Catheter ablation for atrial fibrillation: Prevention of thromboembolic complications

INTRODUCTION — 

Ischemic stroke and systemic thromboembolic events are major causes of death and disability in patients with atrial fibrillation (AF). This topic will focus on management to prevent thromboembolic complications in patients undergoing catheter ablation (CA) for AF.

There are three periods for management of embolic risk in a patient undergoing CA for AF: preprocedural, periprocedural, and postprocedural.

Prevention of thromboembolic complications in the broad population of patients with AF is discussed separately. (See "Atrial fibrillation in adults: Use of oral anticoagulants" and "Atrial fibrillation: Left atrial appendage occlusion".)

Other aspects of CA are discussed separately:

●(See "Atrial fibrillation: Catheter ablation".)

●(See "Catheter ablation for the treatment of atrial fibrillation: Periprocedural issues".)

●(See "Maintenance of sinus rhythm in atrial fibrillation: Catheter ablation versus antiarrhythmic drug therapy".)

●(See "Overview of catheter ablation of cardiac arrhythmias".)

RISK OF EMBOLIC COMPLICATIONS — 

Catheter ablation (CA) entails a risk of thromboembolism. Most of the available data on embolism in this setting are for cerebral emboli. Emboli during or following CA may or may not cause any symptoms.

Symptomatic embolism — The risk of stroke is increased during and early after CA and is in the range of 0.1 to 2.0 percent; rates in the lower end of this range were reported by studies with confirmed uninterrupted anticoagulation [1-4]. These rates would be higher without periprocedural anticoagulation.

Most strokes occur within 24 to 48 hours after the procedure [3]. However, embolic events thought to be attributable to the procedure may occur up to one week after the procedure [5]. This one-week timeframe does not include continued low risk of paradoxical embolism in patients who develop an iatrogenic atrial septal defect that may remain open for several months after the CA procedure. (See 'Causes of embolism' below.)

Asymptomatic embolism — Not all emboli to the brain are symptomatic. Magnetic resonance imaging (MRI) studies performed within 24 hours after CA have demonstrated new cerebral lesions in 7 to 44 percent of asymptomatic patients [6-13]. These lesions are presumed secondary to microemboli [14].

Studies have not established a relationship between microemboli caused by CA for AF and impaired neurocognitive function [13]. Analyses of the effect of cerebral microemboli after CA on cognitive function may be confounded by other conditions affecting cognitive function (eg, chronic conditions) and other effects of CA (eg, the stress associated with the CA procedure and the effect of changes in burden of AF resulting from the procedure), as discussed separately. (See "Atrial fibrillation: Catheter ablation".)

The type of uninterrupted periprocedural oral anticoagulant therapy (in addition to routine intraprocedural intravenous heparin) does not appear to impact development of silent acute brain lesions, as demonstrated by a multicenter trial which randomly assigned 674 patients undergoing AF CA (largely radiofrequency or cryoablation) to uninterrupted direct oral anticoagulant therapy (apixaban) or uninterrupted vitamin K antagonist (VKA; eg, warfarin) [15]. Brain MRI was performed within 3 to 24 hours after ablation. Findings were described in a subset of 321 patients with analyzable MRI studies:

●The frequency of one or more acute brain lesions detected on MRI was similar in patients treated with apixaban (27.2 percent) and those treated with VKA (24.8 percent). Median Montreal Cognitive Assessment (MoCA) scores at three months were similar in patients with or without acute brain lesions.

●Evidence of chronic cerebral white matter damage was present in 40.5 percent of patients and was associated with lower median MoCA scores prior to and after ablation, but this association was not significant after adjustment for age and sex.

The risk of silent cerebral events appears to be similar among various energy sources as demonstrated by a network meta-analysis including 86 studies involving 10,456 patients [12]. The pooled silent cerebral event rate was 19.1 percent. Although there were nominal differences in silent cerebral events among various energy sources (pulsed field ablation [PFA], radiofrequency ablation, cryoballoon ablation, and laser ablation), the differences were not statistically significant.

The causes of cerebral emboli resulting from application of various ablation energy sources have not been established. Thermal ablation with radiofrequency energy can result in char formation with associated thrombus and risk of thromboembolism. The sources of cerebral emboli in patients undergoing PFA have not been determined. PFA is a newer ablation energy source that is intended to be nonthermal to reduce the risk of collateral injury to adjacent structures such as the esophagus. However, some PFA ablation systems may generate heat during multiple applications to the same cardiac tissue. Other postulated types of emboli which might be induced by PFA are gaseous microemboli and red blood cell microparticles [16].

