Cardio · arrhythmias
Cardioversion and anticoagulation timing
Fellowship-level guide to cardioversion of atrial fibrillation under the 2024 ESC AF guideline and the 2023 ACC/AHA/ACCP/HRS AF guideline, with the 2026 ESC heart failure and 2025 ESC pregnancy guidelines and the 2018 NHFA/CSANZ summary: the unstable patient, the 24-hour and 48-hour duration thresholds, transoesophageal echocardiography-guided cardioversion, anticoagulation before and after cardioversion, the wait-and-see approach, electrical technique, drug choice and doses for pharmacological cardioversion, and the trials behind them.
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Red flags
- AF with acute or worsening haemodynamic instability: ESC 2024 recommends electrical cardioversion to improve immediate patient outcomes (Class I, Level C); ACC/AHA 2023 says immediate electrical cardioversion should be performed to restore sinus rhythm when the instability is attributable to AF (COR 1, LOE C-LD)
- Early cardioversion is not recommended without appropriate anticoagulation or transoesophageal echocardiography if AF has lasted longer than 24 h, or if there is scope to wait for spontaneous cardioversion (ESC 2024, Class III, Level C)
- Intracardiac thrombus on pre-cardioversion imaging should prompt cancellation of the planned cardioversion (ACC/AHA 2023 text); when cardioversion is deferred because of LAA thrombus, therapeutic anticoagulation should be instituted for at least 3 to 6 weeks, after which imaging should be repeated before cardioversion (ACC/AHA 2023, COR 1, LOE C-LD)
- Pre-excited AF: atrioventricular nodal blocking agents (verapamil, diltiazem, amiodarone, digoxin, adenosine or beta blockers) are contraindicated because of the risk of precipitating ventricular fibrillation or haemodynamic deterioration (ACC/AHA 2023, COR 3: Harm, LOE B-NR)
- Electrical cardioversion: energy delivery should be confirmed to be synchronised to the QRS to reduce the risk of inducing ventricular fibrillation (ACC/AHA 2023, COR 1, LOE C-LD)
Abbreviations
| Abbreviation | Meaning |
|---|---|
| AF | atrial fibrillation |
| AFL | atrial flutter |
| OAC | oral anticoagulation |
| DOAC | direct oral anticoagulant |
| VKA | vitamin K antagonist |
| INR | international normalised ratio |
| TOE (ESC) / TEE (ACC/AHA) | transoesophageal echocardiography |
| LAA | left atrial appendage |
| LAAO | left atrial appendage occlusion |
| ECV | electrical cardioversion |
| HFrEF | heart failure with reduced ejection fraction |
| LVEF | left ventricular ejection fraction |
| LVH | left ventricular hypertrophy |
| ACS | acute coronary syndrome |
| DHF | decompensated heart failure |
| VF | ventricular fibrillation |
| MI | myocardial infarction |
| TIA | transient ischaemic attack |
| AV | atrioventricular (ACC/AHA) |
| AVN | atrioventricular node (ESC) |
| QTc | corrected QT interval |
| SBP | systolic blood pressure |
| NYHA | New York Heart Association |
| CrCl | creatinine clearance |
| HCM | hypertrophic cardiomyopathy |
| LMWH | low molecular weight heparin |
| SVT | supraventricular tachycardia |
| OR / CI | odds ratio / confidence interval |
| COR / LOE | ACC/AHA class of recommendation / level of evidence |
| ESC | European Society of Cardiology |
| ACC/AHA | American College of Cardiology/American Heart Association |
| NHFA/CSANZ | National Heart Foundation of Australia and Cardiac Society of Australia and New Zealand |
Overview and definitions
This page goes deep on one set of decisions: when to cardiovert AF, how, and how long to anticoagulate before and after. Diagnosis, stroke-risk scoring, rate control, long-term rhythm control and ablation are taught in the Atrial fibrillation topic. The 2024 ESC guideline defines rhythm control as therapies dedicated to restoring and maintaining sinus rhythm, including cardioversion, antiarrhythmic drugs, catheter ablation, endoscopic and hybrid ablation, and open surgical approaches.[1] The ESC adds that rhythm control is never a strategy on its own; it should always be part of the AF-CARE approach.[1]
Cardioversion comes in two forms.[2] The 2023 ACC/AHA/ACCP/HRS guideline calls electrical cardioversion a strategy for acute rhythm control and says that, compared with pharmacological cardioversion alone, synchronised direct current cardioversion is more rapid and efficacious for restoring sinus rhythm from AF.[2] The ESC describes pharmacological cardioversion as an elective procedure in haemodynamically stable patients.[1]
ESC 2024 rows, grouped by clinical situation:
Unstable or unscheduled
- ESC 2024: electrical cardioversion is recommended in AF with acute or worsening haemodynamic instability, to improve immediate patient outcomes (I, C)
- ESC 2024: initiation of therapeutic anticoagulation should be considered as soon as possible in unscheduled cardioversion for AF or atrial flutter, to prevent procedure-related thromboembolism (IIa, B)
Stable, recent onset
- ESC 2024: wait-and-see for spontaneous conversion within 48 h of AF onset should be considered without haemodynamic compromise, as an alternative to immediate cardioversion (IIa, B)
- ESC 2024: early cardioversion is not recommended without appropriate anticoagulation or TOE if AF lasted longer than 24 h, or if there is scope to wait for spontaneous cardioversion (III, C)
Scheduled or persistent AF
- ESC 2024: therapeutic OAC for at least 3 weeks is recommended before scheduled cardioversion of AF and atrial flutter, to prevent procedure-related thromboembolism (I, B)
- ESC 2024: cardioversion (electrical or pharmacological) should be considered in symptomatic patients with persistent AF as part of a rhythm control approach (IIa, B)
Why cardioversion carries a thromboembolic risk
The ESC states that any rhythm control procedure has an inherent risk of thromboembolism.[1] The ACC/AHA adds that thromboembolic risk and anticoagulation considerations apply to both pharmacological and electrical cardioversion.[2]
The ACC/AHA names four sources of risk around acute cardioversion: pre-existing thrombus, the change in atrial mechanical function with restoration of sinus rhythm, atrial stunning after cardioversion, and a transient prothrombotic state.[2] Spontaneous echocardiographic contrast with atrial dysfunction on TEE after cardioversion raised concern about atrial stunning, with mechanical atrial systole recovering over the ensuing month.[2]
- Speed of recovery: the ACC/AHA says recovery of mechanical atrial systole may be influenced by clinical variables, the duration of the AF episode leading to cardioversion, and the extent of comorbid conditions that are risk factors for atrial myopathy.[2]
- Timing of risk: thromboembolic risks are elevated around the time of cardioversion, especially within the 30 days after cardioversion (ACC/AHA).[2]
- Why anticoagulate on both sides: the ACC/AHA bases anticoagulation before cardioversion and for 4 weeks afterwards on elevated thromboembolic risk, high early recurrence of AF, and atrial dysfunction during this period.[2]
How large is the risk?
