- 1.Anticoagulation in the context of cardioversion of AF;
- 2.The management of antithrombotic therapy for patients with AF in the context of coronary artery disease (CAD);
- 3.Investigation and management of subclinical AF (SCAF);
- 4.The use of antidotes for the reversal of non-vitamin K antagonist oral anticoagulants (NOACs);
- 5.Acute pharmacological cardioversion of AF;
- 6.Catheter ablation for AF, including patients with concomitant AF and heart failure (HF);
- 7.Integrated approach to the patient with AF and modifiable cardiovascular risk factors.
I. Anticoagulation in the Context of Cardioversion
OAC use before and after cardioversion
- 1.We recommend that in addition to appropriate rate control, most hemodynamically stable patients with AF or AFL for whom elective electrical or pharmacological cardioversion is planned should receive therapeutic anticoagulation for 3 weeks before cardioversion (Strong Recommendation, Moderate-Quality Evidence).
- 2.We suggest that pharmacological or electrical cardioversion of symptomatic AF or AFL without at least 3 weeks of previous therapeutic anticoagulation be reserved for patients with the following characteristics (Weak Recommendation, Low-Quality Evidence):
- i.Patients with NVAF who present with a clear AF onset within 12 hours in the absence of recent stroke or transient ischemic attack (within 6 months);
- ii.Patients with NVAF and a CHADS2 score < 2 who present after 12 hours but within 48 hours of AF onset.
- 3.We suggest that, as an alternative to at least 3 weeks of therapeutic anticoagulation before cardioversion, transesophageal echocardiography (TEE) may be used to exclude cardiac thrombus (Weak Recommendation, Moderate-Quality Evidence).
- 4.We recommend that immediate electrical cardioversion be considered for patients whose recent-onset AF/AFL is the direct cause of instability with hypotension, acute coronary syndrome (ACS), or pulmonary edema (Strong Recommendation, Low-Quality Evidence).
- 5.When a decision has been reached that a patient will be undergoing unplanned cardioversion of AF/AFL, we suggest that therapeutic anticoagulation therapy be initiated immediately (preferably before cardioversion) with either a NOAC, or with heparin followed by adjusted-dose warfarin (Weak Recommendation, Low-Quality Evidence).
- 6.We suggest that, in the absence of a strong contraindication, all patients who undergo cardioversion of AF/AFL receive at least 4 weeks of therapeutic anticoagulation (adjusted-dose warfarin or a NOAC) after cardioversion. (Weak Recommendation, Low-Quality Evidence). Thereafter, we recommend that the need for ongoing antithrombotic therapy should be on the basis of the risk of stroke as determined by the CCS Algorithm (“CHADS-65”; Strong Recommendation, Moderate-Quality Evidence).
The use of TEE to exclude left atrial thrombus
NOACs vs warfarin for cardioversion
II. Management of Antithrombotic Therapy in Patients With AF and CAD
- 7.We recommend that patients who have concomitant AF and coronary/arterial vascular disease (peripheral vascular disease or aortic plaque), receive an antithrombotic therapy regimen that is on the basis of a balanced assessment of their risk of AF-related stroke, ischemic coronary event, and clinically relevant bleeding associated with the use of antithrombotic agents (Strong Recommendation, High-Quality Evidence [Fig. 2]).
Stable vascular disease and AF in patients at low risk of SSE
- 8.For patients with NVAF/AFL aged < 65 years with no CHADS2 risk factors, we suggest no antithrombotic therapy for stroke prevention (Weak Recommendation, Moderate-Quality Evidence), with management of their coronary or arterial vascular disease as directed by the 2018 CCS/CAIC focused update of the guidelines for the use of antiplatelet therapy.52
Stable vascular disease and AF in patients at high risk of SSE
- Brouwer M.A.
- van den Bergh P.J.
- Aengevaeren W.R.
- et al.