CAUSES OF EMBOLISM — 

The following are potential causes of embolism (of thrombus or air) occurring during the periprocedural period of a catheter ablation (CA) procedure for AF:

●Lack of anticoagulation or subtherapeutic anticoagulation prior to, during, or following the procedure.

●Catheter manipulation within the left atrium, which may dislodge preexisting atrial thrombus.

●Catheter trauma to the left atrial endothelium, which increases the risk of thrombus formation.

●Char caused by thermal injury from ablation may serve as a nidus for thrombus formation.

●Thrombus formation on the ablation catheters or left atrial guide sheaths.

●Conversion to sinus rhythm during the procedure in some patients. (See "Prevention of embolization prior to and after restoration of sinus rhythm in atrial fibrillation".)

●Transseptal puncture during the CA procedure commonly causes a small iatrogenic atrial septal defect (ASD) that may persist for several months (see "Atrial fibrillation: Catheter ablation"). An iatrogenic ASD may serve as a route for paradoxical embolism of thrombus or air (transit of thrombus from the right atrium to the left atrium), with increased risk in patients with thrombus in the right atrium (eg, thrombus on a cardiac implanted electronic device lead) [17], deep venous thrombosis, or intravenous infusions with careful exclusion of air bubbles.

PREPROCEDURAL MANAGEMENT

Decision to anticoagulate — Since patients with AF develop left atrial thrombus over time, anticoagulation during the weeks prior to catheter ablation (CA) is a key consideration in mitigating the risk of thromboembolism during and following CA.

●General approach

•Continue long-term oral anticoagulant – Many patients with AF undergoing CA have an indication for long-term anticoagulation (see "Atrial fibrillation in adults: Selection of candidates for long-term anticoagulation", section on 'Recommendations based on score'). This treatment is continued during the weeks prior to CA for AF.

•Start oral anticoagulant in others – For patients planning to undergo CA for AF who have not been receiving anticoagulation for AF (or other indication), we suggest therapeutic anticoagulation for at least three weeks prior to CA irrespective of CHA₂DS₂-VASc score (table 1) or the presence or absence of sinus rhythm. This approach includes patients with low CHA₂DS₂-VASc score (eg, age <65 years plus ≤1 in males or ≤2 in females) who were not previously treated with long-term anticoagulation, including those in sinus rhythm at the time of CA for AF.

The rationale for this approach is that episodes of AF are frequently asymptomatic [18] but may increase the risk of thromboembolism at the time of catheter manipulation.

●Alternative approach for the lowest risk patients – Alternatively, for patients with CHA₂DS₂-VASc score of 0 in males or 1 in females (table 1), who do not have any condition associated with increased risk of atrial thrombus (eg, hypertrophic cardiomyopathy [HCM], rheumatic heart disease, or cardiac amyloidosis) and are in sinus rhythm and deemed likely to remain in sinus rhythm for three weeks prior the procedure, it is reasonable to not treat with preprocedural anticoagulation.

Choice of oral anticoagulant

●For most patients – For most patients treated with oral anticoagulant (OAC) therapy prior to catheter ablation, we treat with a direct oral anticoagulant (DOAC) rather than a vitamin K antagonist (VKA). This preference is based on evidence favoring DOAC therapy in the general AF population (see "Atrial fibrillation in adults: Use of oral anticoagulants", section on 'Choice of anticoagulant') as well on the following evidence from studies of patients undergoing CA for AF.

A meta-analysis of six randomized controlled trials with a total 2256 enrolled patients compared uninterrupted DOAC versus uninterrupted VKA in patients undergoing CA for AF [19]. With DOAC versus VKA therapy there was a borderline significant decrease in major bleeding events (relative risk 0.45, 95% CI 0.20-0.99; p = 0.05). The frequencies of thromboembolic events (stroke), minor bleeding events, and silent cerebral infarction were similar in the two treatment arms.

Similar findings were obtained by a meta-analysis that included 12 studies (including three of the randomized trials included in the above meta-analysis and nine observational studies) with a total of 4962 patients comparing uninterrupted DOAC with uninterrupted VKA in patients undergoing CA for AF [4]. Major bleeding was less frequent in DOAC-treated patients compared with those treated with VKA (0.9 versus 2 percent; odds ratio 0.50, 95% CI 0.30-0.84). The rates of stroke or transient ischemic attack, minor bleeding events, and silent cerebral embolic events were similar in DOAC and VKA groups.

