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Cardio Topicsarrhythmias

Cardio · arrhythmias

Atrial flutter: cavotricuspid isthmus and atypical circuits

Fellowship-level guide to atrial flutter under the 2019 ESC SVT, 2024 ESC AF, 2023 ACC/AHA/ACCP/HRS AF and 2015 ACC/AHA/HRS SVT guidelines: typical cavotricuspid isthmus-dependent versus atypical circuits, the ECG, acute rate control, cardioversion, pacing and drugs, anticoagulation, CTI ablation and AF afterwards, atypical flutter after AF ablation, and intra-atrial re-entrant tachycardia in adults with congenital heart disease (2020 ESC and 2025 ACC/AHA ACHD), with pregnancy and ANZCOR guidance.

medium15 referencesUpdated 9 Oct 202651 min readVerification in progress

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Red flags

  • Haemodynamically unstable atrial flutter: synchronized DC cardioversion is recommended (ESC 2019, Class I, Level B)
  • Class IC drugs should not be used in the absence of AV-blocking agents because of the risk of slowing the atrial rate, which may result in 1:1 AV conduction (ESC 2019 text)
  • Adenosine in flutter with 2:1 block can produce a rebound increase in AV conduction to 1:1 and may precipitate AF; use only if necessary for diagnosis, with resuscitation equipment available (ESC 2019 text)
  • Adults with Fontan circulation and new-onset atrial flutter or AF: timely cardioversion (pharmacological or electrical) is recommended to prevent clinical decompensation (ACC/AHA 2025 ACHD, COR 1, LOE C-LD)
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Target exams

  • EECC
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Red flags

  • Haemodynamically unstable atrial flutter: synchronized DC cardioversion is recommended (ESC 2019, Class I, Level B)
  • Class IC drugs should not be used in the absence of AV-blocking agents because of the risk of slowing the atrial rate, which may result in 1:1 AV conduction (ESC 2019 text)
  • Adenosine in flutter with 2:1 block can produce a rebound increase in AV conduction to 1:1 and may precipitate AF; use only if necessary for diagnosis, with resuscitation equipment available (ESC 2019 text)
  • Adults with Fontan circulation and new-onset atrial flutter or AF: timely cardioversion (pharmacological or electrical) is recommended to prevent clinical decompensation (ACC/AHA 2025 ACHD, COR 1, LOE C-LD)
Key answer
  • Typical common flutter, the most frequent cavotricuspid isthmus (CTI)-dependent flutter, is a macro-re-entry circuit around the tricuspid annulus using the CTI as a critical passage (ESC 2019); atypical flutter is not dependent on the CTI (ACC/AHA 2023).[1][4]
  • Haemodynamically unstable flutter: synchronized DC cardioversion is recommended (ESC 2019, Class I, Level B).[1]
  • Stable flutter: i.v. ibutilide, i.v. or oral (in-hospital) dofetilide, and low-energy (≤100 J biphasic) cardioversion are each recommended for conversion to sinus rhythm (ESC 2019, Class I, Level B), and the table footnotes contraindicate i.v. ibutilide and i.v. and oral dofetilide with a prolonged QTc interval; propafenone and flecainide are not recommended for conversion (Class III, Level B).[1]
  • Anticoagulation: oral anticoagulation is recommended in atrial flutter at elevated thromboembolic risk to prevent ischaemic stroke and thromboembolism (ESC 2024 AF, Class I, Level B); for typical (CTI-dependent) AFL, ACC/AHA 2023 recommends anticoagulant therapy according to the same risk profile used for AF (COR 1, LOE B-NR).[3][4]
  • Ablation: catheter ablation is recommended for symptomatic, recurrent episodes of CTI-dependent flutter (ESC 2019, Class I, Level A) and should be considered after the first symptomatic episode of typical flutter (Class IIa, Level B).[1]
  • After AF ablation, ESC 2019 says ablation of focal or macro-re-entrant atrial tachycardia should be deferred for ≥3 months, when possible.[1]

ESC 2024 AF calls atrial flutter among the most common atrial tachyarrhythmias.[3] This page covers atrial flutter in adults: the CTI-dependent (typical) circuits and the atypical circuits, how flutter presents, the acute options, anticoagulation, CTI ablation, flutter after AF ablation, and intra-atrial re-entrant tachycardia (IART) in adults with congenital heart disease. Atrial fibrillation (AF) itself is covered in Atrial fibrillation, and AF ablation in AF ablation: indications, technique and anticoagulation. Drug classes and proarrhythmia are covered in Antiarrhythmic drugs: class actions and proarrhythmia, and flutter conducted over an accessory pathway in Wolff–Parkinson–White and ventricular pre-excitation.

What atrial flutter is: one circuit, two families

Flutter is traditionally defined by its ECG appearance.[1] ESC 2019 says atrial flutter and focal atrial tachycardia (AT) are traditionally defined by ECG appearance: continuous regular electrical activity, most commonly a saw-tooth pattern, versus discrete P waves with an isoelectric line in between.[1] It adds that flutter-like ECGs are mostly due to macro-re-entrant atrial circuits, but micro-re-entry is also possible.[1] ACC/AHA/HRS 2015 defines atrial flutter as a macroreentrant atrial arrhythmia with a regular atrial rate and constant P-wave morphology.[2]

The next question is whether the circuit needs the CTI.[2] ACC/AHA/HRS 2015 says that when the flutter circuit involves the CTI, it is labelled CTI-dependent atrial flutter.[2] ACC/AHA/HRS 2015 calls the counterclockwise CTI-dependent circuit around the tricuspid valve (up the septum and down the free wall) typical; less commonly it rotates clockwise, which it says is sometimes called reverse typical.[2] ESC 2019 says typical common flutter is the most frequent CTI-dependent flutter: a macro-re-entry circuit around the tricuspid annulus that uses the CTI as a critical passage at the inferior boundary.[1] Activation runs down the right atrial (RA) free wall, through the CTI and up the right septum, and left atrial (LA) activation is passive.[1] Seen from the apex this is counter-clockwise; when the circuit runs the opposite way (clockwise), the ECG differs and ESC 2019 calls it typical reverse flutter.[1]

Typical (CTI-dependent) flutter

Circuit needs the isthmus

  • ACC/AHA 2023 defines typical AFL as counterclockwise or clockwise flutter whose macroreentrant circuit is dependent on the CTI
  • Counter-clockwise (common) or clockwise (reverse) typical flutter (ESC 2019 Table 5)
  • Other CTI-dependent MRAT includes lower-loop re-entry around the inferior vena cava, which may be clockwise or counter-clockwise (ESC 2019)

Atypical (non-CTI-dependent) flutter

Circuit elsewhere

  • ACC/AHA 2023: not dependent on the CTI; may arise from a macroreentrant circuit in the LA, such as perimitral or LA roof flutter, or could be dependent on scar from previous ablation or surgery
  • RA MRAT or LA MRAT (ESC 2019 Table 5)
  • ESC 2019: true atypical flutter is a post hoc diagnosis, made when the circuit has been outlined and dependence on the CTI has been ruled out
[4] [1]

ESC 2019 Table 5 (Conventional classification of supraventricular tachycardias): the MRAT rows (selected)

ESC 2019 Table 5 groupEntries listed
MRATCavotricuspid isthmus-dependent MRAT (typical atrial flutter, counter-clockwise (common) or clockwise (reverse); other cavotricuspid isthmus-dependent MRAT); non-cavotricuspid isthmus-dependent MRAT (RA MRAT; LA MRAT)
[1]

ESC 2019 notes that the terms non-CTI-dependent macro-re-entrant atrial tachycardia (MRAT) and atypical flutter are used interchangeably, to describe flutter waves on the ECG not suggestive of typical circuits.[1] It warns of a pitfall in this use: an atypical ECG may happen when typical circuits develop in diseased atria, most frequently after surgery or extensive ablation, or under antiarrhythmic drugs.[1] Conversely, upper-loop re-entry may mimic a typical flutter ECG without being CTI-dependent.[1]

[4] [1]

How common it is, and its link with AF

  • ESC 2024 AF: atrial flutter (AFL) is among the most common atrial tachyarrhythmias, with an overall incidence rate of 88 per 100 000 person-years, rising to 317 per 100 000 person-years in people over 50 years of age.[3]
  • ESC 2024 AF: risk factors for AFL and AF are similar, and more than half of all patients with AFL will develop AF.[3]
  • ACC/AHA 2023: AFL is 2.5 times more common in men than in women, and is significantly more likely to occur in patients with underlying heart failure (HF) or chronic obstructive pulmonary disease (COPD).[4]
  • ESC 2019: typical flutter and AF occur in similar clinical settings and coexist in the same patients; AF may trigger flutter, and AF is frequent after typical flutter ablation.[1]

Antiarrhythmic drugs given for AF can produce flutter.[1][2] ESC 2019 says typical flutter may frequently occur in patients treated for AF with class IC drugs or amiodarone.[1] In that case the flutter rate may be reduced to <200 b.p.m., which facilitates 1:1 AV conduction, and the drug effect on ventricular activation may give a wide QRS tachycardia.[1] ACC/AHA/HRS 2015 says atrial flutter may result from antiarrhythmic therapy of AF, particularly with flecainide, propafenone or amiodarone, and that in these patients ablation of CTI-dependent flutter may prevent recurrent flutter while antiarrhythmic therapy for AF is continued.[2]

Why flutter is hard to rate-control, and what it does to the ventricle

ACC/AHA/HRS 2015 says it is often more difficult to achieve rate control for atrial flutter than for AF.[2] ACC/AHA/HRS 2015 says the relatively slower atrial rate of flutter compared with AF often paradoxically results in more rapid AV-nodal conduction, because there is less concealed AV-nodal conduction.[2] Therefore, it says, achieving adequate rate control can be difficult.[2] ESC 2024 AF agrees that rate control can be difficult to achieve in AFL, despite combination therapy.[3]

Reversible systolic dysfunction and subsequent tachycardiomyopathy are not unusual in typical flutter.[1] ESC 2019 says that, beyond the symptoms of a high rate and loss of atrial kick, reversible systolic dysfunction and subsequent tachycardiomyopathy (TCM) are not unusual.[1] In its chronic-therapy rows, catheter ablation is recommended in patients with persistent atrial flutter or with depressed LV systolic function due to TCM (ESC 2019, Class I, Level B).[1]

