Approach

The main elements in the management of new-onset atrial fibrillation (AF) are:[1]​​[102][103][104]

  1. Ventricular rate control

  2. Restoration and maintenance of sinus rhythm

  3. Prevention of thromboembolic events.

As an initial step, identification and treatment of any potential triggers of new-onset AF is very important, because rate and rhythm control measures are less likely to succeed if the acute precipitant persists.[43]

Ventricular rate control

Management of new-onset AF depends on the nature of its presentation, so the urgency of the treatment required should be assessed. Most cases of new-onset AF revert to sinus rhythm spontaneously, but treatment may still be needed to restore adequate ventricular rate, with drugs such as beta-blockers, calcium-channel blockers, and occasionally digoxin.[105] Digoxin is not considered a first-line agent for the purpose of rate control, but it can be useful in patients with heart failure. One study explored whether digoxin use was independently associated with increased mortality in patients with AF; compared with propensity score–matched control participants, the risk of death and sudden death was significantly higher in new digoxin users.[106] In patients with AF taking digoxin, the risk of death was independently related to serum digoxin concentration and was highest in patients with concentrations of ≥1.2 ng/mL (≥1.54 nmol/L).[106]

Cases that revert spontaneously usually do so in the first 24 hours.[105] Patients whose AF does not revert, or who present with significant symptoms and hemodynamic instability, may require either direct current (DC) cardioversion or pharmacologic cardioversion.[1]​​[105]​ There is no significant difference in terms of outcome between DC and pharmacologic cardioversion. Timing of cardioversion in patients who are hemodynamically stable and minimally symptomatic is a topic of research. Some studies suggest no benefit of early cardioversion over a "wait and see" approach; others suggest outcomes are improved when cardioversion is performed early.[107][108]​ New-onset AF may be the first symptomatic presentation of paroxysmal AF, in patients with high risk substrates of stroke, it is reasonable to perform transesophageal echocardiography (TEE) before cardioversion to rule out left atrial (LA) clots.[109]​​

[Figure caption and citation for the preceding image starts]: Transesophageal echocardiogram showing left atrial appendage clot. LA=left atrium; LAA=left atrial appendage; LV=left ventricleFrom the collection of Dr Bharat Kantharia [Citation ends].com.bmj.content.model.Caption@78ce4856

Restoration and maintenance of sinus rhythm

Depending on further risks for AF, patients may require treatment with an antiarrhythmic agent to prevent AF and maintain sinus rhythm once it has been restored.[1]​ Antiarrhythmics are reasonable for long-term maintenance of sinus rhythm for patients with AF who are not candidates for, or decline, catheter ablation or who prefer antiarrhythmic therapy.[1] For more information on this see Established atrial fibrillation.

One multicenter randomized control trial looked at outcomes of a strategy of initiating rhythm-control therapy in patients with early AF (of less than 1 year duration). This study identified a reduced risk of death, from cardiovascular causes, stroke, and hospitalization for heart failure or acute coronary syndrome over 5 years in patients who received early rhythm-control therapy.[110]

Prevention of thromboembolic events

Anticoagulation is recommended in patients with AF irrespective of whether the AF is paroxysmal, persistent, or permanent, due to the high risk of thromboembolic events. Many patients require anticoagulation before, during, and after cardioversion to prevent thromboembolism.[111][112][113]​ Selection of stroke risk reduction therapy should be guided by the patient’s risk of stroke, risks of bleeding with therapy, and their individual preferences.[1]​ The key options for anticoagulation are a vitamin K antagonist such as warfarin, or a direct oral anticoagulant (DOAC) such as dabigatran, rivaroxaban, apixaban, or edoxaban. Both vitamin K antagonists and DOACs are approved as efficacious agents for stroke prevention in AF and in patients undergoing cardioversion.[1][11]​​​​ In patients with AF who are candidates for anticoagulation and do not have either moderate-severe rheumatic mitral stenosis or mechanical heart valves, DOACs are recommended over warfarin to reduce the risk of mortality, stroke, systemic embolism, and intracranial hemorrhage.[1]