- 9.For patients with AF aged ≥ 65 years or with a CHADS2 score ≥ 1 and coronary or arterial vascular disease (peripheral vascular disease or aortic plaque), we recommend long-term therapy with an OAC alone (Strong Recommendation, High-Quality Evidence).
- 10.When an OAC is indicated in the presence of coronary or arterial vascular disease, we suggest a NOAC in preference to warfarin (Weak Recommendation, Moderate-Quality Evidence).
PCI or ACS in patients with AF
Key trials of dual pathway therapy vs triple therapy in AF with ACS/PCI
Duration of TT
AF patients at higher risk of stroke who undergo PCI without high-risk features
- 11.For patients with AF aged ≥ 65 years or with a CHADS2 score ≥ 1, we suggest dual pathway therapy (an OAC with clopidogrel 75 mg/d) for at least 1 month after BMS implantation and at least 3 months after DES implantation (Weak Recommendation, Moderate-Quality Evidence).
AF patients at higher risk of stroke who undergo PCI for ACS or elective PCI with high-risk features
- 12.For patients with AF aged ≥ 65 years or with a CHADS2 score ≥ 1, we recommend an initial regimen of TT (ASA 81 mg/d with clopidogrel 75 mg/d with an OAC) up to 6 months after PCI (Strong Recommendation, Moderate-Quality Evidence). After ASA discontinuation, which may occur as early as the day after PCI, we suggest that dual pathway therapy (an OAC with clopidogrel 75 mg/d) be continued for up to 12 months after PCI (Weak Recommendation, Moderate-Quality Evidence).
AF patients at higher risk of stroke in association with medically managed type 1 MI
- 13.For patients with AF aged ≥ 65 years or with a CHADS2 score ≥ 1, we suggest that dual pathway therapy (an OAC with clopidogrel 75 mg/d, rather than prasugrel or ticagrelor) be given without concomitant ASA for 12 months after ACS (Weak Recommendation, Low-Quality Evidence).
III. Investigation and Management of SCAF
- 14.We suggest that it is reasonable to prescribe OAC therapy for patients who are aged 65 years or older or with a CHADS2 score of ≥ 1 (CHADS-65) who have episodes of SCAF lasting > 24 continuous hours in duration. Additionally, high-risk patients (such as those with a recent embolic stroke of unknown source) with shorter-lasting episodes might also be considered for OAC therapy (Weak Recommendation, Low-Quality Evidence).
IV. Antidotes for NOACs/NOAC Reversal Agents
- 15.We recommend administering idarucizumab for emergency reversal of dabigatran’s anticoagulant effect in patients with uncontrollable or potentially life-threatening bleeding and/or in patients who require urgent surgery for which normal hemostasis is necessary (Strong Recommendation, Moderate-Quality Evidence).
V. Acute Pharmacological Rhythm Control
|Medication||Dose||Time to conversion||Risks|
|Procainamide||15-18 mg/kg I.V. over 30-60 minutes||Approximately 60 minutes||Hypotension|
|Flecainide||300 mg PO (> 70 kg)|
200 mg PO (≤ 70 kg)
Bradycardia and conversion pauses
1:1 Conduction of atrial flutter
|Propafenone||600 mg PO (> 70 kg)|
450 mg PO (≤ 70 kg)
|Ibutilide||1 mg I.V. over 10 minutes|
May repeat once
|30-60 minutes||QT prolongation|
Torsades de pointes
|Amiodarone||150 mg I.V. bolus then|
60 mg/h for 6 hours then
30 mg/h for 18 hours
Torsades de pointes
|Vernakalant||3 mg/kg I.V. over 10 minutes, followed by 2 mg/kg I.V. if no conversion||12-30 minutes||Hypotension|
Nonsustained ventricular tachycardia
- Priori S.G.
- Wilde A.A.
- Horie M.
- et al.
- January C.T.
- Wann L.S.
- Alpert J.S.