Recognising flutter on the ECG

What typical flutter looks like, as each guideline describes it

CircuitECG descriptionSource
Counter-clockwise typicalRegular atrial activation from 250–330 b.p.m., with negative saw-tooth waves in the inferior leads and positive waves in V1ESC 2019 (Figure 10)
Clockwise typicalFlutter waves in the inferior leads look positive and broad, and are frequently bimodal negative in V1ESC 2019
Counter-clockwise typicalDominant negative flutter waves in the inferior leads (so-called sawtooth waves) and a positive P wave in V1 at atrial rates of 250 bpm to 350 bpmACC/AHA/HRS 2015 (Figure 17)
Clockwise typicalThe opposite pattern: positive flutter waves in the inferior leads and wide, negative flutter waves in V1ACC/AHA/HRS 2015
[1] [2]

The two guidelines print different upper rates for counter-clockwise flutter: 330 b.p.m. in ESC 2019 and 350 bpm in ACC/AHA/HRS 2015.[1][2] ACC/AHA/HRS 2015 adds that flutter rates typically range from 250 bpm to 330 bpm, and may be slower with severe atrial disease, antiarrhythmic agents or after unsuccessful catheter ablation.[2]

The pattern is not always classic.[1] ESC 2019 says the typical ECG may change considerably when atrial activation has been modified, as after cardiac surgery involving atrial tissue, after extensive radiofrequency ablation, or in advanced atrial disease.[1] Antiarrhythmic drugs may also modify it, and in these situations an atypical ECG does not rule out a typical CTI circuit.[1] ACC/AHA/HRS 2015 says that with substantial atrial disease, prior surgery or prior radiofrequency catheter ablation, flutter-wave morphology is not a reliable predictor of whether the circuit involves the CTI.[2] It adds that a typical flutter ECG has good predictive value for CTI-dependent flutter in a patient who has not had prior AF ablation, but is less useful after AF ablation.[2] It says a positive or biphasic (but dominantly positive) deflection in V1, with deflections in other leads inconsistent with typical counterclockwise flutter, suggests atypical flutter, and that definitive diagnosis requires EP study and intracardiac mapping.[2]

Flutter hidden by 2:1 conduction

ESC 2019 says that with 2:1 AV block the diagnosis of atrial flutter may not be obvious on the ECG.[1] In that situation, i.v. adenosine may increase the degree of AV block and reveal the typical pattern.[1] However, adenosine can produce a rebound increase in AV conduction to 1:1 and may also precipitate AF.[1] So ESC 2019 says it should only be used if deemed necessary for diagnosis and resuscitation equipment is available.[1]

ANZCOR Guideline 11.9 lists atrial flutter with regular AV conduction (usually 2:1) among the regular narrow-complex tachycardias.[8] If the patient is unstable with adverse signs caused by the arrhythmia (other than sinus tachycardia), it says to attempt synchronised electrical cardioversion, with sedation as required.[8] In the absence of adverse features, it starts with vagal manoeuvres; if the arrhythmia persists and is not atrial flutter, it uses adenosine.[8] If the ventricular rate slows transiently but the arrhythmia then persists, it says to look for atrial activity such as atrial flutter or other atrial tachycardia and treat accordingly.[8]

Differential diagnosis

Rhythms that can look like, or hide, flutter

Look-alikeWhat the held guideline says
Focal ATMRATs with a significant part of the circuit in protected areas may display a focal AT pattern, with discrete P waves (ESC 2019)
Micro-re-entryFlutter-like ECGs are mostly macro-re-entrant, but micro-re-entry is also possible (ESC 2019); ACC/AHA/HRS 2015 says microreentrant AT (≤2 cm in diameter) may be indistinguishable from focal AT
Upper-loop re-entryMay mimic a typical flutter ECG without being CTI-dependent (ESC 2019)
Figure-of-eight double-loop re-entryMay occur around the inferior vena cava and tricuspid annulus and mimic typical clockwise flutter (ESC 2019)
Flutter with a bystander accessory pathwayIn focal AT, atrial flutter, AF or AVNRT, the QRS complexes can be pre-excited when the accessory pathway is a bystander, not a critical part of the circuit (ESC 2019)
[1] [2]

Pre-excited flutter changes the drug list.[8] ANZCOR Guideline 11.9 says that if pre-excited AF (or atrial flutter) is suspected, adenosine, digoxin, verapamil and diltiazem should be avoided, and that electrical cardioversion is usually the safest treatment option.[8] ANZCOR also says atrial flutter is a related but distinct arrhythmia caused by re-entry within the atria, which may be managed similarly to AF in the emergency setting.[8]

Acute management: rate control, cardioversion, pacing and drugs

Start with how the patient is tolerating the rhythm.[1] ESC 2019 says the first step should be rate control when the ventricular rate is high, but that this may be difficult to achieve.[1] AV-nodal blocking drugs, including amiodarone applied mostly in HF or critically ill patients, may help, but cardioversion may be necessary (ESC 2019 Figure 11, Acute therapy of stable atrial flutter or MRAT).[1] It adds that even the combination of digoxin, beta-blockers and calcium channel blockers may fail, making cardioversion to sinus rhythm necessary.[1]

ESC 2019, Recommendations for the therapy of macro-re-entrant atrial arrhythmias: the acute therapy rows (all 8)

GroupRecommendationClass, Level
Haemodynamically unstable patientsSynchronized DC cardioversion is recommended for haemodynamically unstable patientsI, B
Haemodynamically stable patientsi.v. ibutilide or i.v. or oral (in-hospital) dofetilide are recommended for conversion to sinus rhythmI, B
Haemodynamically stable patientsLow-energy (≤100 J biphasic) electrical cardioversion is recommended for conversion to sinus rhythmI, B
Haemodynamically stable patientsHigh-rate atrial pacing is recommended for termination of atrial flutter in the presence of an implanted pacemaker or defibrillatorI, B
Haemodynamically stable patientsi.v. beta-blockers or non-dihydropyridine calcium channel blockers (verapamil or diltiazem) (i.v.) should be considered for control of rapid ventricular rateIIa, B
Haemodynamically stable patientsInvasive and non-invasive high-rate atrial pacing may be considered for termination of atrial flutterIIb, B
Haemodynamically stable patientsi.v. amiodarone may be tried if the above are not available or desirableIIb, C
Haemodynamically stable patientsPropafenone and flecainide are not recommended for conversion to sinus rhythmIII, B
[1]
  • Table note (ESC 2019): i.v. verapamil and diltiazem are contraindicated in the presence of hypotension or heart failure with reduced ejection fraction (HFrEF).[1]
  • Table note (ESC 2019): i.v. beta-blockers are contraindicated in the presence of decompensated heart failure.[1]
  • Table note (ESC 2019): i.v. ibutilide, and i.v. and oral dofetilide, are contraindicated in patients with a prolonged QTc interval.[1]
  • Table note (ESC 2019): i.v. amiodarone prolongs the QTc but torsades de pointes is rare.[1]
[1] [7]

Why the drugs are ranked this way

  • ESC 2019: dofetilide and ibutilide, pure class III antiarrhythmic drugs, are generally effective in interrupting atrial flutter given i.v. (dofetilide may also be given orally for this purpose), while class IA and IC drugs have little or no effect.[1]
  • ESC 2019: class IC antiarrhythmic drugs should not be used in the absence of AV-blocking agents, because of the risk of slowing the atrial rate, which may result in 1:1 AV conduction.[1]
  • ESC 2019: amiodarone may not be very effective acutely in re-establishing sinus rhythm, but it does help to control the ventricular rate if it is too fast.[1]
  • ESC 2019: low-energy electrical cardioversion is commonly used with haemodynamic compromise or after failure of previous actions, but could be the first choice due to its high efficacy; electrical cardioversion for flutter is more effective, and needs less energy, than for AF.[1]
  • ESC 2019: when atrial electrodes are in place, high-rate stimulation can convert flutter, sometimes through AF; if pacing induces AF, this may allow better control of the ventricular rate than flutter.[1]
  • ESC 2024 AF, Table 13 (Antiarrhythmic drugs for sinus rhythm restoration), ibutilide row: initial dosing 1 mg i.v. over 10 min (0.01 mg/kg if body weight <60 kg); subsequent dosing 1 mg over 10 min (10–20 min after the initial dose); acute success 60–75% in AFL (60 min).[3]
  • The same ibutilide row says it should be used in a cardiac care unit as it may cause QT prolongation and torsades de pointes, with ECG monitoring for at least 4 h after administration, and should not be used with prolonged QT, severe LVH or low LVEF.[3]
  • ESC 2024 AF, Table 13 (Antiarrhythmic drugs for sinus rhythm restoration), flecainide row: an AV-node-blocking agent should be given to avoid 1:1 conduction if transformation to AFL occurs, and flecainide should not be used for conversion of atrial flutter.[3]
  • ESC 2024 AF, Recommendation Table 18 (Recommendations for 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).[3]

ACC/AHA/HRS 2015 rows for acute treatment

ACC/AHA/HRS 2015, Recommendations for Acute Treatment of Atrial Flutter (selected rows)

RecommendationCOR, LOE
Oral dofetilide or intravenous ibutilide is useful for acute pharmacological cardioversion in patients with atrial flutterI, A
Intravenous or oral beta blockers, diltiazem or verapamil are useful for acute rate control in patients with atrial flutter who are hemodynamically stableI, B-R
Elective synchronized cardioversion is indicated in stable patients with well-tolerated atrial flutter when a rhythm-control strategy is being pursuedI, B-NR
Synchronized cardioversion is recommended for acute treatment of patients with atrial flutter who are hemodynamically unstable and do not respond to pharmacological therapiesI, B-NR
Rapid atrial pacing is useful for acute conversion of atrial flutter in patients who have pacing wires in place as part of a permanent pacemaker or implantable cardioverter-defibrillator or for temporary atrial pacing after cardiac surgeryI, C-LD
Intravenous amiodarone can be useful for acute control of the ventricular rate (in the absence of pre-excitation) in patients with atrial flutter and systolic heart failure, when beta blockers are contraindicated or ineffectiveIIa, B-R
[2]