The three cohorts below are retrospective analyses.[2][11][12][13]
- FinCV (Finnish CardioVersion study): 7,660 cardioversions in 3,143 consecutive patients with AF lasting under 48 h; the embolic analysis covered 5,116 successful cardioversions in 2,481 patients with neither OAC nor peri-procedural heparin. There were 38 definite thromboembolic events (0.7%; 31 strokes) within 30 days, at a median of 2 days.[11]
- In FinCV (AF lasting under 48 h, with neither OAC nor peri-procedural heparin; embolic events assessed within 30 days after successful cardioversion), age (OR 1.05), female sex (OR 2.1), heart failure (OR 2.9) and diabetes (OR 2.3) independently predicted definite embolic events.[11]
- In the same FinCV analysis, risk was highest (9.8%) with heart failure and diabetes, and lowest (0.2%) with no heart failure and age under 60 years.[11]
- In a database study of electrical cardioversion within 48 h of AF onset, with thromboembolic events recorded within 30 days, 567 cardioversions without therapeutic anticoagulation were followed by 6 neurological events (1.06%), all in patients on aspirin alone.[12]
- In the same study of electrical cardioversion within 48 h of AF onset (events within 30 days), 898 cardioversions on therapeutic anticoagulation were followed by 2 neurological events (0.22%), both in patients off anticoagulation at the time of stroke; the odds ratio for events without vs with therapeutic anticoagulation was 4.8 (p = 0.03).[12]
- In that study of electrical cardioversion within 48 h of AF onset, no thromboembolic events occurred within 30 days with a CHA2DS2-VASc score below 2 (p = 0.06) or in patients with postoperative AF.[12]
- In a Danish nationwide cohort of 16,274 patients after a first-time direct current cardioversion (2000 to 2008), in the first 30 days after discharge the hazard ratio associated with no prior OAC was 2.25 (95% CI 1.43–3.53); the authors concluded that cardioversion without OAC is associated with a high risk of thromboembolism.[13]
The patients you will meet
- Unstable patients: the ESC includes those with haemodynamic instability caused by the arrhythmia or acute cardiac conditions, and severely ill patients who develop AF (sepsis, trauma, surgery, and particularly cancer-related surgery).[1]
- In unstable patients, the ESC says spontaneous restoration of sinus rhythm has been reported in up to 83% during the first 48 h after appropriate treatment of the underlying cause.[1]
- Stable, recent-onset, symptomatic AF in the emergency department: this was the RACE 7 ACWAS population, with haemodynamically stable AF of under 36 hours.[6][1]
- Uncertain onset: the ESC warns that the definite onset of AF is often not known, and the ACC/AHA raises concern about underestimating the actual duration of an episode because AF can occur without symptoms.[1][2]
- Persistent AF with an unclear link to symptoms: the ESC says restoring sinus rhythm by ECV might confirm the impact of the arrhythmia on symptoms or heart failure, and might help identify truly asymptomatic individuals, assess the impact of AF on LV function in HFrEF, and distinguish AF-related symptoms from heart failure symptoms.[1]
Before you shock: three distinctions
Is AF causing the instability? Is it flutter? Is there pre-excitation? Check:
Instability: is AF the cause?
- ESC 2024 text: rapid electrical cardioversion is recommended in acute or worsening haemodynamic instability thought to be caused by AF
- ACC/AHA 2023: with haemodynamic instability attributable to AF, immediate electrical cardioversion should be performed to restore sinus rhythm (COR 1, LOE C-LD)
- ESC 2024 text, for unstable patients whose AF has another underlying cause (for example sepsis, trauma or surgery): spontaneous restoration of sinus rhythm has been reported in up to 83% during the first 48 h after appropriate treatment of the underlying cause
Atrial flutter
- ESC 2024: therapeutic OAC for at least 3 weeks is recommended before scheduled cardioversion of AF and atrial flutter, to prevent procedure-related thromboembolism (I, B)
- ACC/AHA 2023, section 6.8.6 (typical, CTI-dependent AFL): after successful cardioversion or ablation restoring sinus rhythm, anticoagulation should be continued for at least 4 weeks (COR 1, LOE C-LD); left-sided AFLs or atrial tachycardias after AF ablation should be anticoagulated and managed like AF
- ESC 2024, Table 13: do not use flecainide for conversion of atrial flutter
Pre-excited AF
- ESC 2024 text: risk of fast ventricular rates via the accessory pathway, potentially leading to ventricular fibrillation and sudden death
- ACC/AHA 2023: agents that block atrioventricular nodal conduction (verapamil, diltiazem, amiodarone, digoxin, adenosine or beta blockers) are contraindicated because of the risk of precipitating VF or haemodynamic deterioration (COR 3: Harm, LOE B-NR)
Bedside assessment before cardioversion
Ask these before you consent the patient:
- Is there acute or worsening haemodynamic instability caused by AF? Then ESC 2024 recommends electrical cardioversion to improve immediate patient outcomes (Rec Table 15, Class I, Level C), and ACC/AHA 2023 says immediate electrical cardioversion should be performed to restore sinus rhythm when the instability is attributable to AF (section 8.2.2 recommendations, COR 1, LOE C-LD).[1][2]
- How long has AF lasted, and how sure is the onset? The ESC uses 24 h and warns that the definite onset is often not known; the ACC/AHA uses 48 hours, with 12 hours in its low-risk row.[1][2]
- Has the patient had at least 3 weeks of therapeutic anticoagulation? The ESC row recommends this before scheduled cardioversion to prevent procedure-related thromboembolism, and defines it as adherence to DOACs or INR 2.0 or more for VKAs.[1]
- What is the thromboembolic risk? The ACC/AHA rows use CHA2DS2-VASc (2 or more or equivalent; 0–1 or equivalent), and the ESC text makes post-cardioversion OAC optional only for patients without thromboembolic risk factors whose sinus rhythm was restored within 24 h of AF onset.[2][1]
- Is there a previous LAA occlusion device? The ACC/AHA has separate imaging and anticoagulation rows for it.[2]
- For drug choice: severe LVH, HFrEF, coronary artery disease, recent ACS or severe aortic stenosis (ESC Rec Table 17).[1]
- Sinus node dysfunction, atrioventricular conduction disturbances or prolonged QTc (above 500 ms)? ESC 2024 does not recommend pharmacological cardioversion in these patients unless risks for proarrhythmia and bradycardia have been considered (Rec Table 17, Class III, Level C).[1]
- Is there pre-excitation, pregnancy, cardiac amyloidosis or recent cardiac surgery? Each has its own guidance, covered below.[1][3][2]
Imaging to exclude thrombus
The ESC recommends TOE if 3 weeks of therapeutic OAC has not been provided, for exclusion of cardiac thrombus to enable early cardioversion (Class I, Level B).[1] The ESC text says TOE can be performed in acute settings or when early cardioversion is needed, to exclude cardiac thrombus before cardioversion, and that these approaches (at least 3 weeks of therapeutic anticoagulation, or TOE) have been tested in multiple randomised trials.[1]
With AF of 48 hours or more, the ACC/AHA recommends a 3-week duration of uninterrupted therapeutic anticoagulation or imaging evaluation to exclude intracardiac thrombus before elective cardioversion (COR 1, LOE B-R).[2] Its text adds that cardiac computed tomography, particularly with a delayed contrast-enhanced acquisition protocol, has emerged as an alternative imaging modality to exclude intracardiac thrombus.[2]
Multicentre randomised trial: treatment guided by TEE findings vs conventional treatment (described in the abstract background as warfarin for three weeks before electrical cardioversion)
Population: 1222 patients with AF of more than two days’ duration
Key finding
Primary end point (cerebrovascular accident, TIA or peripheral embolism within eight weeks): no significant difference in embolic events, 5 of 619 (0.8%) with TEE guidance vs 3 of 603 (0.5%) with conventional treatment (P = 0.50). Haemorrhagic events: 2.9% vs 5.5% (P = 0.03). Time to cardioversion: mean 3.0 vs 30.6 days (P < 0.001). At eight weeks, no significant differences in death, maintenance of sinus rhythm or functional status.