- et al.
|Appropriate candidates for PIP|
|Contraindication to PIP|
|PIP administration||Immediate release oral AV nodal blocker (one of diltiazem 60 mg, verapamil 80 mg, or metoprolol tartrate 25 mg) 30 minutes before the administration of a class Ic AAD (300 mg of flecainide or 600 mg of propafenone if ≥ 70 kg; 200 mg of flecainide or 450 mg of propafenone if < 70 kg)|
|Initial ED monitoring||Telemetry for at least 6 hours|
Blood pressure monitoring every 30 minutes
12-Lead ECG monitoring every 2 hours
|Determinants of initial treatment failure|
|Instructions for subsequent out-of-hospital use||Patients should take the AV nodal agent 30 minutes after the perceived arrhythmia onset, followed by the class Ic AAD 30 minutes after the AV nodal agent.|
After AAD administration patients should rest in a supine or seated position for the next 4 hours, or until the episode resolves
Patients should present to the ED in the event that:
VI. Catheter Ablation of AF
- Di Biase L.
- Burkhardt J.D.
- Santangeli P.
- et al.
- 16.We suggest that catheter ablation may be performed using uninterrupted therapeutic oral anticoagulation with either a NOAC or adjusted-dose warfarin (Weak Recommendation, Moderate-Quality Evidence).
Ablation in patients with AF and HF
|MacDonald et al.|
|AV node ablation with biventricular pacing||Medical rate control||Medical rate control||Medical rate control||Amiodarone rhythm control||Medical rate control||Medical therapy (rate or rhythm control)|
|• Persistent AF||48%||100%||100%||100%||100%||72%||70%|
|• HF hospitalization, RR (95% CI)||2.93 (0.12-69.83)||2.71 (0.12-62.70)||–||–||0.55 (0.39-0.76)||0.20 (0.01-4.01)||0.58 (0.41-0.81)|
|• All-cause mortality, RR (95% CI)||–||–||–||0.31 (0.01-7.23)||0.44 (0.20-0.97)||–||0.54 (0.34-0.84)|
|Standard mean difference in:|
|• LVEF improvement||9.00 (6.26-11.74)||1.70 (−4.17 to 7.57)||5.5 (0.00-11.00)||11.70 (5.62-17.78)||1.90 (0.55-3.25)||14.0 (8.50-19.50)||9.70 (2.57-16.83)|
|• 6-MW distance||55.0 (26.56-83.44)||−1.30 (−54.75 to 52.15)||42.34 (−7.51-92.19)||---||12.0 (0.51-23.49)||27.0 (−28.0 to 82.0)||31.60 (−49.03 to 112.23)|
VII. Integrated Approach to AF and Modifiable Cardiovascular Risk Factors
- 17.We recommend systematic and strict guideline-adherent management of traditional modifiable cardiovascular risk factors and/or conditions associated with AF, to reduce cardiovascular events (eg, stroke, MI, etc; Strong Recommendation, High-Quality Evidence).
|Conventional risk factors|
|• Advancing age|
|• Male sex|
|• HF with reduced ejection fraction|
|• Valvular heart disease|
|• Thyroid disease|
|• Obstructive sleep apnea|
|Emerging risk factors|
|• Chronic obstructive pulmonary disease|
|• Excessive alcohol intake|
|• Increased pulse pressure|
|• HF with preserved ejection fraction|
|• Congenital heart disease|
|• Subclinical hyperthyroidism|
|• Coronary artery disease|
|• Morphometric (increased height, increased birth weight)|
|• Excessive endurance exercise|
|Potential risk factors|
|• Familial/genetic factors|
|• Tobacco Use|
|Left atrial dilatation|
|• Pericardial fat|
|• Subclinical atherosclerosis|
|• Electrocardiographic (atrial conduction delay, PR interval prolongation)|
|• Chronic kidney disease|
- 18.We suggest that, in addition to implementing appropriate rate or rhythm control measures, an approach targeting modifiable risk markers and conditions associated with AF should be applied to prevent recurrence of the arrhythmia and/or decrease its symptom burden (Weak Recommendation, Low-Quality Evidence).
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