The table leaves out one row: acute antithrombotic therapy is recommended in patients with atrial flutter to align with recommended antithrombotic therapy for patients with AF (COR I, LOE B-NR).[2] That row is partly superseded: for typical (CTI-dependent) AFL, the ACC/AHA 2023 rows below on anticoagulation of typical AFL are newer.[2][4] For left-sided AFLs or ATs that develop after AF ablation, the ACC/AHA 2023 table footnote says they should be anticoagulated and managed in a manner similar to AF (no class or level given).[4] No newer general ACC/AHA anticoagulation row naming those or other non-typical flutter was found among the guidelines checked for this topic.[4] For some adults with congenital heart disease, lesion-specific ACC/AHA 2025 ACHD anticoagulation rows are newer, including the d-TGA, Fontan and cor triatriatum sinister rows given below.[6] ACC/AHA/HRS 2015 supportive text adds the numbers: intravenous ibutilide converts atrial flutter in approximately 60% of cases, and its major risk is torsades de pointes, more likely with reduced LV ejection fraction.[2] It says patients given ibutilide should have continuous ECG monitoring during administration and for at least 4 hours after dosing.[2] It calls intravenous diltiazem the preferred intravenous calcium channel blocker for acute rate control because of its safety and efficacy.[2]

  • ACC/AHA/HRS 2015: diltiazem and verapamil should be avoided in advanced HF and in heart block or sinus node dysfunction without pacemaker therapy, and should not be used with known pre-excitation.[2]
  • ACC/AHA/HRS 2015: cardioversion for atrial flutter can be successful at lower energy levels than for AF.[2]
  • ACC/AHA/HRS 2015: atrial pacing is effective at terminating flutter in >50% of cases.[2]

Anticoagulation around cardioversion

ESC 2024 AF, Recommendation Table 15 (Recommendations for general concepts in rhythm control): the two rows naming atrial flutter (selected)

RecommendationClass, Level
Therapeutic oral anticoagulation for at least 3 weeks (adherence to DOACs or INR ≥2.0 for VKAs) is recommended before scheduled cardioversion of AF and atrial flutter to prevent procedure-related thromboembolismI, 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 thromboembolismIIa, B
[3]

Earlier, ESC 2019 said the recommendation to anticoagulate flutter as in AF extends to the acute setting, for cardioversion when flutter lasts for >48 h; this is dated history, and the ESC 2024 AF rows above are newer.[1][3] ACC/AHA 2023 says that in patients with typical (CTI-dependent) AFL who undergo successful cardioversion or ablation restoring sinus rhythm, anticoagulation should be continued for at least 4 weeks postprocedure (COR 1, LOE C-LD).[4] Its supportive text says the incidence of embolism after cardioversion of AFL is similar to that of AF (0.72% versus 0.46%; P not significant).[4]

Anticoagulation

The evidence on stroke risk in flutter is mainly observational.[3][4] ESC 2024 AF says observational studies suggest that thromboembolic risk is elevated in AFL.[3] In direct comparisons with AF, it says some studies suggest a similar stroke risk and others a lower risk in AFL, possibly because of different comorbidity burdens and confounders such as AFL or AF ablation and anticoagulation, which is more frequently stopped in AFL.[3]

ESC 2024 AF, Recommendation Table 30 (Recommendations for prevention of thromboembolism in atrial flutter): its single row

RecommendationClass, Level
Oral anticoagulation is recommended in patients with atrial flutter at elevated thromboembolic risk to prevent ischaemic stroke and thromboembolismI, B
[3]

ESC 2024 AF says that, because of the association between AFL and thromboembolic outcomes and the frequent development of AF in patients with AFL, the management of comorbidities and risk factors in AFL should mirror that for AF.[3] Similarly, it says, prevention of thromboembolism in AFL includes peri-procedural and long-term oral anticoagulation (OAC).[3]

ESC 2019 SVT gave the earlier ESC rows, which are now dated history.[1] It recommended anticoagulation as in AF for flutter with concomitant AF (Class I, Level B).[1] For flutter without AF, it said anticoagulation should be considered, but that the threshold for initiation had not been established (Class IIa, Level C).[1] ESC 2024 AF Recommendation Table 30 is the newer ESC row and covers patients with atrial flutter at elevated thromboembolic risk.[3]

  • ESC 2019 text: data on embolic risk in flutter have usually been derived in the presence of concomitant AF, making individualized risk stratification difficult; LA appendage stunning and thrombi seem to be lower than in AF.[1]
  • ESC 2019 text: the thrombo-embolic risk of flutter, although lower than that of AF, is still significant.[1]
  • ESC 2019 text: there is a lack of prospective, dedicated, randomized studies on the subject.[1]
  • ESC 2019 text: the value of the CHA2DS2-VASc score in preventing ischaemic stroke in flutter has not been established, and without concomitant AF the threshold for starting anticoagulation appears to be higher than in AF.[1]

ACC/AHA 2023: anticoagulation of typical flutter

ACC/AHA 2023, Recommendations for Anticoagulation of Typical AFL (all 5 rows)

RecommendationCOR, LOE
For patients with AFL, anticoagulant therapy is recommended according to the same risk profile used for AF1, B-NR
In patients with AFL who undergo successful cardioversion or ablation resulting in restoration of sinus rhythm, anticoagulation should be continued for at least 4 weeks postprocedure1, C-LD
Patients with typical AFL who have undergone successful CTI ablation and have had AF previously detected before AFL ablation should receive ongoing oral anticoagulation postablation as indicated for AF1, A
Patients with typical AFL who have undergone successful CTI ablation and are deemed to be at high thromboembolic risk, without any known previous history of AF, should receive close follow-up and arrhythmia monitoring to detect silent AF if they are not receiving ongoing anticoagulation in view of significant risk of AF1, B-NR
In patients with typical AFL who have undergone successful CTI ablation without any known previous history of AF who are at high risk for development of AF (eg, LA enlargement, inducible AF, COPD, HF), it may be reasonable to prescribe long-term anticoagulation if thromboembolic risk assessment suggests high risk (>2% annual risk) for stroke2b, B-NR
[4]
  • Section note (ACC/AHA 2023): this section refers to typical right-sided (CTI-dependent) AFL; left-sided AFLs or atrial tachycardias (ATs) that develop after ablation of AF should be anticoagulated and managed in a manner similar to AF.[4]

Its synopsis and supportive text give the reasoning behind these rows.[4] ACC/AHA 2023 says the high effectiveness of CTI ablation may decrease thromboembolic risk, so that many physicians may stop OAC >1 month after ablation in the absence of previously detected AF.[4] It says the high incidence of new-onset AF at some time after CTI ablation places this practice in question.[4] Its supportive text reports that in a population-based retrospective cohort of patients with typical AFL and no history of AF, stroke occurred in 4.1%, compared with 1.2% of a matched general-population cohort (P <0.001).[4] It adds that no large, randomized trials specifically address the thromboembolic risks and benefits of anticoagulation in patients who have only AFL.[4] It also says LA appendage stunning occurs with AFL, although it appears to be less marked than with AF.[4]

[4] [3] [1]

Catheter ablation of the cavotricuspid isthmus

For typical flutter, ablation targets one anatomical isthmus.[2] ESC 2019 says catheter ablation is the most effective therapy to maintain sinus rhythm, and is clearly superior to amiodarone.[1] ACC/AHA/HRS 2015 explains the target: the CTI is the optimal site because a line of ablation between the tricuspid valve annulus and the inferior vena cava can effectively interrupt the circuit.[2] It says successful ablation is often heralded by interruption of the arrhythmia during the procedure and then EP demonstration of bidirectional block across the ablated tissue.[2] ESC 2019 says CTI ablation with confirmed bidirectional conduction block gives a <10% rate of recurrence.[1]

ESC 2019, Recommendations for the therapy of macro-re-entrant atrial arrhythmias: chronic therapy, ablation rows (4 of the 7 chronic rows; the drug and ablate-and-pace rows are in the next section)

RecommendationClass, Level
Catheter ablation should be considered after the first episode of symptomatic typical atrial flutterIIa, B
Catheter ablation is recommended for symptomatic, recurrent episodes of CTI-dependent flutterI, A
Catheter ablation in experienced centres is recommended for symptomatic, recurrent episodes of non-CTI-dependent flutterI, B
Catheter ablation is recommended in patients with persistent atrial flutter or in the presence of depressed LV systolic function due to TCMI, B
[1]

ACC/AHA 2023, Recommendations for AF Catheter Ablation (selected rows)

RecommendationCOR, LOE
In patients with symptomatic or clinically significant AFL, catheter ablation is useful for improving symptoms1, A
In patients who are undergoing ablation for AF, ablation of additional clinically significant supraventricular arrhythmias can be useful to reduce the likelihood of future arrhythmia2a, B-NR
[4]

ACC/AHA 2023 supportive text says AFL is most commonly due to the critical isthmus formed by the inferior vena cava and the tricuspid valve.[4] It says ablation of previously documented or inducible sustained SVT or AFL during AF ablation is useful to reduce the likelihood of recurrent arrhythmias.[4] Conversely, it says prophylactic CTI ablation in patients without documented or inducible AFL likely has minimal benefit.[4]

ACC/AHA/HRS 2015 ablation rows

ACC/AHA/HRS 2015, Recommendations for Ongoing Management of Atrial Flutter: the ablation rows (selected)