If thrombus is found
| Body | What to do |
|---|---|
| ESC 2024 (text) | Therapeutic anticoagulation for a minimum of 4 weeks, followed by repeat TOE to ensure thrombus resolution |
| ESC 2024 (Rec Table 15) | Repeat TOE should be considered before cardioversion if thrombus was identified on initial imaging, to ensure thrombus resolution and prevent peri-procedural thromboembolism (IIa, C) |
| ACC/AHA 2023 (section 8.2.1 recommendations) | When cardioversion is deferred due to LAA thrombus on pre-cardioversion imaging, therapeutic anticoagulation should be instituted for at least 3 to 6 weeks, after which imaging should be repeated before cardioversion (COR 1, LOE C-LD) |
- In patients with AF, the ACC/AHA says detection of intracardiac thrombus should prompt cancellation of planned cardioversion and, in anticoagulant-naïve patients, therapeutic anticoagulation.[2]
- Thrombus despite anticoagulation should prompt assessment of compliance, dosing appropriateness, drug absorption and drug interactions; switching to an alternative anticoagulant can be considered, although the benefit is uncertain (ACC/AHA).[2]
- As cited by the ACC/AHA, in anticoagulant-naïve patients, 61.2% had thrombus resolution on TEE 3 to 12 weeks after starting a VKA in the CLOT-AF registry, and 41.5% after 6 weeks of rivaroxaban in X-TRA.[2]
- Repeat imaging (TEE or computed tomography) is generally pursued after at least 3 to 6 weeks of therapeutic anticoagulation, to assess for resolution of intracardiac thrombus before reconsidering cardioversion (ACC/AHA).[2]
- In EMANATE (apixaban vs heparin/VKA in patients with AF and 48 h or less of anticoagulation before randomisation, undergoing cardioversion), 60 of 61 patients with thrombi on imaging continued randomised treatment, and all 61 were without outcome events.[9]
The unstable patient
| Body and row | Recommendation | Class / COR, level |
|---|---|---|
| ESC 2024, Rec Table 15 | Electrical cardioversion in AF patients with acute or worsening haemodynamic instability, to improve immediate patient outcomes | I, C |
| ACC/AHA 2023, section 8.2.2 recommendations (electrical cardioversion) | Haemodynamic instability attributable to AF: immediate electrical cardioversion should be performed to restore sinus rhythm | COR 1, LOE C-LD |
| ESC 2026 HF, Rec Table 15 (AF in patients with heart failure) | Urgent cardioversion in the setting of DHF in patients presenting with rapid ventricular rates and haemodynamic instability, to restore sinus rhythm | I, C |
| ESC 2024, Rec Table 15 | Unscheduled cardioversion for AF or atrial flutter: initiation of therapeutic anticoagulation should be considered as soon as possible, to prevent procedure-related thromboembolism | IIa, B |
- In unstable patients, the ESC still considers emergency electrical cardioversion the first-choice treatment if sinus rhythm is thought to be beneficial, despite a high rate of immediate relapse; amiodarone is second line because of its delayed activity, although it may be an appropriate alternative in the acute setting.[1]
- The ACC/AHA calls electrical cardioversion the treatment of choice for haemodynamically unstable AF, given its rapidity and efficacy, but notes that direct data on emergency cardioversion of unstable patients are limited by the emergency circumstances.[2]
- The ACC/AHA also states that no studies compare electrical with pharmacological cardioversion in haemodynamically unstable AF.[2]
- In HFrEF with haemodynamic instability, the 2026 ESC heart failure guideline says intravenous amiodarone or digoxin may be used for acute rate control and haemodynamics, although acute electrical cardioversion should be the first choice.[3]
- Pre-excited AF: the ESC says immediate electrical cardioversion is needed for haemodynamically compromised patients and atrioventricular node-modulating drugs should be avoided; the ACC/AHA says pre-excited AF with haemodynamic instability should be treated with electrical cardioversion (COR 1, LOE B-NR).[1][2]
Anticoagulation timing: the ESC 2024 approach
The ESC text explains its 24-hour threshold in three steps.[1] First, when the definite duration of AF is under 48 hours, cardioversion has typically been considered without pre-procedure OAC or TOE for thrombus exclusion.[1] Second, the definite onset is often not known, and observational data suggest stroke or thromboembolism risk is lowest within a much shorter time period.[1] Third, the task force reached consensus that safety should come first.[1]
In its text, the ESC states that cardioversion is not recommended if AF has lasted longer than 24 hours, unless the patient has already had at least 3 weeks of therapeutic anticoagulation or a TOE is performed to exclude intracardiac thrombus.[1]
| ESC 2024 Recommendation Table 15 (general concepts in rhythm control; complete) | Class, level |
|---|---|
| Electrical cardioversion is recommended in AF patients with acute or worsening haemodynamic instability to improve immediate patient outcomes | I, C |
| DOACs are recommended in preference to VKAs in eligible patients with AF undergoing cardioversion for thromboembolic risk reduction | I, A |
| Therapeutic OAC for at least 3 weeks (adherence to DOACs or INR 2.0 or more for VKAs) is recommended before scheduled cardioversion of AF and atrial flutter to prevent procedure-related thromboembolism | I, B |
| TOE is recommended if 3 weeks of therapeutic OAC has not been provided, for exclusion of cardiac thrombus to enable early cardioversion | I, B |
| OAC is recommended to continue for at least 4 weeks in all patients after cardioversion and long-term in patients with thromboembolic risk factor(s) irrespective of whether sinus rhythm is achieved, to prevent thromboembolism | I, B |
| Cardioversion of AF (either electrical or pharmacological) should be considered in symptomatic patients with persistent AF as part of a rhythm control approach | IIa, B |
| A wait-and-see approach for spontaneous conversion to sinus rhythm within 48 h of AF onset should be considered in patients without haemodynamic compromise as an alternative to immediate cardioversion | IIa, B |
| Implementation of a rhythm control strategy should be considered within 12 months of diagnosis in selected patients with AF at risk of thromboembolic events to reduce the risk of cardiovascular death or hospitalisation | IIa, B |
| Initiation of therapeutic anticoagulation should be considered as soon as possible in the setting of unscheduled cardioversion for AF or atrial flutter to prevent procedure-related thromboembolism | IIa, B |
| Repeat TOE should be considered before cardioversion if thrombus has been identified on initial imaging to ensure thrombus resolution and prevent peri-procedural thromboembolism | IIa, C |
| Early cardioversion is not recommended without appropriate anticoagulation or TOE if AF duration is longer than 24 h, or there is scope to wait for spontaneous cardioversion | III, C |
- After cardioversion, the ESC text says most patients should continue OAC for at least 4 weeks.[1]
- Only for those without thromboembolic risk factors and with sinus rhythm restored within 24 h of AF onset is post-cardioversion OAC optional (ESC text).[1]
- In the presence of any thromboembolic risk factor, the ESC says long-term OAC should be instituted irrespective of the rhythm outcome.[1]
- The ESC text sets the pre-cardioversion requirement as at least 3 weeks of therapeutic anticoagulation (adherence to DOACs or INR above 2 if VKA) before the electrical or pharmacological procedure; the Class I row recommends at least 3 weeks of therapeutic OAC (adherence to DOACs or INR 2.0 or more for VKAs) before scheduled cardioversion of AF and atrial flutter, to prevent procedure-related thromboembolism.[1]
Anticoagulation timing: the ACC/AHA 2023 approach
The ACC/AHA duration-based Class 1 row uses an AF duration of 48 hours or more; two COR 2b rows address AF under 48 hours, one by elevated thromboembolic risk and one by low risk combined with a duration under 12 hours.[2]
| ACC/AHA 2023 section 8.2.1 recommendations (prevention of thromboembolism in the setting of cardioversion; complete) | COR, LOE |
|---|---|
| AF duration of 48 hours or more: a 3-week duration of uninterrupted therapeutic anticoagulation or imaging evaluation to exclude intracardiac thrombus is recommended before elective cardioversion | 1, B-R |
| AF undergoing cardioversion: therapeutic anticoagulation should be established before cardioversion and continued for at least 4 weeks afterwards without interruption to prevent thromboembolism | 1, B-NR |
| Cardioversion deferred due to LAA thrombus on pre-cardioversion imaging: therapeutic anticoagulation for at least 3 to 6 weeks, after which imaging should be repeated before cardioversion | 1, C-LD |
| Previous LAAO, not on anticoagulation: imaging to assess the adequacy of LAAO and exclude device-related thrombosis before cardioversion may be reasonable | 2b, B-NR |
| Previous LAAO with residual leak: peri-cardioversion anticoagulation may be considered and continued thereafter | 2b, C-LD |