●For patients with a specific indication for VKA – An exception to the general preference for DOAC versus VKA is for patients who have a specific indication for VKA (eg, a mechanical heart valve, clinically significant mitral stenosis, or concern for DOAC drug interaction (table 2)). (See "Atrial fibrillation in adults: Use of oral anticoagulants", section on 'Choice of anticoagulant'.)

Continue exisiting oral anticoagulant — As noted directly above, for most patients undergoing CA for AF, we prefer a DOAC to a VKA. The choice between these agents for long-term therapy in patients with AF is discussed separately. (See "Atrial fibrillation in adults: Use of oral anticoagulants" and "Atrial fibrillation in adults: Use of oral anticoagulants", section on 'Choice of anticoagulant'.)

For patients receiving long-term warfarin therapy, there is no evidence that switching to DOAC prior to CA improves outcomes. Thus, we do not routinely switch from warfarin to a DOAC.

We do not have a preference for one DOAC over another and, thus, we do not switch DOACs.

Imaging to exclude left atrial thrombus — The presence of left atrial (LA) thrombus is a contraindication for CA given the risk of precipitating thromboembolism. Thus, imaging to exclude LA (particularly left atrial appendage [LAA]) thrombus is an important consideration for preprocedural management. Transesophageal echocardiography (TEE) is the most well-established method for assessment of LA thrombus, although alternative imaging methods are available. (See 'Selection of patients for TEE' below.)

Timing of preprocedural imaging — When preprocedural LA imaging (TEE or an alternative method) is performed, it should be performed within 48 hours prior to the CA procedure [20]. (See 'Selection of patients for TEE' below and 'Alternative imaging techniques' below.)

Of note, when preprocedural TEE is performed, it is often conducted as a separate procedure prior to (generally the day before) the CA procedure. Two reasons to perform TEE as a separate procedure are to avoid lengthening the CA procedure and to reduce the risk of TEE complications, such as a retropharyngeal hematoma, which can be aggravated by treatment with unfractionated heparin required during the CA procedure. (See "Echocardiography in detection of cardiac and aortic sources of systemic embolism", section on 'LA/LAA thrombi'.)

Cardiac computed tomography (CT) and cardiovascular magnetic resonance (CMR) imaging are also generally performed prior to the CA procedure (eg, the day before), since interpretation of these imaging tests to exclude LA thrombus is required prior to proceeding with CA. (See 'Cardiac computed tomography' below and 'Cardiovascular magnetic resonance imaging' below.)

By contrast, since intracardiac echocardiography (ICE) is an invasive procedure that is used in some centers to guide transseptal puncture and identify CA complications, ICE is commonly performed as an intraprocedural adjunct just prior to performance of the ablation.

Selection of patients for TEE — TEE is a highly sensitive and specific method for identifying LA thrombus [21]. However, TEE is a semiinvasive procedure requiring intubation of the esophagus and is generally performed with sedation, with associated risk of complications. All patients referred for TEE are carefully screened to exclude contraindications and minimize the risk of complications, as discussed separately. (See "Transesophageal echocardiography: Indications, complications, and normal views", section on 'Safety of TEE examination'.)

●General approach – Most experts image the LA (particularly the LAA) in all patients prior to CA to confirm the absence of thrombus, even in patients who have received three weeks of therapeutic preprocedural OAC [20]. TEE is the most commonly used method to exclude LA thrombus in this setting [20]. With this approach, TEE is performed even in patients who have received ≥3 weeks of therapeutic anticoagulation, since LA thrombus has been observed in anticoagulated patients [22].

●Alternative approach – Alternatively, some experts perform TEE prior to CA only in selected patients with one or more of the following characteristics [20].

•Patients with one or more of the following conditions, regardless of whether they have received three weeks of therapeutic anticoagulation:

-CHA₂DS₂-VASc score ≥3 – This is based upon the results of a meta-analysis of 35 studies in patients who were therapeutically anticoagulated for at least three weeks, which found an elevated prevalence of LA thrombus in patients with CHA₂DS₂-VASc score ≥3 (table 1) compared with those with scores ≤2 (6.3 versus 1.1 percent) [22].

-Persistent AF – The above-cited meta-analysis of 35 studies in patients who were therapeutically anticoagulated found that LA thrombus was fourfold more common among patients with nonparoxysmal AF compared with patients with paroxysmal AF [22].

-Hypertrophic cardiomyopathy – Patients with HCM and AF are at high risk of stroke. In a study of patients not taking OACs either with AF and HCM (n = 8946) or with AF without HCM (n = 884,559), patients with HCM with a CHA₂DS₂-VASc score 0 in males or 1 in females had a higher risk of stroke than patients with AF without HCM and a CHA₂DS₂-VASc score of 2 [23]. The risk of stroke in patients with HCM is discussed further separately. (See "Hypertrophic cardiomyopathy: Natural history and prognosis", section on 'Stroke'.)