RecommendationCOR, LOECurrency
Catheter ablation of the CTI is useful in patients with atrial flutter that is either symptomatic or refractory to pharmacological rate controlI, B-RPartly superseded: for symptomatic or clinically significant AFL, the ACC/AHA 2023 row (catheter ablation is useful for improving symptoms; COR 1, LOE A) is newer; otherwise (refractory to pharmacological rate control but neither symptomatic nor clinically significant), no newer general ACC/AHA row among the guidelines checked; population-specific rows, such as those below the table, also apply
Catheter ablation is useful in patients with recurrent symptomatic non–CTI-dependent flutter after failure of at least 1 antiarrhythmic agentI, C-LDSuperseded (dated history): the patients are symptomatic, and for symptomatic or clinically significant AFL the ACC/AHA 2023 row (catheter ablation is useful for improving symptoms; COR 1, LOE A), which names AFL without restricting it to CTI-dependent flutter, is newer
Catheter ablation is reasonable in patients with CTI-dependent atrial flutter that occurs as the result of flecainide, propafenone or amiodarone used for treatment of AFIIa, B-NRPartly superseded: for symptomatic or clinically significant AFL, the ACC/AHA 2023 row (catheter ablation is useful for improving symptoms; COR 1, LOE A) is newer; otherwise no newer general ACC/AHA row among the guidelines checked; population-specific rows, such as those below the table, also apply
Catheter ablation is reasonable in patients with recurrent symptomatic non–CTI-dependent flutter as primary therapy, before therapeutic trials of antiarrhythmic drugs, after carefully weighing potential risks and benefits of treatment optionsIIa, C-LDSuperseded (dated history): the patients are symptomatic, and for symptomatic or clinically significant AFL the ACC/AHA 2023 row (catheter ablation is useful for improving symptoms; COR 1, LOE A), which names AFL without restricting it to CTI-dependent flutter, is newer
Catheter ablation may be reasonable for asymptomatic patients with recurrent atrial flutterIIb, C-LDPartly superseded: for clinically significant AFL, the ACC/AHA 2023 row (catheter ablation is useful for improving symptoms; COR 1, LOE A) is newer; otherwise no newer general ACC/AHA row among the guidelines checked; population-specific rows, such as those below the table, also apply
[2] [4]

The currency column is scoped to the ACC/AHA guidelines checked for this topic. The 2015 row on CTI ablation during AF ablation is not shown, because the ACC/AHA 2023 row on ablating additional clinically significant supraventricular arrhythmias during AF ablation is newer.[4] That row says that in patients who are undergoing ablation for AF, ablation of additional clinically significant supraventricular arrhythmias can be useful to reduce the likelihood of future arrhythmia (COR 2a, LOE B-NR).[4] Newer population-specific ACC/AHA rows also apply where their conditions are met.[6][4] ACC/AHA 2025 ACHD: in adults with Fontan circulation and recurrent supraventricular tachycardia, catheter ablation performed by an electrophysiologist with experience in ACHD is reasonable to reduce arrhythmia recurrence and associated morbidity (COR 2a, LOE C-LD).[6] ACC/AHA 2023: in adults with congenital heart disease with AF undergoing PVI, it may be reasonable to include an ablative strategy in the right atrium directed at reentrant arrhythmia secondary to atriotomy scars and the CTI (COR 2b, LOE C-LD).[4] ESC 2019 adds that when typical CTI-dependent flutter ensues during class IC or amiodarone therapy for AF, CTI ablation is a reasonable choice to ensure that the antiarrhythmic drugs can be continued for AF control.[1]

Success, risk and AF afterwards

ESC 2019 Table 11 (Average success and complication rates of catheter ablation for SVT): the cavotricuspid-dependent atrial flutter row (selected)

Acute success (%)Recurrence (%)Complications (%)Mortality (%)
95102 (vascular complications, stroke, myocardial infarction and pericardial effusion)0.2
[1]
  • ESC 2019: no procedure-related mortality was detected in early studies, but recent studies report mortality and stroke rates of 0.2–0.34 and 0.19–0.5%, respectively (Table 11).[1]
  • ESC 2019: in a recent registry, ablation for flutter had a higher mortality than ablation for AF (0.3 vs. 0.05%), but this might have been due to the comorbidities or advanced ages of patients referred for flutter ablation.[1]
  • ACC/AHA 2023: in a meta-analysis, the acute success rate for catheter ablation of typical AFL is reported to be 92% with a single procedure and 97% with multiple procedures.[4]
  • ACC/AHA/HRS 2015: catheter ablation of atrial flutter is highly effective, with single-procedure success rates >90% and an excellent safety profile.[2]

Ablating the flutter does not remove the AF risk.[1][3] ESC 2019 says the incidence of AF is high in the long term after CTI ablation.[1] ESC 2024 AF says recurrence of AFL is uncommon after achieving and confirming bidirectional block in typical CTI-dependent AFL, but the majority of patients (50%–70%) have manifested AF during long-term follow-up in observational studies after AFL ablation.[3] Hence, it says, all patients with AFL need long-term dynamic re-evaluation in keeping with the AF-CARE approach.[3]

  • ACC/AHA 2023: in a meta-analysis, AF occurred after CTI-dependent AFL ablation in 34% over 14 months; it adds that the incidence is significantly higher with a history of AF before ablation than without (53% versus 23% after 16–18 months; P <0.05).[4]
  • ACC/AHA 2023: by 5 years, AF developed in 60% to 70% of patients, whether or not they had a history of AF before the AFL ablation.[4]
  • ACC/AHA 2023: in 1 study, 82% of patients who underwent typical AFL ablation experienced new-onset AF during long-term follow-up (mean, 39 months).[4]
  • ACC/AHA/HRS 2015: after CTI ablation, 22% to 50% of patients have been reported to develop AF after a mean follow-up of 14 to 30 months, although 1 study reported 82% manifesting AF within 5 years.[2]
  • ACC/AHA/HRS 2015: risk factors for AF after flutter ablation include prior AF, depressed LV function, structural or ischemic heart disease, inducible AF and increased LA size.[2]
[4] [1] [3]

The trials behind first-line ablation

Natale 2000

J Am Coll Cardiol

PMID 10841241
2000

Prospective randomised trial: patients with at least two episodes of symptomatic atrial flutter in the last four months were randomised to antiarrhythmic drug therapy or first-line RF ablation; 61 patients, 30 to drugs and 31 to ablation.

Key finding

After a mean follow-up of 21 ± 11 months, 36% of the drug group and 80% of the ablation group were in sinus rhythm (p < 0.01); AF developed in 29% after ablation and in 53% of those receiving drugs (p < 0.05).

Practice change

The authors conclude that in a selected group of patients with atrial flutter, RF ablation could be considered first-line therapy.

[10]

LADIP (Da Costa 2006)

Circulation

PMID 17030680
2006

Multicentre prospective randomised trial, October 2002 to February 2006: 104 patients (aged 78 ± 5 years; 20 women) after a single episode of symptomatic AFL, 52 to first-line RF ablation and 52 to cardioversion and amiodarone.

Key finding

Over a mean follow-up of 13 ± 6 months, AFL recurred in 3.8% after ablation versus 29.5% with amiodarone (P<0.0001); significant AF beyond 10 minutes occurred in 25% versus 18% (P=0.3); five complications (10%) occurred in the amiodarone group and none after ablation (P=0.03).

Practice change

The authors conclude that RF ablation should be considered first-line therapy even after the first episode of symptomatic AFL.

[9]

ESC 2019 cites both trials (its references 262 and 263) for its Class IIa, Level B row on ablation after the first symptomatic episode of typical flutter.[1] ESC 2024 AF describes the randomized evidence as small trials showing that CTI ablation is superior to antiarrhythmic drugs.[3]

Long-term rate control and antiarrhythmic drugs

Some patients will not have, or will not want, ablation.[1] ESC 2019 says rate control is part of the approach, using AV-nodal blocking agents such as diltiazem, verapamil or beta-blockers (Figure 12, Chronic therapy of atrial flutter or MRAT).[1] When ablation is not feasible or not the patient’s preference, antiarrhythmic drugs may also be used to maintain sinus rhythm.[1] ESC 2019 calls dofetilide and sotalol useful but notes concerns about pro-arrhythmia, and says amiodarone may have a role but should be restricted to HF or significant structural heart disease.[1]

ESC 2019, Recommendations for the therapy of macro-re-entrant atrial arrhythmias: chronic therapy, drug and ablate-and-pace rows (3 of the 7 chronic rows)

RecommendationClass, Level
Beta-blockers or non-dihydropyridine calcium channel blockers (verapamil or diltiazem, in the absence of HFrEF) should be considered if ablation is not desirable or feasibleIIa, C
Amiodarone may be considered to maintain sinus rhythm if the above measures failIIb, C
AV nodal ablation with subsequent pacing (ablate and pace), either biventricular or His-bundle pacing, should be considered if all the above fail and the patient has symptomatic persistent macro-re-entrant atrial arrhythmias with fast ventricular ratesIIa, C
[1]

ACC/AHA/HRS 2015, Recommendations for Ongoing Management of Atrial Flutter: the drug rows (selected)

RecommendationCOR, LOE
Beta blockers, diltiazem or verapamil are useful to control the ventricular rate in patients with hemodynamically tolerated atrial flutterI, C-LD
The following drugs can be useful to maintain sinus rhythm in patients with symptomatic, recurrent atrial flutter, with the drug choice depending on underlying heart disease and comorbidities: amiodarone, dofetilide, sotalolIIa, B-R
Flecainide or propafenone may be considered to maintain sinus rhythm in patients without structural heart disease or ischemic heart disease who have symptomatic recurrent atrial flutterIIb, B-R
[2]

The ongoing-management antithrombotic row of ACC/AHA/HRS 2015 is not in the table: ongoing management with antithrombotic therapy is recommended in patients with atrial flutter to align with recommended antithrombotic therapy for patients with AF (COR I, LOE B-NR).[2] Like the acute row, it is partly superseded: the ACC/AHA 2023 rows above on anticoagulation of typical (CTI-dependent) AFL are newer for that flutter, and lesion-specific ACC/AHA 2025 ACHD anticoagulation rows are newer for some adults with congenital heart disease.[2][4][6] For left-sided AFLs or ATs after AF ablation, which the ACC/AHA 2023 table footnote covers without a class or level, and for other non-typical flutter, no newer general ACC/AHA anticoagulation or antithrombotic row naming them was found among the guidelines checked for this topic.[4] ACC/AHA/HRS 2015 warns that flecainide and propafenone may slow the flutter cycle length, which may lead to a rapid 1:1 ventricular response.[2] Because of this, it advises caution with these drugs in patients with atrial flutter at risk of 1:1 conduction.[2]

Atypical (non-CTI-dependent) flutter

Atypical flutter often occurs in patients with atrial scarring from prior surgery or ablation.[2] ACC/AHA/HRS 2015 says non–isthmus-dependent flutter describes macroreentrant ATs not dependent on conduction through the CTI.[2] The described circuits include a path around the mitral annulus (perimitral flutter), re-entry involving the LA roof, and re-entry around regions of scarring in the right or left atrium.[2] It says these flutters often occur with atrial scarring from prior heart surgery or ablation, but also may occur in any form of heart disease or may be idiopathic.[2]