DOACs are nonvitamin K-dependent and they fall into two classes: oral direct thrombin inhibitors (e.g., dabigatran) and oral direct factor Xa inhibitors (e.g., rivaroxaban, apixaban, edoxaban).[114] DOACs are approved for stroke prevention and have a more favorable side-effect profile than vitamin K antagonists in patients with nonvalvular AF. The fast onset of action of DOACs is also a benefit, which could reduce delays to cardioversion, as well as negating the need for an interim alternative anticoagulant.[115] DOACs are recommended over warfarin in eligible patients (i.e., patients who do not have moderate-to-severe mitral stenosis or a mechanical heart valve).[1]​​[116][117][118]​ The use of DOACs in this setting is supported by data from several studies, most notably:

  • The GARFIELD-AF study: a prospective registry of more than 52,000 patients with newly diagnosed AF. Data from GARFIELD-AF suggest that DOACs are associated with lower risks of all-cause death and bleeding than vitamin K antagonists such as warfarin.[119]

  • The RE-LY trial: compared dabigatran, an oral direct thrombin inhibitor, with warfarin. The trial included 18,113 patients and had a median follow-up of 2 years.[104] The results of RE-LY suggest that compared with warfarin, dabigatran showed noninferiority at a low dose, and superiority at a high dose regarding rates of stroke and systemic embolism (warfarin 1.69% per year, lower-dose dabigatran 1.53% per year, and higher-dose dabigatran 1.11% per year for primary end point of stroke and systemic embolism). Adverse bleeding event rates were lower with a lower dose and similar with a higher dose of dabigatran compared with warfarin. The rate of myocardial infarction was higher with both doses of dabigatran than with warfarin.[104][114]​​[120]

  • The ROCKET AF, ARISTOTLE, and ENGAGE-AF trials: the oral direct factor Xa inhibitors rivaroxaban, apixaban, and edoxaban were compared with warfarin for stroke prevention in patients with nonvalvular AF in the ROCKET AF (14,264 patients, median follow-up of 1.9 years), ARISTOTLE (18,201 patients, median follow-up of 1.8 years), and the ENGAGE-AF (21,105 patients, median follow-up of 2.8 years) trials, respectively.[121][122][123][124] The primary end point of stroke and/or systemic embolism were 1.7% per year with rivaroxaban compared with 2.2% per year with warfarin in the ROCKET AF trial, 1.3% per year with apixaban compared with 1.6% per year with warfarin in the ARISTOTLE trial, and 1.6% per year with a lower dose and 1.2% per year with a higher dose of edoxaban compared with 1.5% per year with warfarin in the ENGAGE-AF trial.[121][122][123][124]

  • One prospective cohort study comparing rivaroxaban to vitamin K antagonists for bleeding risk in patients over 80 years of age, with nonvalvular AF: the primary end point of major bleeding occurred in 6.5% of patients treated with rivaroxaban and 11.2% treated with vitamin K antagonists.[125] Fatal bleeding occurred in 0.9% of rivaroxaban patients and 3.3% of patients treated with vitamin K antagonists.[125]

These studies, together with results from meta-analyses and systematic reviews, have shown that DOACs are noninferior to warfarin for stroke prevention in patients with nonvalvular AF, and may be associated with a reduced risk of fatal bleeding.[120][125][126][127][128] [ Cochrane Clinical Answers logo ] [Evidence A] It is, therefore, reasonable to use DOACs as first-line agents or as a subsequent replacement for warfarin in patients with AF.[1]​ Based on the current evidence, dabigatran is favored as a first-line agent or subsequent replacement for warfarin in suitable patients who do not have marked renal insufficiency, and who do not have mechanical prosthetic valves.[114][120]

