAC undergoing elective PCI/stenting, where bleeding risk is high (HAS-BLED ≥3), we suggest triple therapy for one month, followed by dual therapy with OAC plus single antiplatelet (preferably clopidogrel) for 6 months, following which OAC monotherapy can be used. (W-L)
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In AF patients requiring OAC undergoing elective PCI/stenting , where bleeding risk is unusually high and thrombotic risk relatively low, we suggest use of OAC plus single antiplatelet (preferably clopidogrel) for 6 months, following which OAC monotherapy can be used. (W-L)
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In AF patients requiring OAC presenting with an ACS, undergoing PCI/stenting, where bleeding risk is low (HAS-BLED 0-2) relative to risk for ACS or stent thrombosis, we suggest triple therapy for 6 months, followed by dual therapy with OAC plus single antiplatelet (preferably clopidogrel) until 12 months, following which OAC monotherapy can be used. (W-L)
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In AF patients requiring OAC presenting with an ACS, undergoing PCI/stenting, where bleeding risk is high (HAS-BLED ≥3), we suggest triple therapy for 1-3 months, followed by dual therapy with OAC plus single antiplatelet (preferably clopidogrel) up to 12 months, following which OAC monotherapy can be used. (W-L)
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In AF patients requiring OAC presenting with an ACS, undergoing PCI/stenting where bleeding risk is unusually high and thrombotic risk low, we suggest OAC plus single antiplatelet (preferably clopidogrel) for 6-9 months may be considered, following which OAC monotherapy can be used. (W-L)
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In AF patients with ACS or undergoing PCI in whom OAC is recommended, we suggest using VKA with TTR>65-70% (INR range 2.0-3.0), or to use a NOAC at a dose licensed for stroke prevention in AF. (W-L)
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In AF patients in which aspirin is concomitantly used with OAC, we suggest a dose 2167 of 75-100mg qd with concomitant use of PPI to minimize gastrointestinal bleeding. (W-L)
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In AF Patients in which a P2Y12 inhibitor is concomitantly used with OAC, we suggest the use of clopidogrel. (W-L)
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For patients with AF and stable coronary artery disease (eg, no acute coronary syndrome within the previous year) and who choose oral anticoagulation, we suggest OAC with either a NOAC or adjusted dose VKA therapy alone (target international normalized ratio [INR] range, 2.0-3.0) rather than the combination of OAC and aspirin. (W-L)
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CATHETER OR SURGICAL ABLATION, ELECTROPHYSIOLOGICAL PROCEDURES

In patients with AF in whom catheter ablation of AF or implantation of cardiac electronic implantable devices is planned, we suggest performing the procedure on uninterrupted VKA in the INR therapeutic range, dabigatran or rivaroxaban. (W-L)
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In patients in whom sinus rhythm has been restored, we suggest that long-term anticoagulation should be based on the patient’s CHA2DS2VASc thromboembolic risk profile, regardless of whether sinus rhythm has been restored via ablation, cardioversion (even spontaneous), or other means. (W-L)
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CEREBROVASCULAR DISEASE

In AF patients with acute ischaemic stroke, we suggest that very early anticoagulation (<48h) using heparinoids or VKA should not be used. (U-CBS)
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In AF patients with acute stroke without contraindications, we recommend that long term oral anticoagulation is indicated as secondary prevention. (S-H)
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In AF patients with acute ischaemic stroke, We suggest that oral anticoagulation should usually be started within 2 weeks of acute ischaemic stroke, but the optimal timing within this period is not known. (U-CBS)
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In patients with AF and high ischaemic stroke risk, we suggest anticoagulation with a NOAC after acute spontaneous ICH (which includes subdural, subarachnoid and intracerebral haemorrhages) after careful consideration of the risks and benefits. (U-CBS)
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In ICH survivors at high risk of recurrent ICH (e.g. those with probable cerebral amyloid angiopathy), we suggest left atrial appendage occlusion. (U-CBS)
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In patients with AF and symptomatic carotid stenosis (>50%), we suggest carotid revascularisation with endarterectomy or stenting in addition to OAC as indicated. (W-M)
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In patients with AF and carotid stenosis treated with revascularisation, we suggest OAC therapy, without long-term antiplatelet therapy. (U-CBS)
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ATRIAL HIGH-RATE EPISODES DETECTED BY CARDIAC IMPLANTED ELECTRONIC DEVICES

For patients that present with a clinically documented episode of AF (12-lead ECG or other means, eg. external devices with validated rhythm detection), we suggest that the presence or absence of symptoms must not influence the process of decision making with regard to the need for anticoagulation based on risk stratification. (U-CBS)
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In cases of AHRE (atrial high rate episodes) detected by a CIED of at least 5 min duration, we suggest that direct analysis of electrograms corresponding to AHRE is clinically indicated to exclude artifacts or other causes of inappropriate detection of atrial tachyarrhythmias or AF. (U-CBS)
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In patients with AF, we suggest that prescription of oral anticoagulants could be considered as a result of an individualized clinical assessment taking into account overall AHRE burden (in the range of hours rather than minutes) and specifically, the presence of AHRE >24 hours, individual stroke risk (using CHA2DS2VASc), predicted risk benefit of oral anticoagulation and informed patient preferences. (U-CBS)
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ATRIAL FLUTTER