-Rheumatic mitral stenosis – Patients with rheumatic mitral stenosis and AF are at high risk for thromboembolism, even when they receive anticoagulant therapy. (See "Rheumatic mitral stenosis: Overview of management", section on 'Prevention of thromboembolism'.)

-Cardiac amyloidosis – Patients with cardiac amyloidosis and AF have high rates of intracardiac thrombus, even when they have receive anticoagulant therapy. (See "Cardiac amyloidosis: Treatment and prognosis", section on 'Atrial fibrillation'.)

•Patients who have CHA₂DS₂-VASc score ≥1 in males and ≥2 in females (table 1) and have not received three weeks of therapeutic anticoagulation.

When employing a selective approach to TEE imaging, some experts use one of the alternative imaging methods to exclude LA thrombus in those patients who do not undergo TEE. (See 'Alternative imaging techniques' below.)

An observational study to assess the need for preprocedural TEE in patients at low risk for embolization included 1058 patients imaged by TEE within 24 hours of CA for AF [24]. The frequency of LA thrombus or sludge was evaluated according to the CHADS₂ score (see "Echocardiography in detection of cardiac and aortic sources of systemic embolism"). A CHADS₂ score of 0 was present in 47 percent of patients. LA or LAA thrombus or sludge was found in 0.6 and 1.5 percent of all patients, and the frequency increased with ascending CHADS₂ scores (percents in parentheses): 0 (0), 1 (2), 2 (5), 3 (9), 4 to 6 (11).

Alternative imaging techniques — Alternative methods of imaging the LAA prior to CA are used in patients who have a contraindication for TEE, and some clinicians use these methods in patients who are determined to have sufficiently low risk for LA thrombus to forgo TEE. The alternative imaging options are cardiac CT, CMR, and ICE [20]. The alternative imaging technique is chosen largely based on local resources and expertise.

Cardiac computed tomography — Delayed phase cardiac CT protocols have evolved to provide high levels of sensitivity (98 percent; 95% CI 0.94-1.00) and specificity (99 percent; 95% CI 0.94-1.00) in identifying LAA thrombus compared with TEE, as identified by a meta-analysis [25]. Although early phase cardiac CT provides similar sensitivity as late delayed phase cardiac CT, it should be not used in this setting because it yields lower specificity for thrombus detection (92 percent; 95% CI 0.86-0.95) than delayed phase cardiac CT [25,26].

Intracardiac echocardiography — ICE is a sensitive and specific method for identifying LA or LAA thrombus in patients preparing for CA for AF [20]. The preferred position for the ICE catheter to identify LA thrombus is the pulmonary artery, as the LA may be incompletely visualized from the coronary sinus and is commonly not well visualized from right atrium [27,28].

Cardiovascular magnetic resonance imaging — Data on the accuracy of CMR for identifying LAA thrombus compared with TEE are more limited than for cardiac CT, with fewer studies, smaller sample sizes, and greater heterogeneity of CMR imaging protocols [25,29]. As an example, in a meta-analysis of four CMR studies with a total of 433 patients comparing diagnostic performance of CMR with TEE, the sensitivity of CMR was 80 percent (95% CI 0.63-0.91) and specificity was 98 percent (95% CI 0.97-0.99) [25].

Among various CMR techniques, delayed-enhancement CMR is the most sensitive (100 percent) and specific (99 percent) method of identifying LAA, as indicated by a meta-analysis including seven studies with a total of 582 patients examining the diagnostic accuracy of various CMR imaging techniques (cine-CMR, first-pass contrast-enhanced three-dimensional CMR angiography [CE-MRA], delayed-enhancement CMR [DE-CMR], and CMR regardless of the magnetic resonance sequences used) compared with TEE [29-31].

PERIPROCEDURAL MANAGEMENT — 

Periprocedural management to reduce the list of thromboembolic complications includes oral anticoagulant (OAC) therapy and administration of intravenous heparin. (See 'Management of oral anticoagulants' below and 'Intravenous heparin' below.)

Management of oral anticoagulants — As discussed above, the choice of OAC prescribed prior to, during, and following catheter ablation (CA) is based largely on the chosen long-term anticoagulant (a direct oral anticoagulant [DOAC] for most patients, with vitamin K antagonist [VKA] prescribed only in patients with a specific indication for VKA therapy). (See 'Choice of oral anticoagulant' above and 'Continue exisiting oral anticoagulant' above.)