Right atrial MRAT

ESC 2019

  • Atrial sutures and patches from complex congenital heart surgery, with progressive atrial damage, create obstacles and protected isthmuses for complex and multiple MRAT
  • Usually around RA free wall scars; extensive scarring in complex congenital heart disease hinders the distinction between focal AT and MRAT
  • May also occur without previous intervention, mostly around areas of electrical silence in the RA free wall, probably due to fibrosis

Left atrial MRAT

ESC 2019

  • Most usually due to electrically silent areas of abnormal tissue after medical interventions or progressive atrial degeneration or fibrosis; anatomical obstacles such as the pulmonary vein ostia and the mitral annulus are often involved
  • Also created after surgery for conditions including mitral valve disease, related to incisions or cannulation; AF surgery may also cause macro-re-entry circuits and focal AT
  • Peri-mitral flutter is ablated in a similar way to peri-tricuspid circuits, but a stable line of block at critical isthmuses is more challenging
[1]

Ablation is the most effective treatment of right atrial MRAT.[1] ESC 2019 says rate control is often difficult due to the regularity and usually slow rate of the tachycardia, and antiarrhythmic drugs are often ineffective or limited by structural heart disease and comorbidities.[1] It calls radiofrequency ablation of often several critical isthmuses the most effective treatment, but says these procedures should be restricted to experienced operators and centres.[1] ACC/AHA/HRS 2015 says ablation of non–CTI-dependent flutter requires more extensive mapping than CTI ablation, and success rates are lower.[2] An ESC 2019 key message says patients with macro-re-entrant tachycardias following atrial surgery should be referred to specialized centres for ablation.[1]

Atypical flutter after AF ablation

Owing to its widespread use, AF ablation is the procedure that frequently causes the lesions that sustain these circuits.[1] ESC 2019 adds that this usually follows linear ablation or extensive defragmentation, and that pre-existing atrial disease is also predictive of macro-re-entry.[1] It says circumferential antral ablation may also create MRAT due to gaps in the lines.[1] ACC/AHA/HRS 2015 says microreentrant or macroreentrant left AT after AF ablation occurs in approximately 5% of patients, less often when ablation is limited to pulmonary vein isolation.[2] It says these arrhythmias are more common with longer-duration persistent AF, more dilated left atria, or linear ablation lesions.[2]

  • ESC 2019: AT due to a small re-entrant circuit after AF ablation may possibly be distinguished from macro-re-entry by a shorter P-wave duration; RA MRATs more often show negative polarity in at least one precordial lead than LA macro-re-entry.[1]
  • ACC/AHA/HRS 2015: it may be very difficult to achieve rate control in post–AF ablation non–CTI-dependent flutter (far more so than in pre-ablation AF); when the ventricular response cannot be controlled with common rate-control drugs, attempts at restoring sinus rhythm with drugs and cardioversion are often required.[2]
  • ESC 2024 AF: after any ablation for AF, recurrence may manifest as AF or as AT; an early recurrence after pulmonary vein isolation (AT, AF or flutter) is conventionally considered potentially transitory.[3]
  • ESC 2024 AF: discussion of management options for AT after ablation should ideally involve a multidisciplinary team with experience in interventional management of complex arrhythmias.[3]

The timing of ablation comes next. ESC 2019 says intervention for these tachycardias should be delayed, if possible, for ≥3 months.[1] It adds that, as part of the maturation of the lesions, some tachycardias may be transient, and initial rate control and/or antiarrhythmic drugs are favoured.[1] ACC/AHA/HRS 2015 says many flutters seen in the first 3 months after catheter ablation or cardiac surgery will not recur, so it advises deferring ablation of flutter after AF ablation until after the 3-month waiting period.[2] Rarely, it says, drugs fail to control flutter during those 3 months, and early repeat ablation is then warranted.[2] ESC 2024 AF adds a newer note: an early recurrence after pulmonary vein isolation (AT, AF or flutter) is conventionally considered potentially transitory.[3] It reports the conclusion of recent trials that used continuous implantable loop recorders for peri-procedural monitoring: they have confirmed a link between early and later recurrence.[3]

Anticoagulation follows the AF rules.[4] ACC/AHA 2023 says left-sided AFLs or ATs that develop after AF ablation should be anticoagulated and managed in a manner similar to AF.[4] Its synopsis adds that ablation of non–CTI-dependent AFL is technically more difficult, and that atypical AFL or AT often occurs after AF ablation.[4]

[4] [1] [3] [2]

Adults with congenital heart disease: intra-atrial re-entrant tachycardia

Atrial incisions contribute to atrial tachycardia after congenital heart surgery.[5] ESC 2020 adult congenital heart disease (ACHD) says right atrial incisions, with remodelling from haemodynamic overload, contribute to the high prevalence of AT in various forms of congenital heart disease (CHD).[5] It says the most frequent is late IART, in particular CTI-dependent atrial flutter.[5] Atrial rates between 150 and 250 beats per minute may lead to rapid AV conduction, haemodynamic compromise and sudden cardiac death (SCD).[5]

  • ESC 2019 SVT: tetralogy of Fallot, Ebstein’s anomaly, transposition of the great arteries after atrial switch, and univentricular hearts with Fontan palliation are especially prone to late arrhythmias such as incisional or intra-atrial re-entry tachycardia.[1]
  • ESC 2019 SVT, atrial septal defect: patients commonly present with RA MRAT, the leading mechanism is CTI-dependent tachycardia, and CTI-dependent and incisional flutter may coexist; closure of an existing defect, in isolation, is generally insufficient to abolish an existing AT, and catheter ablation should be considered before defect closure.[1]
  • ESC 2019 SVT, Mustard or Senning repair: atrial re-entrant tachycardias are common; ablation has a high acute success rate, but recurrence rates approach 30% during long-term follow-up.[1]
  • ESC 2019 SVT, Fontan: patients with a classic (atriopulmonary) Fontan are at especially high risk, with ≤60% developing SVTs after 15 years of follow-up, and AT is poorly tolerated haemodynamically with univentricular hearts.[1]
  • ACC/AHA/HRS 2015: the most common mechanism of SVT in ACHD is macroreentrant AT (also called flutter), which accounts for at least 75% of SVT and frequently involves the CTI.[2]
  • ACC/AHA 2025 ACHD, repaired tetralogy of Fallot: atrial flutter most commonly involves a prior atriotomy, the anatomic tricuspid annulus, or both, and can be definitively treated with catheter ablation.[6]
  • ESC 2020 ACHD, atrial septal defect: late post-operative arrhythmias after surgical repair at age <40 years are most frequently IART or atrial flutter, which can be successfully treated with radiofrequency or cryoablation; without repair or with repair after age 40 years, AF becomes more common.[5]
  • ESC 2020 ACHD, atrial septal defect: in patients with atrial flutter or AF, cryo- or radiofrequency ablation (modified maze procedure) should be considered at the time of surgery (text; no class or level given).[5]
  • ESC 2024 AF: in patients with atrial septal defect, closure may be performed before the fourth decade of life to decrease the risk of AF or AFL.[3]
  • ESC 2020 ACHD, atrial switch: the dominant mechanism of supraventricular arrhythmias is CTI atrial flutter, often requiring baffle puncture to achieve isthmus block.[5]

ESC 2020 ACHD rows

ESC 2020 ACHD, Recommendations for treatment of arrhythmias in adult congenital heart disease: rows on SVT, IART and referral (selected)

GroupRecommendationClass, Level
(opening rows, no sub-heading; selected)In patients with moderate and severe CHD complexity (Table 4) and documented arrhythmias, referral to a centre with a multidisciplinary team and expertise in ACHD patients and ACHD-related arrhythmia is indicatedI, C
(opening rows, no sub-heading; selected)In mild CHD, catheter ablation is recommended over long-term medical therapy for symptomatic, sustained recurrent SVT (AVNRT, AVRT, AT and IART), or if SVT is potentially related to SCD (Table 7)I, C
(opening rows, no sub-heading; selected)In moderate and severe CHD, catheter ablation should be considered for symptomatic, sustained recurrent SVT (AVNRT, AVRT, AT and IART), or if SVT is potentially related to SCD (Table 7), provided that the procedure is performed in experienced centresIIa, C
PacemakerPM implantation should be considered in ACHD patients with bradycardia-tachycardia syndrome to prevent IART, if ablation fails or is not possibleIIa, C
[5]
  • Table note: ESC 2020 ACHD Table 7 is titled Risk estimates for arrhythmic events and bradycardias in ACHD; PM, pacemaker.[5]

ESC 2020 ACHD Table 4 (Classification of congenital heart disease complexity): selected entries

ESC 2020 Table 4 classLesions relevant to IART (selected entries)
MildIncludes repaired secundum atrial septal defect (ASD), sinus venosus defect, VSD or PDA without residuae or sequellae (the examples given include chamber enlargement and ventricular dysfunction)
ModerateIncludes ASD secundum, moderate or large unrepaired (excluding pulmonary vascular disease); Ebstein anomaly; tetralogy of Fallot, repaired; transposition of the great arteries after arterial switch operation
SevereIncludes Fontan circulation; transposition of the great arteries (except for patients with arterial switch operation)
[5]

So the complexity class decides the strength of the ESC 2020 ablation row.[5] For example, an adult after an atrial switch for transposition, or with a Fontan circulation, falls in the severe group, where ablation for symptomatic, sustained recurrent IART should be considered in experienced centres (ESC 2020 ACHD, Class IIa, Level C).[5]