For patients with atrial flutter, we suggest that antithrombotic therapy decisions follow the same risk-based recommendations as for AF. (U-CBS)
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PREGNANCY

For women receiving OAC for prevention of stroke/TE in AF who become pregnant, we suggest discontinuation of OAC with a VKA between weeks 6 and 12 and replacement by LMWH twice daily (with dose adjustment according to weight and target anti-Xa level 4-6 hours post-dose 0.8-1.2 U/mL), especially in patients with a warfarin dose required of >5 mg/day (or phenprocoumon >3 mg/day or acenocoumarol >2mg/day). OAC should then be discontinued and replaced by adjusted-dose LMWH (target anti-Xa level 4-6 hours post-dose 0.8-1.2 U/mL) in the 36th week of gestation. (U-CBS)
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For women on treatment with long-term vitamin K antagonists who are attempting 2740 pregnancy and are candidates for LMWH substitution, we suggest performing frequent pregnancy tests and use LMWH instead of VKA when pregnancy is achieved rather than switching to LMWH while attempting pregnancy. (U-CBS)
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For pregnant women, we suggest avoiding the use of NOACs. (U-CBS)
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For lactating women using warfarin, acenocoumarol, or UFH who wish to breastfeed, we suggest continuing the use of warfarin, acenocoumarol, LMWH or UFH. (U-CBS)
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For breast-feeding women, we suggest alternative anticoagulants rather than NOACs. (U-CBS)
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ATRIAL FIBRILLATION AND CHRONIC KIDNEY DISEASE

For mild CKD (Stage II, CrCl 60-89 ml/min), we suggest that oral anticoagulation clinical decision making and treatment recommendations match that of patients without CKD. (W-VL)
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For moderate CKD (Stage III, CrCl 30-59 ml/min), we suggest oral anticoagulation in patients with a CHA2DS2VASc ≥2 with label-adjusted NOACs or dose adjusted vitamin K antagonists. (W-VL)
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In severe non-dialysis CKD (Stage IV CrCl 15-30), we suggest using VKAs and selected NOACs (rivaroxaban 15mg QD, apixaban 2.5mg bid, edoxaban 30mg QD and (in USA only) dabigatran 75mg bid) with caution, based on pharmacokinetic data. (U-CBS)
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In end-stage renal disease (CrCl <15 or dialysis-dependent), we suggest that individualized decision-making is appropriate. (U-CBS)
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In end-stage renal disease (CrCl <15 or dialysis-dependent , we suggest using well managed VKA with TTR>65-70%. (U-CBS)
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AF WITH ASSOCIATED VALVULAR HEART DISEASE

In patients with AF at high risk of ischaemic stroke who have absolute contraindications for OAC, we suggest using LAA occlusion. (W-L)
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In AF patients at risk of ischaemic stroke undergoing cardiac surgery, we suggest considering surgical exclusion of the LAA for stroke prevention, but the need for long term OAC is unchanged. (W-L)
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In AF patients taking warfarin without high risk of thromboembolism or do not have a mechanical valve, we suggest pre-operative management without bridging. (W-L)
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In AF patients on antithrombotic prophylaxis with warfarin with a high risk of thromboembolism or with a mechanical valve, we suggest pre-operative management with bridging. (W-L)
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In AF patients on antithrombotic prophylaxis with a NOAC, we suggest pre-operative management without bridging. (W-L)
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THE PATIENT

In AF patients who have previously refused OAC, we suggest reinforcing educational messages at each contact with the patient and revisit OAC treatment decisions. (U-CBS)
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Recommendation Grading

Overview

Title

Antithrombotic Therapy For Atrial Fibrillation

Authoring Organization

Publication Month/Year

February 1, 2012

Last Updated Month/Year

January 23, 2024

Document Type

Guideline

External Publication Status

Published

Country of Publication

US

Document Objectives

The risk of stroke varies considerably across different groups of patients with atrial fibrillation (AF). Antithrombotic prophylaxis for stroke is associated with an increased risk of bleeding. We provide recommendations for antithrombotic treatment based on net clinical benefit for patients with AF at varying levels of stroke risk and in a number of common clinical scenarios.

Target Patient Population

Patients with AF

Inclusion Criteria

Female, Male, Adolescent, Adult, Older adult

Health Care Settings

Ambulatory, Emergency care, Hospice, Hospital, Long term care, Outpatient

Intended Users

Nurse, nurse practitioner, physician, physician assistant

Scope

Assessment and screening, Prevention, Management, Treatment

Diseases/Conditions (MeSH)

D001281 - Atrial Fibrillation, D000925 - Anticoagulants, D020521 - Stroke, D011655 - Pulmonary Embolism

Keywords

atrial fibrillation, anticoagulation, stroke, afib, Stroke Prevention, Antithrombotic Agents, Anticoagulation

Supplemental Methodology Resources

Data Supplement, Data Supplement

Methodology

Number of Source Documents
175
Literature Search Start Date
January 1, 2005
Literature Search End Date
October 1, 2009