| Reported AF duration under 48 hours (not in the setting of cardiac surgery), not on anticoagulation: pre-cardioversion imaging to exclude intracardiac thrombus may be considered in those at elevated thromboembolic risk (CHA2DS2-VASc 2 or more or equivalent) | 2b, C-LD |
| Low thromboembolic risk (CHA2DS2-VASc 0–1 or equivalent) and AF duration under 12 hours: the benefit of pre-cardioversion imaging or peri-cardioversion anticoagulation is uncertain, given the low incidence of peri-cardioversion thromboembolic events in this population | 2b, C-LD |
- The ACC/AHA says the safety of cardioversion without further assessment or previous anticoagulation for AF under 48 hours has been challenged, and that thromboembolic risks in this group were not homogeneous but varied with the patient’s risk profile and AF duration.[2]
- Time to cardioversion of more than 12 hours has been reported as an independent predictor of thromboembolic complications (ACC/AHA text).[2]
- The ACC/AHA cites retrospective observational data from the FinCV (Finnish CardioVersion) study, a study of cardioversion of acute AF (AF lasting under 48 h), showing 30-day peri-cardioversion thromboembolic event rates of 0.4% with CHA2DS2-VASc 0 to 1 and 0.3% with AF of under 12 hours; the combination of a score of 0 to 1 and AF under 12 hours may identify a population at particularly low risk.[2][11]
- The ACC/AHA suggests that a more nuanced assessment may integrate a patient’s substrate for atrial myopathy and thromboembolic risk, instead of strict dependence on the previously used 48-hour threshold.[2]
- History (ACC/AHA text): early experience showed thromboembolism was less frequent in chronically anticoagulated patients, which led to an empiric recommendation for 3 weeks of anticoagulation before cardioversion in the ACUTE study of patients with more than 2 days of AF.[2]
ESC 2024
- Threshold: 24 h; early cardioversion is not recommended without appropriate anticoagulation or TOE if AF has lasted longer than 24 h, or if there is scope to wait for spontaneous cardioversion (III, C)
- Before scheduled cardioversion: therapeutic OAC for at least 3 weeks is recommended, to prevent procedure-related thromboembolism (I, B); if not provided, TOE is recommended to exclude cardiac thrombus and enable early cardioversion (I, B)
- After: OAC is recommended for at least 4 weeks in all, and long-term with thromboembolic risk factor(s) irrespective of whether sinus rhythm is achieved, to prevent thromboembolism (I, B); the ESC text makes it optional only without risk factors and with sinus rhythm restored within 24 h of onset
ACC/AHA 2023
- Threshold: 48 hours; a 3-week duration of uninterrupted therapeutic anticoagulation or imaging to exclude intracardiac thrombus is recommended before elective cardioversion (COR 1, LOE B-R)
- Reported duration under 48 hours (not after cardiac surgery), not on anticoagulation: imaging to exclude intracardiac thrombus may be considered in those at elevated thromboembolic risk, CHA2DS2-VASc 2 or more or equivalent (COR 2b); CHA2DS2-VASc 0–1 or equivalent and under 12 hours: benefit of imaging or peri-cardioversion anticoagulation uncertain (COR 2b)
- After: therapeutic anticoagulation should be established before and continued for at least 4 weeks without interruption, to prevent thromboembolism (COR 1, LOE B-NR)
NHFA/CSANZ 2018
- Published summary: cardioversion remains first-line choice for acute rhythm control when clinically indicated
- Published summary: if anticoagulation is indicated, non-vitamin K oral anticoagulants are recommended in preference to warfarin
Which anticoagulant?
The ESC recommends DOACs in preference to VKAs in eligible patients with AF undergoing cardioversion, for thromboembolic risk reduction (Class I, Level A).[1] The ACC/AHA says DOACs are alternatives to VKAs as thromboprophylaxis around cardioversion, and that, given rapid time to therapeutic efficacy, reliable maintenance of efficacy and ease of continuation, DOACs may be preferentially considered over VKAs for patients with AF planned for cardioversion, barring contraindications.[2] The ACC/AHA adds that at least 3 weeks of pre-cardioversion anticoagulation may be achieved with either VKAs or DOACs.[2]
The ESC summarises the trial evidence: three underpowered trials showed non-significantly lower cardiovascular event rates with DOACs than warfarin.[1] In a meta-analysis of these 5203 patients, predominantly undergoing electrical cardioversion, the composite of stroke, systemic embolism, MI and cardiovascular death was significantly lower with a DOAC (0.42% vs 0.98% with a VKA; risk ratio 0.42), with no significant difference in major bleeding.[1]
Randomised 2:1, rivaroxaban 20 mg once daily (15 mg if creatinine clearance 30–49 mL/min) vs dose-adjusted VKA; investigators chose an early (target 1–5 days after randomisation) or delayed (3–8 weeks) cardioversion strategy
Population: 1504 patients with AF undergoing elective cardioversion
Key finding
Composite of stroke, TIA, peripheral embolism, MI and cardiovascular death: 5 of 978 (0.51%) vs 5 of 492 (1.02%), risk ratio 0.50 (95% CI 0.15–1.73). Major bleeding 0.6% vs 0.8%. Time to cardioversion significantly shorter with rivaroxaban (P < 0.001).
Open-label, blinded-endpoint randomised trial: edoxaban 60 mg per day (30 mg with creatinine clearance 15–50 mL/min, weight 60 kg or less, or P-glycoprotein inhibitors) vs enoxaparin-warfarin; randomisation stratified by cardioversion approach (TEE or not), anticoagulant experience, edoxaban dose and region
Population: 2199 patients undergoing electrical cardioversion of non-valvular AF
Key finding
Stroke, systemic embolic event, MI and cardiovascular mortality: 5 (<1%) vs 11 (1%), OR 0.46 (95% CI 0.12–1.43). Major and clinically relevant non-major bleeding: 16 of 1067 (1%) vs 11 of 1082 (1%), OR 1.48 (95% CI 0.64–3.55). Results independent of the TEE-guided strategy and anticoagulation status.
Randomised: apixaban 5 mg twice daily (2.5 mg twice daily with two of age 80 years or more, weight 60 kg or less, serum creatinine 133 µmol/L or more) vs heparin/VKA; imaging and/or a 10 mg loading dose (down-titrated to 5 mg) allowed at investigator discretion to expedite cardioversion
Population: 1500 patients with AF and 48 h or less of anticoagulation before randomisation, undergoing cardioversion
Key finding
Full analysis set, apixaban vs heparin/VKA: strokes 0 of 753 vs 6 of 747 (nominal P = 0.015). Safety population: major bleeding 3 of 735 vs 6 of 721 (nominal P = 0.338). 855 patients had imaging and 342 received a loading dose.
The X-VeRT authors (AF undergoing elective cardioversion) concluded that rivaroxaban appears to be an effective and safe alternative to VKAs and may allow prompt cardioversion.[7] The ENSURE-AF authors (electrical cardioversion of non-valvular AF) and the EMANATE authors (AF with 48 h or less of anticoagulation before randomisation, undergoing cardioversion) reported low bleeding and thromboembolic event rates in both arms.[8][9]
After cardioversion: how long?
- ESC 2024: OAC is recommended for at least 4 weeks in all patients after cardioversion, and long-term in patients with thromboembolic risk factor(s), irrespective of whether sinus rhythm is achieved, to prevent thromboembolism (Class I, Level B).[1]
- ACC/AHA 2023: therapeutic anticoagulation should be established before cardioversion and continued for at least 4 weeks afterwards without interruption, to prevent thromboembolism (COR 1, LOE B-NR).[2]
- Atrial flutter: ACC/AHA 2023 section 6.8.6, which refers to typical right-sided (CTI-dependent) AFL, says anticoagulation should be continued for at least 4 weeks after successful cardioversion or ablation that restores sinus rhythm (COR 1, LOE C-LD); separately, ESC 2024 Recommendation Table 30 (prevention of thromboembolism in atrial flutter, not specific to cardioversion) recommends OAC in atrial flutter at elevated thromboembolic risk to prevent ischaemic stroke and thromboembolism (Class I, Level B).[2][1]
- The ESC text says thromboembolism prevention in atrial flutter includes peri-procedural and long-term OAC.[1]
The wait-and-see approach
The ESC cites spontaneous restoration of sinus rhythm in 76%–83% of patients with recent-onset AF: 10%–18% within the first 3 h, 55%–66% within 24 h and 69% within 48 h.[1] In the ESC text, these spontaneous conversions are likely to bias the limited contemporary data on the efficacy of pharmacological cardioversion.[1]
The ESC row says a wait-and-see approach for spontaneous conversion to sinus rhythm within 48 h of AF onset should be considered in patients without haemodynamic compromise, as an alternative to immediate cardioversion (Class IIa, Level B).[1]
Multicentre, randomised, open-label non-inferiority trial: wait-and-see (rate-control medication only, delayed cardioversion if AF did not resolve within 48 hours) vs early cardioversion
Population: Patients in the emergency department with haemodynamically stable, recent-onset (under 36 hours), symptomatic AF
Key finding
Sinus rhythm at 4 weeks: 193 of 212 (91%) with wait-and-see vs 202 of 215 (94%) with early cardioversion; difference −2.9 percentage points (95% CI −8.2 to 2.2; P = 0.005 for non-inferiority, margin −10).