  • ESC 2020 ACHD text: arrhythmias causing haemodynamic instability require immediate termination irrespective of duration or anticoagulation; sinus arrest or bradycardia may occur after conversion, and availability of back-up pacing needs to be considered in patients at risk of sinus node dysfunction.[5]
  • ESC 2020 ACHD text: if IART or AF is tolerated and lasting ≥48 h, cardiac thrombus needs to be ruled out by transoesophageal echocardiography and/or appropriate anticoagulation (>3 weeks) and pharmacological rate control started before cardioversion, using a beta blocker or calcium channel blocker (in patients with normal systemic ventricular function and absent pre-excitation).[5]
  • ESC 2020 ACHD text: maintenance of sinus rhythm is the aim in all CHD patients, and catheter ablation is recommended as first-line therapy over long-term drugs for amenable, circumscribed substrates (text; the formal rows are above).[5]
  • ESC 2020 ACHD text: class IC drugs may slow IART without blocking AV conduction, allowing 1:1 conduction with worsening haemodynamics.[5]
  • ESC 2020 ACHD text: amiodarone may be considered to prevent AT or AF recurrence with systemic ventricular dysfunction, systemic ventricular hypertrophy or coronary artery disease when ablation fails or is not an option; long-term amiodarone is not advised in young CHD patients.[5]
  • ESC 2020 ACHD text: anticoagulation is recommended in paroxysmal and persistent AF or IART with moderate or severe CHD, with an individualized approach; in mild CHD, CHA2DS2-VASc and HAS-BLED should be used as per general recommendations (text; no class or level given).[5]

ESC 2024 AF, Recommendation Table 29 (Recommendations for patients with AF and congenital heart disease): its single row

RecommendationClass, Level
Oral anticoagulation should be considered in all adult congenital heart disease patients with AF/AFL and intracardiac repair, cyanosis, Fontan palliation, or systemic right ventricle to prevent ischaemic stroke and thromboembolism, regardless of other thromboembolic risk factorsIIa, C
[3]

ESC 2020 ACHD, Special considerations and recommendations for intervention after Fontan operation: rows on arrhythmias (selected)

RecommendationClass, Level
Sustained atrial arrhythmia with rapid AV conduction is a medical emergency and should be promptly treated with electrical cardioversionI, C
Anticoagulation is indicated in the presence, or with a history, of atrial thrombus, atrial arrhythmias, or thromboembolic eventsI, C
In patients with arrhythmias, a proactive approach of electrophysiologic evaluation and ablation (where appropriate) should be consideredIIa, C
[5]

For AF or atrial flutter after a Fontan operation, the newer ESC 2024 AF Recommendation Table 29 row applies: oral anticoagulation should be considered to prevent ischaemic stroke and thromboembolism, regardless of other thromboembolic risk factors (Class IIa, Level C).[3] For that population, the ESC 2020 ACHD row saying anticoagulation is indicated in the presence, or with a history, of atrial arrhythmias (Class I, Level C) is dated history.[5][3] In the presence, or with a history, of atrial thrombus, thromboembolic events or other atrial arrhythmias after a Fontan operation, no newer ESC row was found among the guidelines checked for this topic.[5][3] In those cases, the ESC 2020 ACHD row applies: anticoagulation is indicated (Class I, Level C).[5]

ESC 2024 AF text adds that 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.[3] ESC 2021 pacing says current evidence on devices with atrial antitachycardia pacing to treat IART in CHD is too limited to make general recommendations.[13]

ESC 2019 SVT rows for adults with congenital heart disease

ESC 2019, Recommendations for the therapy of supraventricular tachycardia in congenital heart disease in adults (selected rows)

GroupRecommendationClass, Level
(opening row, before Acute therapy; dated history for atrial flutter, and for focal AT after a Fontan operation)Anticoagulation for focal AT or atrial flutter should be similar to that for patients with AFI, C
Acute therapy: haemodynamically unstable patientsSynchronized DC cardioversion is recommended for haemodynamically unstable patientsI, B
Chronic therapyBeta-blockers should be considered for recurrent focal AT or atrial flutter, if ablation is not possible or successfulIIa, C
Chronic therapyIn patients with SVT planned for surgical repair of a congenital heart disease anomaly, pre-operative catheter ablation or intraoperative surgical ablation should be consideredIIa, C
Chronic therapyAmiodarone may be considered for prevention if ablation is not possible or successfulIIb, C
Chronic therapySotalol is not recommended as a first-line antiarrhythmic drug as it is related to an increased risk of pro-arrhythmias and mortalityIII, C
Chronic therapyFlecainide and propafenone are not recommended as first-line antiarrhythmic drugs in patients with ventricular dysfunction and severe fibrosisIII, C
[1]

ESC 2019 also has a chronic-therapy ablation row for adults with congenital heart disease (Class IIa, Level C); the ESC 2020 ACHD rows above are newer and split by CHD complexity.[1][5] The newer ESC 2024 AF Recommendation Table 29 row above says oral anticoagulation should be considered in all adults with congenital heart disease and AF/AFL with intracardiac repair, cyanosis, Fontan palliation or a systemic right ventricle (Class IIa, Level C).[3] That row aims to prevent ischaemic stroke and thromboembolism, regardless of other thromboembolic risk factors.[3] For atrial flutter, the ESC 2019 row saying anticoagulation for focal AT or atrial flutter should be similar to that for patients with AF (Class I, Level C) is dated history.[1] The newer ESC 2024 AF rows cover it: Recommendation Table 29 for that subgroup, and for other adults the general Recommendation Table 30 row, which recommends oral anticoagulation in atrial flutter at elevated thromboembolic risk to prevent ischaemic stroke and thromboembolism (Class I, Level B).[3] For focal AT after a Fontan operation, the newer ESC 2020 ACHD Fontan row above applies (anticoagulation is indicated in the presence, or with a history, of atrial arrhythmias, Class I, Level C).[1][5] For focal AT in other adults with CHD, no newer ESC row was found among the guidelines checked for this topic.[1] ESC 2019 says it is recommended that patients with complex incisional tachycardias are referred to specialist centres with adequate experience, ablation volumes and advanced mapping capabilities (text; no class or level given).[1] It says ablation in ACHD has lower success rates than in the general cohort with AF or atrial flutter, but ablation of CTI-related arrhythmias has been reported to have a high acute success rate (>95%), although mid-term recurrence may approach 20%.[1]

ACC/AHA 2025 ACHD rows for specific lesions

ACC/AHA/HRS/ISACHD/SCAI 2025 ACHD: rows on atrial arrhythmias in d-TGA with atrial switch, Fontan circulation and cor triatriatum sinister (selected)

PopulationRecommendationCOR, LOE
d-TGA with atrial switchIn adults with d-TGA and atrial switch who have atrial arrhythmias, rhythm control strategies are preferable to rate control strategies to reduce symptoms and prevent heart failure1, B-NR
d-TGA with atrial switchIn adults with d-TGA and atrial switch who have sustained intra-atrial reentrant arrhythmias or atrial fibrillation, oral anticoagulation can be useful to prevent embolic events2a, C-LD
Fontan circulationIn adults with Fontan circulation and new-onset or worsening atrial tachyarrhythmias, evaluation with imaging and follow-up cardiac catheterization as indicated is recommended to assess for potential contributory anatomic or hemodynamic abnormalities and Fontan-pathway thrombosis1, C-EO
Fontan circulationIn adults with Fontan circulation and a known or suspected thrombus, atriopulmonary Fontan, a history of thromboembolism, or a history of sustained atrial flutter or fibrillation, anticoagulation is recommended to reduce the likelihood of thromboembolic disease1, B-NR
Fontan circulationIn adults with Fontan circulation and the absence of high-risk features (history of thromboembolism, sustained atrial flutter/fibrillation, or atriopulmonary Fontan) or bleeding contraindications, treatment with either aspirin or anticoagulation is recommended to reduce the probability of thromboembolic disease1, B-NR
Fontan circulationIn adults with Fontan circulation with new-onset atrial flutter or atrial fibrillation, timely cardioversion (pharmacological or electrical) is recommended to prevent clinical decompensation1, C-LD
Fontan circulationIn adults with Fontan circulation and recurrent supraventricular tachycardia, catheter ablation performed by an electrophysiologist with experience in ACHD is reasonable to reduce arrhythmia recurrence and associated morbidity2a, C-LD
Fontan circulationIn adults with an atriopulmonary Fontan, preserved ventricular function, and acceptable surgical risk with atrial arrhythmias refractory to medical and catheter-based therapies, Fontan conversion surgery may be considered to reduce arrhythmia recurrence2b, C-LD
Unrepaired cor triatriatum sinisterIn adults with unrepaired cor triatriatum sinister and atrial fibrillation or atrial flutter, prior stroke, or left atrial thrombus, chronic anticoagulation is recommended to prevent embolic stroke, whether or not conventional thromboembolic risk factors are present1, C-LD
Unrepaired cor triatriatum sinisterIn adults with unrepaired cor triatriatum sinister and atrial fibrillation or atrial flutter, a rhythm control strategy can be beneficial to avoid clinical decompensation2a, C-LD
[6]
  • ACC/AHA 2025 ACHD supportive text, d-TGA with atrial switch: sustained IART is common and can cause rapid decompensation and death, depending on the ventricular rate and underlying clinical status, and atrial arrhythmias also carry a risk of thromboembolism.[6]
  • ACC/AHA 2025 ACHD supportive text, Fontan: atrial arrhythmias can occur in up to 60% of adults with Fontan circulation, and acute cardioversion of new-onset flutter or IART or AF can be performed safely and is recommended to prevent progressive ventricular dysfunction or Fontan circulatory failure.[6]
  • The same text says that, because of the high thrombosis risk in the Fontan population, transesophageal echocardiography before cardioversion is necessary to rule out thrombosis regardless of arrhythmia duration or cardioversion strategy.[6]
  • ACC/AHA 2025 ACHD supportive text, Fontan: scar-mediated IART and focal ATs predominate, and treatment frequently requires integration of multiple interventions, including anticoagulation, cardioversion, antiarrhythmic medical therapy, pacing and catheter ablation.[6]
  • ACC/AHA 2025 ACHD take-home message: rhythm control is typically preferred over rate control for atrial arrhythmias in complex patients, such as those with a systemic right ventricle or Fontan circulation.[6]
  • ACC/AHA 2023 AF: in adults with congenital heart disease and AF undergoing pulmonary vein isolation, it may be reasonable to include an ablative strategy in the right atrium directed at reentrant arrhythmia from atriotomy scars and the CTI (COR 2b, LOE C-LD).[4]
  • ACC/AHA/HRS 2015 text: because the CTI is involved in >60% of atrial reentry circuits in ACHD, an initial ablation strategy targeting this region is often used.[2]
  • ACC/AHA/HRS 2015 text: intravenous adenosine is unlikely to terminate atrial reentry tachycardia or flutter in ACHD, but may be diagnostic by producing transient AV block.[2]