DOACs are generally safe in older patients; however, dabigatran may be associated with an increased risk of gastrointestinal bleeding compared with warfarin in patients ages >75 years.[129][130] DOACs should be used with caution in patients with renal impairment. In patients with nonvalvular AF and mild or moderate renal impairment, the use of DOACs has been found to be associated with a reduced risk of stroke or systemic embolism and a reduced risk of major bleeding compared with warfarin, which suggests a favorable risk profile of these agents in patients with mild-to-moderate renal disease.[131] Some DOACs may be used in patients with renal impairment. If a DOAC is suitable, depending on the degree of renal impairment and the indication for use, a dose adjustment may be required; consult the prescribing information for specific guidance on use in patients with renal impairment. DOACs should not be used in patients with mechanical prosthetic valves or moderate-to-severe mitral stenosis, due to an increased risk of stroke, heart attack, and blood clot in these patients, nor should they be used in combination with heparin (including low molecular weight heparin), heparin derivatives, or warfarin.[111] Patients with diabetes are at risk of complications of diabetes when treated with oral anticoagulants; this risk seems to be lower with DOACs compared with vitamin K antagonists. Dabigatran is favored for its efficacy and lower rates of adverse effects in this patient group.[132][133]

Warfarin remains the first-line therapy in patients with AF and moderate-severe rheumatic mitral stenosis or mechanical heart valves. Warfarin takes several days to have a therapeutic effect, so patients presenting with new-onset AF treated with warfarin are treated with intravenous heparin (activated partial thromboplastin time [aPTT] of 45-60 seconds) or subcutaneous low-molecular-weight heparin while they are awaiting cardioversion and being evaluated for long-term anticoagulation. Once the patient is established on warfarin, the efficacy and safety of anticoagulation with warfarin is highly dependent on the quality of anticoagulation control, as reflected by the average time in therapeutic range (TTR) of INR 2-3. The SAMe-TT₂R₂ scoring system (based on sex, age, medical history, treatment interactions, tobacco use, and race) is a tool that may help identify anticoagulation-naive patients who are less likely to maintain TTR >70% and who should, therefore, be managed with DOACs instead of warfarin.[134][135] SAMe-TT₂R₂ score Opens in new window

If there are no risk factors for stroke, aspirin (either alone or in combination with clopidogrel) is not recommended to reduce the risk of stroke or to prevent thromboembolic events.[1]

The choice of anticoagulation strategy depends on the presentation. Factors in the patient's presentation and diagnostic assessment that guide appropriate treatment include the following:

  • Whether the patient is hemodynamically stable or unstable

  • If hemodynamically stable, whether the patient is symptomatic or asymptomatic

  • If symptomatic, the onset of the symptoms (<48 hours, ≥48 hours, or unknown)

  • The presence of associated heart failure

  • The presence of a thrombus on TEE

  • If a thrombus is absent on TEE, thromboembolic risk is stratified. [ Atrial Fibrillation CHA(2)DS(2)-VASc Score for Stroke Risk Opens in new window ]

If the AF is of unknown duration, or if TEE cannot be performed, the patient should be treated as for presumed thrombus and recommendations for confirmed LA thrombus should be followed.

In the setting of AF, the left atrial appendage can play a role in blood stasis and clot formation, and consequently be a source of emboli.[11]​ Although oral anticoagulation is the standard of care to reduce the risk of ischemic stroke in patients with AF, it is contraindicated in some patients due to an excess risk of major bleeding.[1]​ Left atrial appendage occlusion (LAAO) may be considered as an alternative for stroke prevention in patients with a moderate to high risk of stroke (CHA₂DS₂-VASc score ≥2) when there are absolute contraindications to the use of anticoagulants (due to a nonreversible cause), or the risk of bleeding outweighs the benefits.[1][2][18]​​[136]​ For more information on this treatment see Established atrial fibrillation.

Need for hospital admission

Patients who present with new-onset AF who are at low risk for major clinical consequences (young patients with no structural heart diseases, no major cardiac symptoms, or hemodynamic compromise) may be discharged directly from the emergency department after stable sinus rhythm is restored.

Admission to the hospital is indicated for the following patient groups:

  • Patients with underlying heart disease who have hemodynamic consequences or symptoms of angina, heart failure, or syncope or who are at risk for a complication resulting from therapy of the arrhythmia

  • Older patients

  • Associated or precipitant medical conditions that require further treatment, such as heart failure, pulmonary problems (e.g., pneumonia, pulmonary embolism), hypertension, or hyperthyroidism.