- In RACE 7 ACWAS (haemodynamically stable, recent-onset symptomatic AF of under 36 hours in the emergency department), conversion within 48 hours in the wait-and-see group was spontaneous in 150 of 218 (69%) and followed delayed cardioversion in 61 (28%); in the early group, 36 of 219 (16%) converted spontaneously before cardioversion and 171 (78%) after cardioversion.[6][1]
- In the same RACE 7 ACWAS population, among patients who completed 4 weeks of remote monitoring, AF recurred in 49 of 164 (30%) with wait-and-see and 50 of 171 (29%) with early cardioversion; cardiovascular complications within 4 weeks after randomisation occurred in 10 and 8 patients, respectively.[6][1]
- The ESC summarises RACE 7 ACWAS, in patients with recent-onset symptomatic AF without haemodynamic compromise, as showing that waiting for spontaneous conversion until 48 h after the onset of AF symptoms was non-inferior to immediate cardioversion at 4 weeks follow-up.[1]
RACE 7 ACWAS wait-and-see arm (the trial protocol)
- 1
Rate control only
Initial treatment with rate-control medication only
- 2
Wait up to 48 hours
Delayed cardioversion if AF did not resolve within 48 hours
Electrical cardioversion: doing it well
| ACC/AHA 2023 section 8.2.2 recommendations (electrical cardioversion; complete) | COR, LOE |
|---|---|
| Haemodynamic instability attributable to AF: immediate electrical cardioversion should be performed to restore sinus rhythm | 1, C-LD |
| Haemodynamically stable AF: electrical cardioversion can be performed as initial rhythm-control strategy or after unsuccessful pharmacological cardioversion | 1, B-R |
| Energy delivery should be confirmed to be synchronised to the QRS to reduce the risk of inducing VF | 1, C-LD |
| Elective electrical cardioversion: biphasic energy of at least 200 J as initial energy can be beneficial to improve success of the initial shock | 2a, B-R |
| Elective cardioversion with longer duration of AF or unsuccessful initial shock: optimising the electrode vector, higher energy and pretreatment with antiarrhythmic drugs can facilitate success | 2a, B-NR |
| Obesity and AF: manual pressure augmentation and/or further escalation of electrical energy may be beneficial to improve success | 2b, C-LD |
- Sedation and setting: the ESC says ECV can be safely applied in elective and acute settings with sedation by intravenous midazolam, propofol or etomidate.[1]
- Monitoring: the ESC says blood pressure monitoring and oximetry should be used routinely, and intravenous atropine or isoproterenol, or temporary transcutaneous pacing, should be available in case of post-cardioversion bradycardia.[1]
- Waveform and energy: in the ESC text, biphasic defibrillators are standard because of their superior efficacy over monophasic defibrillators, and a randomised trial showed maximum fixed-energy shocks were more effective than low-escalating energy.[1]
- Pads: the ESC finds no single optimal electrode position (a meta-analysis of 10 randomised trials showed no difference in sinus rhythm restoration between anterior-posterior and antero-lateral positions), while active compression of the pads is associated with lower defibrillation thresholds and higher success rates.[1]
- Vector by AF duration: the ACC/AHA says that with biphasic maximal output and recent-onset AF either vector may be reasonable, but with longer AF duration the anterior-posterior vector may be favourable.[2]
- Body weight: increased body weight has been associated with reduced success, and in a small randomised study paddles, manual pressure augmentation and further energy escalation improved success in obese patients (ACC/AHA text).[2]
- Refractory cases: the ACC/AHA mentions two defibrillators used simultaneously, effectively doubling the delivered energy.[2]
Single-centre, single-blinded randomised trial: maximum-fixed (360-360-360 J) vs low-escalating (125-150-200 J) biphasic truncated exponential shocks
Population: 276 patients with elective cardioversion of AF
Key finding
Sinus rhythm 1 min after cardioversion: 114 of 129 (88%) vs 97 of 147 (66%); after the first shock: 75% vs 34%. No significant difference in any safety endpoint.
Antiarrhythmic pretreatment
- The ESC says immediate vernakalant, or 3–4 days of pretreatment with flecainide, ibutilide, propafenone or amiodarone, improves the rate of successful ECV and can facilitate long-term maintenance of sinus rhythm by preventing early recurrent AF.[1]
- In a meta-analysis cited by the ESC, amiodarone before cardioversion (200–800 mg/day for 1–6 weeks) and after (200 mg/day) significantly improved restoration and maintenance of sinus rhythm after ECV of AF.[1]
- The ACC/AHA says that with a longer duration of AF, immediate recurrence of AF, a previous unsuccessful electrical cardioversion, or a wish to make all reasonable efforts to avoid recurrence, antiarrhythmic pretreatment and continuation, to facilitate success of acute cardioversion and promote maintenance of sinus rhythm afterwards, may be pursued with shared decision-making.[2]
Diagnostic cardioversion
| Body and row | Recommendation | Class / COR, level |
|---|---|---|
| ESC 2024 AF, Rec Table 16 | Electrical cardioversion as a diagnostic tool should be considered in persistent AF where there is uncertainty about the value of sinus rhythm restoration on symptoms, or to assess improvement in LV function | IIa, C |
| ESC 2026 heart failure, Rec Table 4 (specialised investigations in established heart failure; under its investigations for HFrEF) | Electrical cardioversion as a diagnostic tool may be considered in persistent AF where there is uncertainty about the value of sinus rhythm restoration on symptoms or to assess improvement in LV function | IIb, C |
| ACC/AHA 2023, section 8.1 recommendations (goals of therapy with rhythm control) | Where symptoms associated with AF are uncertain, a trial of rhythm control (e.g. cardioversion or pharmacological therapy) may be useful to determine what, if any, symptoms are attributable to AF | 2b, C-LD |
For patients with HFrEF (listed under investigations for HFrEF in its table of specialised investigations in established heart failure), the newer 2026 ESC heart failure guideline says diagnostic electrical cardioversion may be considered (Class IIb) in these same circumstances.[3] The 2024 ESC AF guideline says it should be considered (Class IIa).[1] The 2024 ESC AF guideline lists the value of diagnostic cardioversion for persistent AF in steering AF management as a gap in evidence.[1]
Pharmacological cardioversion: choosing the drug
Why choose a drug at all? The ESC says pharmacological cardioversion does not require fasting, sedation or anaesthesia, but is less effective than electrical cardioversion, with timing a significant determinant of success.[1] The ESC bases the choice of drug on the type and severity of concomitant heart disease.[1]
| ESC 2024 Recommendation Table 17 (pharmacological cardioversion; complete) | Class, level |
|---|---|
| Intravenous flecainide or propafenone is recommended when pharmacological cardioversion of recent-onset AF is desired, excluding patients with severe LVH, HFrEF or coronary artery disease | I, A |
| Intravenous vernakalant is recommended when pharmacological cardioversion of recent-onset AF is desired, excluding patients with recent ACS, HFrEF or severe aortic stenosis | I, A |
| Intravenous amiodarone is recommended when cardioversion of AF in patients with severe LVH, HFrEF or coronary artery disease is desired, accepting there may be a delay in cardioversion | I, A |
| A single self-administered oral dose of flecainide or propafenone (pill-in-the-pocket) should be considered for patient-led cardioversion in selected patients with infrequent paroxysmal AF, after efficacy and safety assessment and excluding those with severe LVH, HFrEF or coronary artery disease | IIa, B |
| Pharmacological cardioversion is not recommended for patients with sinus node dysfunction, atrioventricular conduction disturbances or prolonged QTc (above 500 ms), unless risks for proarrhythmia and bradycardia have been considered | III, C |
- Speed: in a meta-analysis cited by the ESC, intravenous vernakalant and flecainide had the highest conversion rate within 4 h, possibly allowing discharge from the emergency department.[1]