For patients taking a DOAC — DOAC dosing is uninterrupted (or minimally interrupted) for CA [32]. This approach is supported by a meta-analysis of eight studies (six randomized, two observational) identifying similar rates of thromboembolic and bleeding events with uninterrupted DOAC as with minimally interrupted DOAC use [33].

●For most patients taking a DOAC who present for CA, we suggest continuing the DOAC uninterrupted or with minimal interruption (holding the DOAC for ≤24 hours).

•For most patients taking once-a-day DOACs, we either continue the DOAC uninterrupted or hold one dose (either the day before or on the morning of the procedure).

•For most patients taking a twice-a-day DOACs, we either continue the DOAC uninterrupted or hold two doses (eg, both doses the day before the procedure, or one dose the evening before the procedure and one dose the morning of the procedure).

●However, for patients with elevated risk of a periprocedural stroke (eg, patients with a CHA₂DS₂-VASc score ≥1 in males and ≥2 in females with planned intraprocedural cardioversion) who are taking a DOAC, we suggest uninterrupted DOAC.

For patients taking a VKA — For patients taking a VKA prior to CA, we continue uninterrupted therapeutic VKA (goal international normalized ratio [INR] 2.0 to 3.0) in the periprocedural period [32]. Doses of VKA are held only if the INR is >3.0.

One randomized trial [34] and most observational studies [3,35,36] have shown that continuous anticoagulation with warfarin, compared with warfarin discontinuation with a heparin bridge, is associated with a lower rate of embolization and an equivalent or lower bleeding rate [37]. In the COMPARE trial, 1584 patients with paroxysmal or persistent AF and CHADS₂ score ≥1 were randomly assigned to warfarin discontinuation two to three days before ablation and bridging with low molecular weight heparin (1 mg/kg enoxaparin twice daily until the evening before the procedure) or continuation of therapeutic warfarin (three to four weeks with an INR 2.0 to 3.0) [34]. The primary endpoint of the incidence of thromboembolic events (stroke, transient ischemic attack, or systemic thromboembolism) in the 48 hours after ablation occurred more frequently with warfarin discontinuation (4.9 versus 0.25 percent; odds ratio [OR] 13, 95% CI 3.1-55.6). The incidence of major bleeding complications was similar in the two groups (0.76 versus 0.38 percent, respectively). The majority of events occurred in patients with persistent AF. One limitation of the trial is that operators were not blinded to the anticoagulation strategy.

For patients receiving uninterrupted warfarin anticoagulation during CA, the optimal immediate-preprocedural range for the INR has not been established. In a retrospective study of 1113 patients undergoing catheter ablation for AF, bleeding and vascular complications were less prevalent when the INR was ≥2.0 and ≤3.0 (5 percent), compared with ≤2.0 (10 percent) or ≥3.0 (12 percent) [38]. The optimal INR range was calculated to be 2.1 to 2.5.

Intravenous heparin — As CA is associated with a risk of periprocedural thromboembolic complications (see 'Risk of embolic complications' above), all patients undergoing CA (irrespective of the patient’s baseline thromboembolic risk and whether or not the procedure is performed on uninterrupted OAC) are treated with a continuous intravenous (IV) unfractionated heparin (UFH):

●Heparinized sheath irrigation – Most experts flush the transseptal sheath prior to IV insertion using 1000 U/cc heparin [20]. This approach is based on an observational study in which flushing the transseptal sheath using 1000 u/cc heparin was associated with lower incidence of thrombus formation on the transseptal sheath as detected by intracardiac echocardiography than using a 2 U/cc heparin flush (although OAC was not uninterrupted in this study) [39].

●Loading dose – We start with an IV loading dose of 100 units UFH/kg at the beginning of the procedure. Others administer the loading dose just before transeptal puncture, while others give half the dose before and half the dose after transeptal puncture [40].

●Continuous infusion – After administration of the loading dose, a continuous infusion of UFH is started to maintain the activated clotting time (ACT) >300 s; the first ACT is performed 10 to 15 minutes after the loading dose. The target ACT >300 s is supported by the results of a meta-analysis of 19 studies of a total of 7150 patients taking a variety of OACs undergoing CA [41]. An ACT >300 was associated with lower rates of thromboembolic complications (OR 0.51, 95% CI 0.35-0.75) and bleeding (OR 0.70, 95% CI 0.60-0.83) compared with an ACT <300.

Evaluate for pericardial effusion — Intracardiac echocardiography is done at the end of the CA procedure to ensure that there is no pericardial effusion. If a pericardial effusion is found we take the following approach:

●For small effusions, we observe and continue with the anticoagulation protocol.