Hemodynamically unstable AF

AF with a rapid ventricular rate causing ongoing chest pain, hypotension, shortness of breath, dizziness, or syncope requires immediate DC cardioversion. This is performed under adequate short-acting general anesthesia and involves delivery of an electrical shock synchronized with the intrinsic activity of the heart by sensing the R wave of the ECG (i.e., synchronized). The energy output for successful termination of new-onset AF varies from 200 J to a maximum of 400 J depending on the body size and the presence of other comorbid conditions. Lower energy of 100 J may be used as the starting level when biphasic energy is used.

For patients with hemodynamically unstable AF, initiation of anticoagulation should not delay DC cardioversion. It is reasonable to consider administering an intravenous bolus of unfractionated heparin followed by infusion, or low-molecular-weight heparin or DOAC and to continue this after cardioversion unless contraindicated.[1]

Hemodynamically stable AF: symptomatic

Patients require rate-control therapy until cardioversion is successful. If there is no evidence of heart failure, beta-blockers (e.g., intravenous esmolol, propranolol, metoprolol; oral atenolol, metoprolol, nadolol, propranolol, bisoprolol, carvedilol) or nondihydropyridine calcium-channel blockers (i.e., diltiazem, verapamil) are the preferred choice.[1] Nondihydropyridine calcium-channel blockers are useful in ventricular rate control in the absence of preexcitation. They provide reasonable rate control and also improve AF-related symptoms compared with beta-blockers.[1]​ If rate control is inadequate with monotherapy, a combination of a beta-blocker and calcium-channel blockers may be used. Patients should be carefully monitored to prevent excess atrioventricular nodal blockade.[1] If there is evidence of decompensated heart failure, nondihydropyridine calcium-channel blockers are contraindicated.[1] Certain beta-blockers, digoxin, or amiodarone may be used for rate control in patients with AF and heart failure.[1][15]

Patients presenting with new-onset AF of <48 hours' duration and no evidence of LA thrombus on TEE should have DC or pharmacologic cardioversion. DC cardioversion is fast, safe, and efficient. Pharmacologic cardioversion is accomplished with the use of antiarrhythmic agents.[137] However, these must be used with caution, as they may cause bradycardia or tachyarrhythmias. Antiarrhythmic agents with variable, but demonstrated, efficacy for cardioversion of new-onset AF include flecainide, propafenone, ibutilide, and amiodarone.[138][139][140]​ Class III agents (including amiodarone and ibutilide) are less efficacious than class IC agents (flecainide and propafenone) in conversion to sinus rhythm.[141][142][143][144]

The strategy for managing anticoagulation in patients presenting with new-onset AF of <48 hours' duration and with no evidence of LA thrombus is as follows:[1]​​

  • If CHA₂DS₂-VASc score is 0-1, no anticoagulation is required.

  • If CHA₂DS₂-VAS-VASc score is ≥2, intravenous heparin (aPTT of 45-60 seconds) or subcutaneous low-molecular-weight heparin should be started before cardioversion. Once sinus rhythm is restored, the patient should preferably be started on a DOAC, unless they are not eligible for a DOAC (e.g., presence of moderate-to-severe mitral valve stenosis or mechanical prosthetic valves), or DOACs are unavailable. After the heparin is stopped, the first dose of the DOAC is usually given at the next scheduled dose time; however, local guidance should be consulted for each DOAC. If not using DOACs, start warfarin, and continue heparin until the warfarin levels are therapeutic (INR 2-3).​

  • DOACs should not be used in patients with mechanical prosthetic valves or mitral stenosis. In such cases, warfarin is the recommended anticoagulant. The concomitant use of DOACs with heparin (including low molecular weight heparin), heparin derivatives, or warfarin is not recommended. DOACs should be used with caution in patients with renal impairment; consult prescribing information for specific guidance.