- Class IC drugs (flecainide more so than propafenone) are superior for conversion within 12 h, while amiodarone works in a delayed fashion, within 24 h (ESC).[1]
- Anticoagulation still applies: the ESC says it should be started or continued according to a formal (re-)assessment of thromboembolic risk.[1]
| Drug (ESC 2024, Table 13) | Route and dosing | Acute success and time to sinus rhythm | Contraindications and precautions |
|---|---|---|---|
| Flecainide | Oral 200–300 mg; intravenous 1–2 mg/kg over 10 min | Oral 50%–60% at 3 h and 75%–85% at 6–8 h (3–8 h); intravenous 52%–95% (up to 6 h) | Not in severe structural or coronary artery disease, Brugada syndrome or severe renal failure (CrCl under 35 mL/min/1.73 m²); prior inpatient documentation of safety and efficacy before pill-in-the-pocket use; an AVN-blocking agent should be given to avoid 1:1 conduction if the rhythm transforms to AFL; stop the infusion if QRS widens by more than 25% or bundle branch block occurs; caution in sinus node disease and AVN dysfunction; do not use for conversion of atrial flutter |
| Propafenone | Oral 450–600 mg; intravenous 1.5–2 mg/kg over 10 min | Oral 45%–55% at 3 h, 69%–78% at 8 h (3–8 h); intravenous 43%–89% (up to 6 h) | The same cell as flecainide (shared in Table 13) |
| Amiodarone | Intravenous 300 mg over 30–60 min, then 900–1200 mg intravenous over 24 hours (or 200 mg oral three times daily for 4 weeks) | 44% (8–12 h to several days) | May cause phlebitis (use a large peripheral vein, avoid intravenous administration beyond 24 h, preferably a volumetric pump); may cause hypotension, bradycardia/atrioventricular block, QT prolongation; in hyperthyroidism only if no other option (risk of thyrotoxicosis); consider the broad range of drug interactions |
| Ibutilide | Intravenous 1 mg over 10 min (0.01 mg/kg if body weight under 60 kg); then 1 mg over 10 min, 10–20 min after the initial dose | 31%–51% (30–90 min) in AF; 60–75% in AFL (60 min) | Use in a cardiac care unit, as it may cause QT prolongation and torsades de pointes; ECG monitoring for at least 4 h after administration to detect any proarrhythmic effects; not in prolonged QT, severe LVH or low LVEF |
| Vernakalant | Intravenous 3 mg/kg over 10 min (maximum 339 mg); then 2 mg/kg over 10 min, 10–15 min after the initial dose (maximum 226 mg) | 50% within 10 min | Not in arterial hypotension (SBP under 100 mmHg), recent ACS (within 1 month), NYHA III or IV heart failure, QT prolongation or severe aortic stenosis; may cause arterial hypotension, QT prolongation, QRS widening or non-sustained ventricular tachycardia |
Table 13 also lists long-term doses in square brackets (flecainide 50–150 mg twice daily, propafenone 150–300 mg three times daily, amiodarone 200 mg oral daily); these are long-term doses for maintenance of sinus rhythm.[1]
The ACC/AHA rows and doses
| ACC/AHA 2023 section 8.2.3 recommendations (pharmacological cardioversion; complete) | COR, LOE |
|---|---|
| Pharmacological cardioversion is reasonable as an alternative to electrical cardioversion in those who are haemodynamically stable, or when electrical cardioversion is preferred but cannot be performed | 2a, C-LD |
| Ibutilide is reasonable for pharmacological cardioversion in patients without depressed LV function (LVEF under 40%) | 2a, A |
| Intravenous amiodarone is reasonable for pharmacological cardioversion, although time to conversion is generally longer than with other agents (8–12 hours) | 2a, A |
| Recurrent AF outside hospital: the pill-in-the-pocket approach with a single oral dose of flecainide or propafenone, with a concomitant AV nodal blocking agent, is reasonable if previously tested in a monitored setting | 2a, A |
| Intravenous procainamide may be considered for pharmacological cardioversion when other intravenous agents are contraindicated or not preferred | 2b, B-R |
| Drug (ACC/AHA 2023, Table 22) | Route and loading dose | Maintenance dose | Approximate time to sinus rhythm | Major adverse effects |
|---|---|---|---|---|
| Amiodarone | Intravenous 5–7 mg/kg or 300 mg | 1200–3000 mg by continuous infusion over 24 h | 8–12 h | Bradycardia, hypotension, QT prolongation, phlebitis, torsades de pointes |
| Flecainide | Oral, single dose: 200 mg if under 70 kg, 300 mg if over 70 kg | Not applicable | 3–8 h | Atrial flutter, AV block, dizziness, dyspnoea, exacerbation of HFrEF, headache, nausea, QT prolongation, ventricular tachycardia, visual disturbances |
| Ibutilide | Intravenous: 60 kg or more, 1 mg over 10 min; under 60 kg, 0.01 mg/kg over 10 min; a second equal dose may be given if the arrhythmia has not terminated within 10 min after the end of the first infusion | Not applicable | 30–90 min | Non-sustained ventricular tachycardia, QT prolongation, torsades de pointes |
| Procainamide | Intravenous 1 g over 30 min | 2 mg/min continuous infusion over 1 h | 30–60 min | Agranulocytosis, AV block, exacerbation of HFrEF, hypotension, neutropenia, QT prolongation, rash, thrombocytopenia, torsades de pointes |
| Propafenone | Oral, single dose: 450 mg if under 70 kg, 600 mg if over 70 kg | Not applicable | 3–8 h | Atrial flutter, AV block, dizziness, dyspnoea, exacerbation of HFrEF, nausea, taste disturbances, ventricular tachycardia, visual disturbances |
Table 22 footnotes: some studies have given intravenous amiodarone for 24 h followed by oral administration, and flecainide is available in an intravenous form in Europe.[2]
- Ibutilide: the ACC/AHA reports conversion rates of about 30% in AF (2% with placebo), greater efficacy in AFL (38%–63%), and most conversions within 30 to 90 minutes.[2]
- Ibutilide risk: torsades de pointes is more frequent with reduced LVEF, so the ACC/AHA says ibutilide is best avoided with LVEF 40% or less; a magnesium infusion immediately before ibutilide may mitigate the risk of torsades and excessive QT prolongation.[2]
- Amiodarone: the ACC/AHA says intravenous amiodarone needs 8 to 12 hours to convert AF, a much longer response time than ibutilide.[2]
- Single oral doses: the ACC/AHA cites 3- to 4-hour conversion rates of 58%–68% for flecainide (18%–29% with placebo) and 45%–57% for propafenone (17%–29% with placebo).[2]
- Procainamide: more effective than placebo (conversion at 1 hour 69% vs 38%) but less effective than ibutilide (14% vs 76%), with clinically significant hypotension in 5%–12% and potential to exacerbate HFrEF (ACC/AHA).[2]
- Not for acute use: the ACC/AHA says dofetilide, oral amiodarone and oral sotalol take several days to work and are not practical for acute pharmacological cardioversion, and data do not support intravenous sotalol.[2]
Pill-in-the-pocket
- The ESC says a single self-administered oral dose of flecainide or propafenone is effective in symptomatic patients with infrequent, recent-onset paroxysmal AF, and that safe use requires screening to exclude sinus node dysfunction, atrioventricular conduction defects or Brugada syndrome, plus prior in-hospital validation of efficacy and safety.[1]
- ESC 2024 Recommendation Table 18 (antiarrhythmic drugs for long-term maintenance of sinus rhythm): concomitant use of a beta-blocker, diltiazem or verapamil should be considered in AF patients treated with flecainide or propafenone, to prevent 1:1 conduction if their rhythm is transformed to atrial flutter (Class IIa, Level C).[1]
- ACC/AHA 2023 section 8.3.2 recommendations (inpatient initiation of antiarrhythmic agents): when starting pill-in-the-pocket flecainide or propafenone with an AV nodal blocking drug, it is reasonable to give the first dose in a facility with continuous ECG monitoring, given the potential for proarrhythmia (COR 2a, LOE B-NR).[2]
- The ACC/AHA says a beta blocker or non-dihydropyridine calcium channel blocker is generally given at least 30 minutes before flecainide or propafenone, to prevent 1:1 AV conduction during AFL.[2]
- In the study the ACC/AHA cites (268 emergency department patients with stable AF of recent onset; the 210 successfully treated were discharged with the plan), single-dose flecainide or propafenone was successful in 94% of episodes over 15 ± 5 months.[2]
- The ACC/AHA notes that the incidence of adverse effects across studies is not insignificant (6%–17%), so the strategy should only be used for highly selected patients after it has first been observed to be safe and effective in an inpatient setting.[2]
Electrical or pharmacological?