●If moderate, we reverse anticoagulation and observe with follow-up echocardiography. (See "Pericardial effusion: Approach to management", section on 'Indications for pericardial fluid removal'.)

●If large, we reverse anticoagulation and perform pericardiocentesis. (See "Pericardial effusion: Approach to management", section on 'Choice of pericardial drainage procedure'.)

●For patients with cardiac tamponade (pericardial effusion with associated hemodynamic compromise), we perform pericardiocentesis and reverse anticoagulation, regardless of the size of the effusion. (See "Cardiac tamponade", section on 'Management'.)

EARLY POSTPROCEDURAL MANAGEMENT

Discontinuing IV heparin — Intravenous (IV) unfractionated heparin (UFH) is stopped at the end of the procedure and the sheaths are pulled when the activated clotting time is <200 to 250 s or after heparin effect reversal with protamine [20].

Resuming oral anticoagulant — The approach to anticoagulation within the first 24 hours after a CA procedure is largely determined by the anticoagulant the patient was taking prior to the procedure (provided the choice of oral anticoagulant [OAC] was appropriate). (See 'Choice of oral anticoagulant' above.)

In the absence of bleeding complications, we suggest the following approach:

●DOAC – For patients who have been taking a direct oral anticoagulant (DOAC), DOAC may generally be restarted four to six hours after sheath removal. (See 'For patients taking a DOAC' above.)

●VKA – For patients who have been taking a vitamin K antagonist (VKA) with a therapeutic international normalized ratio (INR), the next VKA dose is given approximately 24 hours after the prior dose. (See 'For patients taking a VKA' above.)

For those patients in whom the INR was <2.0 prior to the procedure, we administer IV UFH without a bolus six hours after sheath pull, restart oral VKA (at an increased dose) the night of the procedure, and continue UFH until the INR is 2.0. Another reasonable approach is to stop UFH the morning after the procedure and start low molecular weight heparin, usually at half the typical dose (0.5 mg/kg twice daily) to avoid bleeding.

●No prior oral anticoagulant – For patients previously not taking any OAC, an appropriate agent is chosen (as discussed above). (See 'Choice of oral anticoagulant' above.)

A first dose of either DOAC or warfarin can be given six hours after an uncomplicated procedure. Patients started on warfarin will need to receive bridging heparin treatment for a few days, as described directly above.

LONGER TERM MANAGEMENT

Initial months of anticoagulation — For patients who have undergone AF catheter ablation (CA), we continue oral anticoagulant (OAC) therapy for at least two [20,42] or three months [32] regardless of CHA₂DS₂-VASc score to ensure that the increased risk of embolization associated with the procedure has returned to a baseline risk and that there has been adequate time to document an absence of recurrence of AF for those patients in whom practitioners and patients are contemplating discontinuing anticoagulation. (See 'Risk of embolic complications' above.)

Long-term options — After the initial two or three months of anticoagulation, we assess the need for continued anticoagulation. Management options for patients deemed to have continued risk of thromboembolism (based largely upon CHA₂DS₂-VASc score) depend upon whether or not the patient has a contraindication to long-term anticoagulation (ie, an ongoing and unresolvable high risk for bleeding) [32]. For patients who are treated with long-term anticoagulation, their prior anticoagulant is generally continued. Choice of long-term anticoagulation is discussed further separately. (See "Atrial fibrillation in adults: Use of oral anticoagulants", section on 'Choice of anticoagulant'.)

●Documented recurrent AF – For patients with documented recurrent AF after CA, we treat with OAC according to the approach for long-term anticoagulation for patients with AF (based upon CHA₂DS₂-VASc score (table 1) and burden of AF). (See "Atrial fibrillation in adults: Selection of candidates for long-term anticoagulation", section on 'Approach to deciding whether to anticoagulate'.)

●No documented recurrent AF – Since patients with no documented recurrent AF after CA may have undetected AF and/or atrial myopathy and still be at risk for thromboembolism, we stratify risk similarly in these patients:

•For patients with a CHA₂DS₂-VASc score of ≥2 in males or ≥3 in females, we suggest long-term OAC [43,44]. This approach is supported by the meta-analyses discussed below. (See 'Outcomes with long-term anticoagulation' below.)

•For patients with CHA₂DS₂-VASc score of 1 in males or 2 in females, we consider the heterogeneity of thromboembolic risk associated with various components of the score and the burden of AF. Age 65 to 74 confers greater thromboembolic risk than other factors with a one-point value (table 1).