  • Anticoagulation should be established before cardioversion and continued for at least 4 weeks afterward, and may be required for longer in some patients.​[43]​​​[145]​​

If the onset of symptoms is 48 hours or more, a 3-week regimen of uninterrupted anticoagulant therapy or imaging evaluation is recommended to rule out intracardiac thrombus before electively opting for cardioversion.[1]​ CHA₂DS₂-VASc score also predicts risk of cardiovascular complications post cardioversion.[146] The strategy for managing anticoagulation in these patients is as follows:

  • If CHA₂DS₂-VASc score is 0-1, heparin should be started, and cardioversion should be delayed until the patient is established on heparin with a target aPTT of 45-60 seconds. Following successful cardioversion, heparin can be discontinued. There is currently no evidence to support longer-term anticoagulation in patients with a score of 1 or lower. However, therapeutic decisions should be based on an individual assessment of thromboembolic versus bleeding risk; long-term anticoagulation is always required for patients with any form of cancer, irrespective of CHA₂DS₂-VASc score, even after sinus rhythm has been restored.[145]​​[147][148][149]​​​​ If the decision is made to continue long-term anticoagulation in patients with a CHA₂DS₂-VASc score of 1, DOACs have a superior net benefit compared with vitamin K antagonists.[147][148]

  • If CHA₂DS₂-VASc score is ≥2, all eligible patients should preferably be started on a DOAC.[1]​ DOACs are recommended over warfarin in all cases other than for mitral stenosis and mechanical heart valve.​[28]​ If warfarin is used as an oral anticoagulant, the target INR should be established for 3-4 weeks before cardioversion is attempted.[28] DOACs should not be used in patients with mechanical prosthetic valves and mitral stenosis.[1]​ The concomitant use of DOACs with heparin (including low molecular weight heparin), heparin derivatives, or warfarin is contraindicated. DOACs should be used with caution in patients with renal impairment; consult prescribing information for specific guidance.  

  • Anticoagulation should be established before cardioversion and continued for at least 4 weeks afterward, and may be required for longer in some patients.[1]​​[43]​​​​[145]​​​​​

If there is evidence of LA thrombus on TEE, or the presence of thrombus is unknown or the duration of AF is unknown or for 48 hours or more, all eligible patients should preferably be put on a DOAC for at least 3-6 weeks; after this, imaging such as TEE should be repeated to rule out intracardiac thrombus before elective cardioversion.[1][43]​​​​​

Hemodynamically stable AF: asymptomatic

Patients with CHA₂DS₂-VASc score 0-1 can be observed. Most cases of new-onset AF revert to sinus rhythm spontaneously, usually in the first 24 hours.[105] If AF does not resolve spontaneously, rate-control therapy is required until cardioversion is successful. However, rate- and rhythm-control strategies have comparable clinical outcomes in many patients with AF; shared decision-making with the patient is recommended.[1]​​[105]​

Anticoagulation should be established before cardioversion and continued for at least 4 weeks afterward, and may be required for longer in some patients. If there is evidence of LA thrombus on TEE, or the presence of thrombus is unknown or the duration of AF is unknown or for 48 hours or more, all eligible patients should preferably be put on a DOAC for at least 3-6 weeks; after this, imaging such as TEE should be repeated to rule out intracardiac thrombus before elective cardioversion. DOACs are recommended over warfarin in all cases other than for mitral stenosis and mechanical heart valve. DOACs should not be used in patients with mechanical prosthetic valves and mitral stenosis. Further, If CHA₂DS₂-VASc score is ≥2, all eligible patients should preferably be started on a DOAC.[1][43]​ 

Postcardioversion management

  • Patients with a newly detected first episode of new-onset AF converted to sinus rhythm are usually not continued on rhythm maintenance antiarrhythmic therapy. However, based on AF burden, severity of presentation, and after shared decision, antiarrhythmics to maintain sinus rhythm may be considered on an individual basis especially in patients who are deemed not suitable for catheter ablation or those who refuse.

  • Therapeutic decisions should always be based on an individual assessment of thromboembolic versus bleeding risk.

  • Long-term anticoagulation is required for patients with identified high risk for thromboembolism (CHA₂DS₂-VASc score ≥1 in patients with nonvalvular AF, those with valvular AF, with prosthetic mitral valve, patients with hypertrophic cardiomyopathy; any form of cancer irrespective of CHA₂DS₂-VASc score), even after sinus rhythm has been restored.[1][145][147][148][149]

The Canadian Association of Emergency Physicians acute atrial fibrillation checklist is a helpful resource for assessing and treating new onset atrial fibrillation.  CAEP: acute atrial fibrillation/flutter best practices checklist Opens in new window

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