- ACC/AHA 2023: in haemodynamically stable AF, electrical cardioversion can be performed as the initial rhythm-control strategy or after unsuccessful pharmacological cardioversion (COR 1, LOE B-R), and pharmacological cardioversion is reasonable as an alternative (COR 2a, LOE C-LD).[2]
- The ACC/AHA favours electrical over pharmacological cardioversion when the patient can tolerate sedation, wants more immediate conversion, or has failed or not met candidacy for pharmacological cardioversion.[2]
- After an unsuccessful drug, the ACC/AHA says electrical cardioversion should be the next step, instead of switching to another antiarrhythmic drug with the risk of potentiating adverse effects such as QT prolongation or bradycardia.[2]
- In a retrospective propensity score-matched analysis of 374 haemodynamically stable emergency department patients cited by the ACC/AHA, successful cardioversion occurred in 78.2% with direct current cardioversion, 59.2% with pharmacological conversion and 37.9% with wait-and-watch (P under 0.001).[2]
- In its key messages (section 11), the ESC says: use electrical cardioversion in haemodynamic instability; otherwise choose electrical or pharmacological cardioversion based on patient characteristics and preferences.[1]
Partial factorial randomised trial at 11 Canadian emergency departments: intravenous procainamide (15 mg/kg over 30 min) then electrical cardioversion if necessary (up to three shocks of 200 J or more), vs placebo then electrical cardioversion; nested open-label comparison of anteroposterior vs anterolateral pad positions
Population: 396 adults with acute AF in the emergency department
Key finding
Conversion to sinus rhythm for at least 30 min: 96% drug-shock vs 92% shock-only (absolute difference 4%, 95% CI 0–9; p = 0.07); 52% of the drug-shock group converted with the infusion alone; discharge home 97% vs 95%; no serious adverse events; in Protocol 2 (n = 244), anterolateral vs anteroposterior pads 94% vs 92% (p = 0.68).
Specific scenarios
Previous left atrial appendage occlusion
- ACC/AHA 2023: with previous LAAO and no anticoagulation, imaging to assess the adequacy of LAAO and exclude device-related thrombosis before cardioversion may be reasonable (COR 2b, LOE B-NR); with a residual leak, peri-cardioversion anticoagulation may be considered and continued thereafter (COR 2b, LOE C-LD).[2]
- The ACC/AHA text calls pre-cardioversion imaging prudent after LAAO in patients not on anticoagulation, while noting that data to guide peri-cardioversion anticoagulation with LAAO are limited.[2]
- In a small multicentre retrospective analysis of patients with a Watchman device, TEE before electrical cardioversion detected device-related thrombus in 2.7% (4 of 148).[2]
Pre-excited AF
- ACC/AHA 2023: haemodynamically stable pre-excited AF: intravenous ibutilide or intravenous procainamide is recommended as an alternative to elective cardioversion (COR 1, LOE C-LD).[2]
- ESC 2024 text: pharmacological cardioversion can be attempted with ibutilide or flecainide, propafenone should be used with caution because of its effects on the atrioventricular node, and amiodarone should be avoided in pre-excited AF because of its delayed action.[1]
Heart failure and cardiac amyloidosis
- The 2026 ESC heart failure guideline says pharmacological and electrical cardioversion seem to have similar outcomes in decompensated heart failure with rapid AF and instability, although specific studies in heart failure populations are lacking.[3]
- The 2026 ESC heart failure text says amiodarone is recommended in HFrEF requiring pharmacological cardioversion, while propafenone, flecainide and dronedarone are associated with poorer outcomes in HFrEF and should be avoided.[3]
- Cardiac amyloidosis (ESC 2026 heart failure text): anticoagulation is indicated in patients with AF regardless of CHA2DS2-VA score, due to high thromboembolic risk, and TOE is necessary before cardioversion to exclude intracardiac thrombus, regardless of the duration of anticoagulation before the procedure.[3]
After cardiac surgery and in congenital heart disease
- ACC/AHA 2023: poorly tolerated AF after cardiac surgery: direct current cardioversion with antiarrhythmic drug therapy is recommended, considering imaging to rule out LAA thrombus where AF has been present more than 48 hours without anticoagulation (COR 1, LOE B-R).[2]
- ACC/AHA 2023: AF after cardiac surgery treated with rate control: at 30- to 60-day follow-up it is reasonable to assess the rhythm and, if AF has not reverted spontaneously, consider cardioversion after an adequate duration of anticoagulation (COR 2a, LOE C-LD).[2]
- The ACC/AHA under-48-hour imaging row excludes the setting of cardiac surgery.[2]
- Congenital heart disease (ESC 2024 text): when cardioversion is planned, both 3 weeks of OAC and TOE should be considered, because thrombi are common in congenital heart disease with atrial arrhythmias.[1]
Complications and pitfalls
- Thromboembolism: in FinCV (cardioversion of acute AF lasting under 48 h, with neither OAC nor peri-procedural heparin), definite thromboembolic events within 30 days occurred at a median of 2 days after cardioversion, and the authors of the Danish nationwide cohort (first-time DC cardioversion for AF) describe a high risk in the initial period after cardioversion without OAC.[11][13]
- VF from a poorly timed shock: the ACC/AHA says energy delivery should be confirmed to be synchronised to the QRS to reduce the risk of inducing VF, with synchronisation confirmed before each shock attempt.[2]
- Bradycardia after cardioversion: the ESC says intravenous atropine or isoproterenol, or temporary transcutaneous pacing, should be available.[1]
- The ACC/AHA lists monitoring for rare chronotropic, haemodynamic or thromboembolic complications, and for the effects of anaesthesia given during electrical cardioversion.[2]
- Drug toxicity (ESC Table 13): ibutilide may cause QT prolongation and torsades de pointes; vernakalant may cause arterial hypotension, QT prolongation, QRS widening or non-sustained ventricular tachycardia; amiodarone may cause phlebitis, hypotension, bradycardia or atrioventricular block and QT prolongation; with flecainide, an atrioventricular node-blocking agent should be given to avoid 1:1 conduction if the rhythm transforms to AFL.[1]
- Bleeding: in ACUTE (1222 patients with AF of more than two days), haemorrhagic events were fewer with the TEE-guided strategy than with conventional warfarin for 3 weeks before electrical cardioversion (2.9% vs 5.5%).[10][2]
Outcomes and disposition
- Recurrence: in RACE 7 ACWAS (haemodynamically stable, recent-onset symptomatic AF of under 36 hours in the emergency department), AF recurred within 4 weeks in 30% (wait-and-see) and 29% (early cardioversion) of monitored patients.[1][6]
- Going home: in RAFF2 (adults with acute AF in the emergency department), 97% (drug-shock) and 95% (shock-only) were discharged home.[14]
- Service design: the ESC says structured and integrated care for acute-onset AF in the emergency department is associated with better outcomes without compromising safety.[1]
- Long-term anticoagulation is decided by thromboembolic risk factors, not by the rhythm after cardioversion (ESC).[1]
- For follow-up, rate control and long-term rhythm control, use the Atrial fibrillation topic.