•For patients with CHA₂DS₂-VASc score of 0 in males or 1 in females (table 1) and no high risk conditions for thromboembolism, we suggest stopping anticoagulation. (See "Atrial fibrillation in adults: Selection of candidates for long-term anticoagulation", section on 'CHA2DS2-VASc score'.)

●Role of LAA occlusion – For patients with AF who have undergone CA who have an indication for long-term anticoagulation but who have increased risk of bleeding complications (eg, history of major bleed or high risk of falls), left atrial appendage (LAA) occlusion (which can be performed at the time of CA) is a potential alternative. However, antithrombotic therapy (eg, an OAC plus an antiplatelet agent for 45 days followed by dual antiplatelet therapy for six months) is required after LAA occlusion. LAA occlusion is discussed further separately. (See "Atrial fibrillation: Left atrial appendage occlusion".)

Outcomes with long-term anticoagulation — The safety and efficacy of long-term OAC compared with no OAC after CA for AF was studied in a 2019 meta-analysis of five studies with nearly 4000 patients during a mean follow-up of nearly 40 months [45]:

●In patients with a CHA₂DS₂-VASc score ≥2, OAC continuation was associated with a decrease in the risk of thromboembolic events (risk ratio [RR] 0.41, 95% CI 0.21-0.82) but an increased risk of intracranial hemorrhage (ICH; RR 5.78, 95% CI 1.33-25.08). The absolute risk decrease in thromboembolic risk was 1.14 percent, while the increase in ICH was 0.7 percent.

●In patients with a CHA₂DS₂-VASc score of 0 or 1, the risk of ICH from OAC exceeded any potential decrease in thromboembolic risk.

A later meta-analysis including 20 studies with a total 22,429 patients (13,505 not treated with OAC) after CA for AF also found that a CHA₂DS₂-VASc score ≥2 favored OAC continuation, given the risk of thromboembolic events [46].

The optimal approach to chronic anticoagulation after successful CA, defined as no evidence of recurrence, is uncertain [47]. It is known that late recurrent AF occurs in 20 to 30 percent of patients, but the methods used in some studies likely underestimate the incidence [48-51]. (See "Atrial fibrillation: Catheter ablation", section on 'Efficacy'.)

The role of long-term anticoagulation was indirectly addressed by studies that found a lower incidence of stroke comparing successful CA with antiarrhythmic drug therapy [52-54]. In a retrospective study of 174 matched pairs of AF individuals with a CHA₂DS₂-VASc score ≥1 who were treated with either antiarrhythmic drug therapy or CA and treated for at least three months with warfarin, the rate of stroke/transient ischemic attack was lower with the CA group (0.59 versus 2.21 percent per year) [52]. In those individuals treated with CA and in whom there was no AF recurrence, the stroke rate was very low compared with those with recurrence (0.8 versus 5.4 percent) after a mean follow-up period of 47 months.

SOCIETY GUIDELINE LINKS — 

Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Atrial fibrillation" and "Society guideline links: Arrhythmias in adults" and "Society guideline links: Catheter ablation of atrial fibrillation".)

SUMMARY AND RECOMMENDATIONS

●Risk of thromboembolism with catheter ablation – The risk of symptomatic and asymptomatic thromboembolism is increased during and early after catheter ablation (CA) for atrial fibrillation (AF). (See 'Risk of embolic complications' above.)

●Preprocedural issues

•Decision to anticoagulate – Many patients with AF undergoing CA have an indication for long-term anticoagulation. Anticoagulation is continued in the weeks prior to CA for AF. (See "Atrial fibrillation in adults: Selection of candidates for long-term anticoagulation", section on 'Recommendations based on score'.)

For patients planning to undergo CA for AF who have not been receiving anticoagulation for AF (or another indication), we suggest therapeutic anticoagulation for at least three weeks prior to CA irrespective of presence or absence of sinus rhythm (Grade 2C). This approach includes patients with low CHA2DS2-VASc score (table 1) (eg, age <65 years plus ≤1 in males or ≤2 in females) who were not previously treated long-term anticoagulation, including those in sinus rhythm at the time of CA for AF. The rationale for this approach is that episodes of AF are frequently asymptomatic but increase the risk of thromboembolism at the time of catheter manipulation. (See 'Decision to anticoagulate' above.)

Alternatively, for patients with CHA₂DS₂-VASc score of 0 in males or 1 in females, who do not have any condition associated with increased risk of atrial thrombus (eg, hypertrophic cardiomyopathy [HCM], rheumatic heart disease, or cardiac amyloidosis) and are in sinus rhythm and deemed likely to remain in sinus rhythm for three weeks prior the procedure, it is reasonable to not treat with preprocedural anticoagulation.