Four rows in the ACC/AHA 2025 ACHD table above are on anticoagulation or antithrombotic therapy: one for d-TGA with atrial switch, two for Fontan circulation (split by the features each row lists) and one for unrepaired cor triatriatum sinister.[6] They are newer than the ACC/AHA 2023 rows on anticoagulation of typical (CTI-dependent) AFL, and each applies only to the adults it names.[6][4]

[4] [5] [1] [6]

Other special populations

Pregnancy

ESC 2025 pregnancy says atrial flutter in pregnant women most often occurs in the presence of ACHD or valvular heart disease, and with metabolic disturbances such as thyrotoxicosis or electrolyte disturbances.[7] It says synchronized direct current cardioversion is indicated in all cases with haemodynamic instability caused by any SVT, including AF and AFL.[7] The indication for anticoagulation with low-molecular-weight heparin (LMWH) before cardioversion, or for transoesophageal echocardiography, should be evaluated as in non-pregnant women and maintained for at least 4 weeks after cardioversion.[7] ESC 2025 pregnancy text says catheter ablation for recurrent drug-refractory CTI-dependent AFL, among other arrhythmias, may be considered to avoid potentially harmful antiarrhythmic drug effects during pregnancy, although it has no role in AF.[7]

ESC 2025 pregnancy, Recommendation Table 14 (Recommendations for supraventricular tachycardia and pregnancy): rows naming AFL or haemodynamic instability (selected)

GroupRecommendationClass, Level
Acute management of SVT and AFImmediate electrical cardioversion is recommended for acute treatment of SVT with haemodynamic instabilityI, C
Acute management of SVT and AFIntravenous digoxin or verapamil (if preserved LVEF) should be considered as a second-line option for initial rate control in pregnant women with AF or AFL and rapid ventricular rateIIa, C
Acute management of SVT and AFIbutilide or flecainide may be considered for termination of AF and AFL in pregnant women without structural heart diseaseIIb, C
Long-term management of SVT and AFBeta-1-selective blockers (except atenolol) are recommended for rate control in pregnant women with AF, AFL or focal atrial tachycardiaI, C
Long-term management of SVT and AFDigoxin or verapamil should be considered for rate control in pregnant women with AF, AFL or focal atrial tachycardia when beta-blockers fail or are not toleratedIIa, C
Long-term management of SVT and AFSotalol may be considered for rhythm management of AF and AFL with controlling for pro-arrhythmic risk factors as in non-pregnant womenIIb, C
[7]

Cardiomyopathy

ESC 2023 cardiomyopathies, Recommendation Table 11 (Recommendations for management of atrial fibrillation and atrial flutter in patients with cardiomyopathy): its four Anticoagulation rows (selected)

GroupRecommendationClass, Level
AnticoagulationOral anticoagulation in order to reduce the risk of stroke and thrombo-embolic events is recommended in all patients with HCM or cardiac amyloidosis and AF or atrial flutter (unless contraindicated)I, B
AnticoagulationOral anticoagulation to reduce the risk of stroke and thrombo-embolic events is recommended in patients with DCM, NDLVC, or ARVC, and AF or atrial flutter with a CHA2DS2-VASc score ≥2 in men or ≥3 in womenI, B
AnticoagulationOral anticoagulation to reduce the risk of stroke and thrombo-embolic events should be considered in patients with RCM and AF or atrial flutter (unless contraindicated)IIa, C
AnticoagulationOral anticoagulation to reduce the risk of stroke and thrombo-embolic events should be considered in patients with DCM, NDLVC, or ARVC, and AF or atrial flutter with a CHA2DS2-VASc score of 1 in men or of 2 in womenIIa, B
[14]

In these rows, HCM is hypertrophic cardiomyopathy, DCM dilated cardiomyopathy, NDLVC non-dilated left ventricular cardiomyopathy, ARVC arrhythmogenic right ventricular cardiomyopathy and RCM restrictive cardiomyopathy.[14] The general ESC 2024 AF row, which recommends oral anticoagulation in patients with atrial flutter at elevated thromboembolic risk to prevent ischaemic stroke and thromboembolism (Class I, Level B), is newer and does not name a cardiomyopathy.[3]

Athletes

ESC 2020 sports cardiology, in its section on AF during sports, says structural heart disease or pre-excitation should always be excluded before advising sport in individuals with recognised AF.[11] It says rapid 1:1 conduction can occur, especially during atrial tachycardia or atrial flutter, so if AFL has been documented, prophylactic CTI ablation should be considered (text; its recommendation tables are images in the held text and are not used).[11] It adds that class I drugs should not be used in monotherapy, because they may increase the propensity to develop AFL, which without adequate rate control may lead to 1:1 AV conduction and high ventricular rates.[11]

Non-cardiac surgery

ESC 2022 non-cardiac surgery, in its section on AF and flutter, says management of atrial flutter follows the same principles as AF with respect to OAC therapy (text; no class or level given).[12] It says rate control is usually the initial approach, but AV-nodal drugs are usually less effective than in AF, and with a high ventricular rate electrical cardioversion is frequently needed.[12] It says amiodarone may be an alternative used to control rate, especially in HF or critically compromised patients.[12] It says dofetilide and ibutilide are effective in converting flutter to sinus rhythm, whereas class IA and IC drugs and amiodarone are less efficient and should not be used.[12]

Pulmonary hypertension and heart failure

  • ACC/AHA 2023: in patients with pulmonary hypertension with pulmonary vascular disease and AF or AFL, a rhythm-control strategy is reasonable to improve functional status and potentially prolong survival (COR 2a, LOE B-NR).[4]
  • ESC/ERS 2022 pulmonary hypertension: catheter ablation is the preferred approach in managing atrial flutter and some other atrial tachycardias, although catheter ablation in pulmonary arterial hypertension (PAH) is often more technically challenging than in a structurally normal right heart chamber (text; no class or level given).[15]
  • ESC/ERS 2022: in the absence of specific evidence for PAH, anticoagulation in PAH with atrial arrhythmia should follow the recommendations for patients with other cardiac conditions (text; no class or level given).[15]
  • ESC 2019: catheter ablation is recommended in persistent atrial flutter or with depressed LV systolic function due to TCM (Class I, Level B).[1]
  • ESC 2019 table note: i.v. verapamil and diltiazem are contraindicated with hypotension or HFrEF, and i.v. beta-blockers with decompensated heart failure.[1]
  • ACC/AHA/HRS 2015: intravenous amiodarone can be useful for acute rate control (in the absence of pre-excitation) in atrial flutter with systolic heart failure when beta blockers are contraindicated or ineffective (COR IIa, LOE B-R).[2]

Complications and pitfalls

Pitfalls that cost marks
  • A class IC drug without AV-nodal cover: ESC 2019 says class IC drugs should not be used in the absence of AV-blocking agents, because of the risk of slowing the atrial rate, which may result in 1:1 AV conduction.[1]
  • Using flecainide or propafenone to cardiovert flutter: ESC 2019 says they are not recommended for conversion to sinus rhythm (Class III, Level B).[1]
  • Adenosine without resuscitation equipment: ESC 2019 says adenosine can produce a rebound increase in AV conduction to 1:1 and may also precipitate AF, so it should only be used if deemed necessary for diagnosis and resuscitation equipment is available.[1]
  • Ibutilide with a long QTc: ESC 2019 says i.v. ibutilide and i.v. and oral dofetilide are contraindicated with a prolonged QTc interval.[1]
  • Trusting an atypical ECG: ESC 2019 says an atypical ECG does not rule out a typical CTI circuit after cardiac surgery involving atrial tissue, after extensive radiofrequency ablation, in advanced atrial disease or on antiarrhythmic drugs.[1]
  • Stopping anticoagulation because the flutter is ablated: ACC/AHA 2023 says patients with typical AFL who have undergone successful CTI ablation and had AF detected before AFL ablation should receive ongoing oral anticoagulation postablation as indicated for AF (COR 1, LOE A).[4]
  • Re-ablating early after AF ablation: ESC 2019 says ablation of post-AF-ablation atrial tachycardias should be deferred for ≥3 months, when possible.[1]

Prognosis

The long-term questions are AF and stroke. ESC 2024 AF says more than half of all patients with AFL will develop AF.[3] After AFL ablation, it says the majority (50%–70%) have manifested AF during long-term follow-up in observational studies.[3] ACC/AHA 2023 reports stroke in 4.1% of a population-based cohort with typical AFL and no AF history, against 1.2% of matched controls.[4] In adults with Fontan circulation, ACC/AHA 2025 ACHD says atrial arrhythmias are associated with significant morbidity and mortality.[6]

Evidence, guidelines and regional differences

  • Anticoagulation. ESC 2024 AF recommends OAC in atrial flutter at elevated thromboembolic risk to prevent ischaemic stroke and thromboembolism (Class I, Level B); for typical (CTI-dependent) AFL, ACC/AHA 2023 recommends anticoagulant therapy according to the same risk profile used for AF (COR 1, LOE B-NR) and adds post-ablation rows by AF history.[3][4]
  • First-line ablation. ESC 2019 says ablation should be considered after the first symptomatic episode of typical flutter (Class IIa, Level B); ACC/AHA 2023 says catheter ablation is useful for symptomatic or clinically significant AFL to improve symptoms (COR 1, LOE A).[1][4]
  • Atypical flutter ablation. ESC 2019 recommends ablation in experienced centres for symptomatic, recurrent non-CTI-dependent flutter (Class I, Level B); for symptomatic or clinically significant AFL, ACC/AHA 2023 says catheter ablation is useful for improving symptoms (COR 1, LOE A).[1][4]
  • Dated ACC/AHA history. The ACC/AHA/HRS 2015 rows on recurrent symptomatic non-CTI-dependent flutter (ablation useful after failure of at least 1 antiarrhythmic agent, COR I, LOE C-LD; reasonable as primary therapy, before therapeutic trials of antiarrhythmic drugs, after carefully weighing potential risks and benefits, COR IIa, LOE C-LD) are dated history.[2][4]
  • Acute pharmacological conversion. For haemodynamically stable patients, ESC 2019 recommends i.v. ibutilide or i.v. or oral (in-hospital) dofetilide for conversion to sinus rhythm (Class I, Level B); ACC/AHA/HRS 2015 calls oral dofetilide or intravenous ibutilide useful (COR I, LOE A).[1][2]
  • Evidence gaps. ESC 2019 says there is a lack of prospective, dedicated, randomized studies on anticoagulation in flutter; ACC/AHA 2023 says no large randomized trials address anticoagulation in patients who have only AFL.[1][4]

ANZ practice: ANZCOR Guideline 11.9 says atrial flutter may be managed similarly to AF in the emergency setting, and that if pre-excited AF (or atrial flutter) is suspected, adenosine, digoxin, verapamil and diltiazem should be avoided.[8] No NHFA/CSANZ guideline on atrial flutter was found in the PubMed census for this topic.