Special populations
Pregnancy
| Body and row | Recommendation | Class / COR, level |
|---|---|---|
| ESC 2024 AF, Rec Table 28 | Immediate electrical cardioversion in AF during pregnancy with haemodynamic instability or pre-excited AF, to improve maternal and foetal outcomes | I, C |
| ESC 2024 AF, Rec Table 28 | Electrical cardioversion should be considered for persistent AF in pregnant women with HCM, to improve maternal and foetal outcomes | IIa, C |
| ESC 2025 pregnancy, Rec Table 5 (cardiomyopathies and pregnancy) | Cardioversion for AF should be considered in pregnant women with HCM | IIa, C |
| ESC 2024 AF, Rec Table 28 | Intravenous ibutilide or flecainide may be considered to terminate AF in stable pregnant patients with a structurally normal heart, to improve maternal and foetal outcomes | IIb, C |
| ESC 2024 AF, Rec Table 28 | Therapeutic anticoagulation with LMWHs or VKAs (except VKAs in the first trimester or beyond week 36) for pregnant patients with AF at elevated thromboembolic risk, to prevent ischaemic stroke and thromboembolism | I, C |
| ESC 2025 pregnancy, Rec Table 14 (long-term management of SVT and AF) | Therapeutic anticoagulation with LMWH for pregnant women with persistent or permanent AF at elevated thromboembolic risk (LMWH only; no VKA option in this row) | I, C |
| ESC 2025 pregnancy, Rec Table 14 (acute management of SVT and AF) | Immediate electrical cardioversion for acute treatment of SVT with haemodynamic instability | I, C |
| ESC 2025 pregnancy, Rec Table 14 (acute management of SVT and AF) | Ibutilide or flecainide may be considered for termination of AF and AFL in pregnant women without structural heart disease | IIb, C |
| ACC/AHA 2023, section 10.13 recommendations (pregnancy) | In pregnant patients with AF, DC cardioversion is safe to patient and fetus and should be performed in the same manner as in patients who are not pregnant | COR 1, LOE B-NR |
| ACC/AHA 2023, section 10.13 recommendations (pregnancy) | Structurally normal heart and haemodynamically stable AF: pharmacological cardioversion with agents with a history of safe use in pregnancy, such as intravenous procainamide, may be considered | COR 2b, LOE C-LD |
- The 2025 ESC pregnancy guideline says electrical cardioversion is safe and effective in all phases of pregnancy because it does not affect foetal circulation or induce foetal arrhythmia; transthoracic impedance does not change in pregnancy, so shock energies should be the same as outside pregnancy, and the foetal heart rate should be monitored afterwards.[4]
- It also says the indication for LMWH before cardioversion, or the need for TOE, should be evaluated as in non-pregnant women, with anticoagulation maintained for at least 4 weeks after cardioversion.[4]
- The 2024 ESC AF text adds that cardioversion should generally be preceded by anticoagulation, that LMWH or unfractionated heparin is preferred because these do not cross the placenta, and that DOACs are not recommended in pregnancy because of safety concerns.[1]
- Anticoagulation rows differ by guideline: ESC 2024 AF recommends therapeutic anticoagulation with LMWHs or VKAs (except VKAs in the first trimester or beyond week 36) for pregnant patients with AF at elevated thromboembolic risk, to prevent ischaemic stroke and thromboembolism (Class I, Level C); the newer ESC 2025 pregnancy guideline recommends therapeutic anticoagulation with LMWH for pregnant women with persistent or permanent AF at elevated thromboembolic risk (Class I, Level C).[1][4]
- Hypertrophic cardiomyopathy: ESC 2024 AF says electrical cardioversion should be considered for persistent AF in pregnant women with HCM, to improve maternal and foetal outcomes (Class IIa, Level C); the newer ESC 2025 pregnancy guideline says cardioversion for AF should be considered in pregnant women with HCM (Class IIa, Level C), and its text adds that AF is poorly tolerated in HCM patients in general, due to the risk of haemodynamic decompensation, and that medical or electrical cardioversion of AF during pregnancy should be considered.[1][4]
Obesity, older patients and children
- Obesity: ACC/AHA 2023 says manual pressure augmentation and/or further escalation of electrical energy may be beneficial to improve success of electrical cardioversion (COR 2b, LOE C-LD).[2]
- Older patients: in FinCV (cardioversion of acute AF lasting under 48 h, with neither oral anticoagulation nor peri-procedural heparin), older age was an independent predictor of definite embolic events within 30 days of successful cardioversion (OR 1.05), and patients under 60 years without heart failure had the lowest risk (0.2%).[11]
- Children: the guideline rows quoted on this page are adult recommendations; no paediatric cardioversion rows are used here.
Guidelines, currency and regional differences
This page quotes the 2024 ESC AF guideline and the 2023 ACC/AHA/ACCP/HRS AF guideline, the newest AF guidelines from each body in the MedVellum cardiology guideline register (census 2026-10-05). The newer 2026 ESC heart failure and 2025 ESC pregnancy guidelines also carry cardioversion rows; where they differ from the AF guidelines, both are shown.[3][4][1]
In Australia and New Zealand
The 2018 NHFA/CSANZ guideline was written to assist Australian practitioners in diagnosing and managing adult patients with AF.[5] Its published summary says cardioversion remains the first-line choice for acute rhythm control when clinically indicated, and that flecainide is preferable to amiodarone for acute and chronic rhythm control.[5] It recommends non-vitamin K oral anticoagulants in preference to warfarin if anticoagulation is indicated, and the sexless CHA2DS2-VA score to assess stroke risk.[5] The full NHFA/CSANZ guideline text could not be retrieved for this page, so no Australian rule on duration thresholds or peri-cardioversion anticoagulation is quoted; no newer NHFA/CSANZ AF guideline was found.
Where the evidence is thin
- The ESC lists as a gap in evidence the uncertainty about AF duration and stroke risk when performing cardioversion.[1]
- Evidence levels: the ESC 24-hour row is Level C, and the ACC/AHA under-48-hour and under-12-hour rows are LOE C-LD.[1][2]
- The ESC describes the three DOAC cardioversion trials as underpowered, each showing only non-significantly lower cardiovascular event rates with DOACs than warfarin; the significant difference in the composite of stroke, systemic embolism, MI and cardiovascular death (DOAC 0.42% vs VKA 0.98%) came from a meta-analysis of these 5203 patients, predominantly undergoing electrical cardioversion.[1]
Exam pearls
- ESC 2024 uses 24 h; ACC/AHA 2023 uses 48 hours, with a 12-hour low-risk group (CHA2DS2-VASc 0–1).[1][2]
- After cardioversion, to prevent thromboembolism, ESC 2024 recommends OAC for at least 4 weeks in all patients and ACC/AHA 2023 says anticoagulation should continue for at least 4 weeks without interruption; the ESC text makes it optional only without thromboembolic risk factors and with sinus rhythm restored within 24 h of onset.[1][2]
- Thrombus on imaging: ESC, at least 4 weeks of anticoagulation then repeat TOE; ACC/AHA, at least 3 to 6 weeks then repeat imaging.[1][2]
- A wait-and-see approach for spontaneous conversion within 48 h of onset, in patients without haemodynamic compromise and as an alternative to immediate cardioversion, should be considered (Class IIa, Level B) in the ESC 2024 guideline, backed by RACE 7 ACWAS (haemodynamically stable, recent-onset symptomatic AF of under 36 hours; sinus rhythm at 4 weeks 91% with wait-and-see, which included delayed cardioversion if AF did not resolve within 48 hours, vs 94% with early cardioversion, non-inferior).[1][6]
- Severe LVH, HFrEF or coronary artery disease: ESC 2024 recommends intravenous amiodarone when cardioversion is desired, accepting there may be a delay (Class I, Level A); the ACC/AHA says ibutilide is best avoided with LVEF 40% or less.[1][2]
- ACC/AHA 2023: energy delivery should be confirmed to be synchronised to the QRS to reduce the risk of inducing VF (COR 1); for elective cardioversion, biphasic energy of at least 200 J as initial energy can be beneficial to improve success of the initial shock (COR 2a).[2]
References15ShowHide
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