•Choice of oral anticoagulant – For most patients treated with oral anticoagulant (OAC) therapy prior to CA, we treat with a direct oral anticoagulant (DOAC) rather than a vitamin K antagonist (VKA). This preference is based on evidence favoring DOAC therapy in the general AF population (see "Atrial fibrillation in adults: Use of oral anticoagulants", section on 'Choice of anticoagulant') as well on evidence from studies of patients undergoing CA for AF.

An exception to the general preference for DOAC versus VKA is for patients who have a specific concomitant indication for VKA (eg, a mechanical heart valve, clinically significant mitral stenosis, or concern for DOAC drug interaction (table 2)). (See "Atrial fibrillation in adults: Use of oral anticoagulants", section on 'Choice of anticoagulant'.)

•Left atrial imaging – Since the presence of left atrial (LA) thrombus is a contraindication for CA, imaging to exclude LA thrombus (particularly in the left atrial appendage [LAA]) is an important consideration for preprocedural management. Transesophageal echocardiography (TEE) is the most well-established method for assessment of LA thrombus. Alternative imaging methods include cardiac computed tomography (CT), intracardiac echocardiography (ICE), and cardiovascular magnetic resonance (CMR) imaging. (See 'Imaging to exclude left atrial thrombus' above.)

●Periprocedural management – Periprocedural management to reduce the list of thromboembolic complications includes OAC therapy and administration of intravenous (IV) heparin. (See 'Management of oral anticoagulants' above and 'Intravenous heparin' above.)

•For patients taking DOAC – For most patients taking a DOAC who present for CA, we suggest continuing the DOAC uninterrupted or with minimal interruption (holding the DOAC for ≤24 hours). (Grade 2B).

However, for patients at elevated risk of periprocedural stroke (eg, patients with a CHA₂DS₂-VASc score ≥1 in males and ≥2 in females (table 1) in whom intraprocedural cardioversion is planned), uninterrupted DOAC is preferred. (See 'For patients taking a DOAC' above.)

•For patients taking VKA – For patients taking long-term VKA (eg, warfarin) who present for CA, we recommend continuing such therapy uninterrupted (Grade 1A). Heparin bridging is not required. (See 'For patients taking a VKA' above.)

•IV heparin for all patients – IV heparin is administered to all patients undergoing AF CA. We suggest a target activated clotting time (ACT) >300. (See 'Intravenous heparin' above.)

●Initial months after catheter ablation – OAC is continued for an initial period at least two to three months after the CA procedure in all patients. (See 'Initial months of anticoagulation' above.)

●Long-term options – We base the decision of long-term therapy after the initial period on the patient's estimated risk of thromboembolism and risk of bleeding. (See 'Long-term options' above.)

•With documented recurrent AF – For patients with documented recurrent AF after CA, we treat with OAC according to the approach for long-term anticoagulation for patients with AF (based upon CHA₂DS₂-VASc score (table 1) and burden of AF). (See "Atrial fibrillation in adults: Selection of candidates for long-term anticoagulation", section on 'Approach to deciding whether to anticoagulate'.)

•No documented recurrent AF – Since patients with no documented recurrent AF after CA may have undetected AF and/or atrial myopathy and still be at risk for thromboembolism, we stratify risk by CHA₂DS₂-VASc score (table 1) similarly in these patients:

-For patients with a CHA₂DS₂-VASc score of ≥2 in males or ≥3 in females, we suggest long-term OAC (Grade 2C). (See 'Outcomes with long-term anticoagulation' above.)

-For patients with CHA₂DS₂-VASc score of 1 in males or 2 in females, we consider the heterogeneity of thromboembolic risk associated with various components of the score and the burden of AF. Age 65 to 74 confers greater thromboembolic risk than other factors with a one-point value (table 1).

-For patients with CHA₂DS₂-VASc score of 0 in males or 1 in females (table 1) and no high risk conditions for thromboembolism, we suggest stopping anticoagulation (Grade 2C). (See "Atrial fibrillation in adults: Selection of candidates for long-term anticoagulation", section on 'CHA2DS2-VASc score'.)

•Role of LAA occlusion – For patients with AF who have undergone CA and have an indication for long-term anticoagulation (as outlined above) but who are not a good candidate for long-term anticoagulation due to high bleeding risk (eg, history of major bleed or fall risk), a LAA occlusion procedure (which can be performed at the time of CA) is a potential alternative option, as discussed separately. (See "Atrial fibrillation: Left atrial appendage occlusion".)