ESC 2024 AF says more detail on the management of AFL is in the 2019 ESC SVT guideline.[3] Guidelines used for this topic: 2019 ESC SVT; 2024 ESC AF; 2023 ACC/AHA/ACCP/HRS AF; 2015 ACC/AHA/HRS SVT (JACC text); 2020 ESC and 2025 ACC/AHA/HRS/ISACHD/SCAI adult congenital heart disease; 2025 ESC cardiovascular disease and pregnancy; and 2023 ESC cardiomyopathies. Also used: 2020 ESC sports cardiology, 2022 ESC non-cardiac surgery, 2022 ESC/ERS pulmonary hypertension and 2021 ESC pacing (text only), and ANZCOR Guideline 11.9. No ESC SVT guideline newer than 2019 and no ACC/AHA SVT guideline newer than 2015 was found in the PubMed census for this topic, run in October 2026. For each source guideline, the held guidelines named below that were published in the same month or later were swept for recommendations on atrial flutter, macro-re-entrant atrial tachycardia, the CTI or IART.

  • Checked, not used: the 2024 EHRA/HRS/APHRS/LAHRS AF ablation consensus statement is held, but it is an expert consensus statement rather than a guideline, and its advice tables are images in the held text.
  • The 2024 AHA/ACC perioperative guideline is held but replaced by the 2026 edition; atrial flutter appears in it only in a reference title.
  • The 2025 AHA/ACC competitive sports scientific statement is held and has no atrial flutter content.
  • The 2018 ACC/AHA/HRS bradycardia guideline is held; its adult congenital pacing rows do not name atrial flutter or IART.
  • The 2023 ESC diabetes guideline is held; atrial flutter appears only in a reference title.
  • Also checked, with no recommendation row on atrial flutter: the 2026 ESC heart failure, 2022 ESC ventricular arrhythmia, 2024 AHA/ACC hypertrophic cardiomyopathy, 2025 ESC myocarditis and pericarditis, 2026 ESC cardiac rehabilitation and 2022 AHA/ACC/HFSA heart failure guidelines.
  • The 2020 ACC/AHA valvular guideline has a row on the left atrial appendage at valve surgery for AF or atrial flutter, which is outside this topic.
  • The 2021 AHA/ASA secondary stroke prevention guideline is held; its rows naming atrial flutter are confined to patients with suspected or established stroke or TIA, a population this topic does not cover.
  • The 2018 NHFA/CSANZ heart failure guideline is held and has no recommendation on atrial flutter; atrial flutter appears only in its cardio-oncology text on taxanes.
  • The NHFA/CSANZ Comprehensive Australian Clinical Guideline for Diagnosing and Managing Acute Coronary Syndromes 2025 (PMID 40180468) is not held as text in its version of record, so it was not checked for this topic.
  • The Medical Journal of Australia summary of that 2025 NHFA/CSANZ acute coronary syndrome guideline (PMID 41693087) is held and has no atrial flutter content.
  • Only the PubMed abstract of the 2023 Cardiac Society of Australia and New Zealand Expert Position Statement on Catheter and Surgical Ablation for Atrial Fibrillation (PMID 38702234) is held; its full text is not held and was not checked for this topic.
  • Only the PubMed abstract of the 2026 AHA/ACC/ACS/ASNC/HRS/SCA/SCCT/SCMR/SVM Guideline for Perioperative Cardiovascular Management for Noncardiac Surgery (PMID 42804570) is held; its full text is not held and was not checked for this topic.
  • The NHFA/CSANZ Australian Clinical Guidelines for the Diagnosis and Management of Atrial Fibrillation 2018 (PMID 30077228) are not held as text in their version of record, so they were not checked for this topic.
  • Only the PubMed abstract of the NHFA/CSANZ Australian clinical guidelines for the diagnosis and management of atrial fibrillation 2018 (PMID 30067936) is held; its full text is not held and was not checked for this topic.
  • The Management of patients with atrial tachycardia: a clinical consensus statement of the European Heart Rhythm Association (EHRA) of the ESC, endorsed by the Heart Rhythm Society (HRS), the Asia Pacific Heart Rhythm Society (APHRS), the Latin American Heart Rhythm Society (LAHRS), and the Association for European Paediatric and Congenital Cardiology (AEPC) (PMID 41435855) is not held as text in the evidence caches, so it was not checked for this topic.
  • The PACES/HRS Expert Consensus Statement on the Recognition and Management of Arrhythmias in Adult Congenital Heart Disease: developed in partnership between the Pediatric and Congenital Electrophysiology Society (PACES) and the Heart Rhythm Society (HRS). Endorsed by the governing bodies of PACES, HRS, the American College of Cardiology (ACC), the American Heart Association (AHA), the European Heart Rhythm Association (EHRA), the Canadian Heart Rhythm Society (CHRS), and the International Society for Adult Congenital Heart Disease (ISACHD) (PMID 24814377) is not held as text in the evidence caches, so it was not checked for this topic.

Exam pearls

250–330b.p.m.: regular atrial activation in counter-clockwise typical flutter (ESC 2019)
<10%Recurrence after CTI ablation with confirmed bidirectional block (ESC 2019)
50%–70%Patients who manifested AF during long-term follow-up in observational studies after AFL ablation (ESC 2024 AF)
≥3 monthsDefer ablation of post-AF-ablation atrial tachycardias, when possible (ESC 2019)
[1] [3]
One-liners
  • True atypical flutter is a post hoc diagnosis: the circuit has been outlined and CTI dependence ruled out (ESC 2019).[1]
  • Slower flutter can mean faster ventricles: in patients treated for AF with class IC drugs or amiodarone, flutter rate may be reduced to <200 b.p.m., facilitating 1:1 AV conduction (ESC 2019).[1]
  • Electrical cardioversion of flutter is more effective, and needs less energy, than for AF (ESC 2019).[1]
  • Left-sided flutter or AT that develops after AF ablation should be anticoagulated and managed in a manner similar to AF (ACC/AHA 2023, table footnote).[4]
  • Late IART, in particular CTI-dependent flutter, is the most frequent atrial tachycardia in CHD (ESC 2020 ACHD).[5]
References15ShowHide
  1. [1]Brugada J, et al. 2019 ESC Guidelines for the management of patients with supraventricular tachycardiaThe Task Force for the management of patients with supraventricular tachycardia of the European Society of Cardiology (ESC). Eur Heart J, 2020.PMID 31504425
  2. [2]Page RL, et al. 2015 ACC/AHA/HRS Guideline for the Management of Adult Patients With Supraventricular Tachycardia: A Report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines and the Heart Rhythm Society. J Am Coll Cardiol, 2016.PMID 26409259
  3. [3]Van Gelder IC, et al. 2024 ESC Guidelines for the management of atrial fibrillation developed in collaboration with the European Association for Cardio-Thoracic Surgery (EACTS). Eur Heart J, 2024.PMID 39210723
  4. [4]Joglar JA, et al. 2023 ACC/AHA/ACCP/HRS Guideline for the Diagnosis and Management of Atrial Fibrillation: A Report of the American College of Cardiology/American Heart Association Joint Committee on Clinical Practice Guidelines. Circulation, 2024.PMID 38033089
  5. [5]Baumgartner H, et al. 2020 ESC Guidelines for the management of adult congenital heart disease. Eur Heart J, 2021.PMID 32860028
  6. [6]Gurvitz M, et al. 2025 ACC/AHA/HRS/ISACHD/SCAI Guideline for the Management of Adults With Congenital Heart Disease: A Report of the American College of Cardiology/American Heart Association Joint Committee on Clinical Practice Guidelines. Circulation, 2026.PMID 41411375
  7. [7]De Backer J, et al. 2025 ESC Guidelines for the management of cardiovascular disease and pregnancy. Eur Heart J, 2025.PMID 40878294
  8. [8]Australian and New Zealand Committee on Resuscitation Guideline 11.9 – Managing Acute Dysrhythmias ANZCOR, 2026.Source
  9. [9]Da Costa A, et al. Results from the Loire-Ardèche-Drôme-Isère-Puy-de-Dôme (LADIP) trial on atrial flutter, a multicentric prospective randomized study comparing amiodarone and radiofrequency ablation after the first episode of symptomatic atrial flutter. Circulation, 2006.PMID 17030680
  10. [10]Natale A, et al. Prospective randomized comparison of antiarrhythmic therapy versus first-line radiofrequency ablation in patients with atrial flutter. J Am Coll Cardiol, 2000.PMID 10841241
  11. [11]Pelliccia A, et al. 2020 ESC Guidelines on sports cardiology and exercise in patients with cardiovascular disease. Eur Heart J, 2021.PMID 32860412
  12. [12]Halvorsen S, et al. 2022 ESC Guidelines on cardiovascular assessment and management of patients undergoing non-cardiac surgery. Eur Heart J, 2022.PMID 36017553
  13. [13]Glikson M, et al. 2021 ESC Guidelines on cardiac pacing and cardiac resynchronization therapy. Eur Heart J, 2021.PMID 34455430
  14. [14]Arbelo E, et al. 2023 ESC Guidelines for the management of cardiomyopathies. Eur Heart J, 2023.PMID 37622657
  15. [15]Humbert M, et al. 2022 ESC/ERS Guidelines for the diagnosis and treatment of pulmonary hypertension. Eur Heart J, 2022.PMID 36017548

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