Version July 2025
INTRODUCTION —
Atrial flutter is a relatively common supraventricular arrhythmia that can impact quality of life and cause stroke or systemic embolization. Restoration and maintenance of sinus rhythm improves symptoms and decreases the risk of embolization if atrial flutter recurrence does not occur. (See "Atrial flutter: Overview of diagnosis and management", section on 'Clinical manifestations' and "Atrial flutter: Risk of thromboembolism and role of anticoagulation", section on 'Thromboembolic risk'.)
Issues related to the indications and therapeutic options for the maintenance of sinus rhythm in atrial flutter will be reviewed here. Causes of atrial flutter, rate control therapy, the restoration of sinus rhythm after cardioversion, and the role of anticoagulation in atrial flutter are discussed separately. (See "Atrial flutter: Overview of diagnosis and management", section on 'Associated conditions' and "Atrial flutter: Restoration of sinus rhythm" and "Atrial flutter: Risk of thromboembolism and role of anticoagulation" and "Control of ventricular rate in atrial flutter".)
INDICATIONS —
We attempt to keep most patients with recurrent atrial flutter in sinus rhythm to decrease symptoms, unlike atrial fibrillation (AF), in which rhythm control and rate control are reasonable strategies. In addition, the long-term maintenance of sinus rhythm may decrease the risk of stroke. Rhythm control with either radiofrequency (RF) catheter ablation or antiarrhythmic drug therapy is necessary; in most cases, RF catheter ablation is preferred because of the high rate of success and low rate of complications. Exceptions include individuals identified as having reversible triggers such as pneumonia, hyperthyroidism, and other acute medical problems. (See "Management of atrial fibrillation: Rhythm control versus rate control".)
Atrial flutter is characterized by rapid, regular atrial depolarizations at a characteristic rate of approximately 300 beats/min. In the absence of rate slowing drugs or atrioventricular (AV) nodal disease, every other depolarization passes through the AV node, and the ventricular rate is usually around 150 beats per minute. Unlike AF, attempts to slow this rate are often unsuccessful or require high doses of rate slowing drugs; thus, the maintenance of sinus rhythm is desirable in most patients to control symptoms. In addition, episodes will often be recurrent unless a reversible cause is present. (See "ECG tutorial: Atrial and atrioventricular nodal (supraventricular) arrhythmias", section on 'Atrial fibrillation and atrial flutter' and "Atrial flutter: Overview of diagnosis and management".)
The discussion in this topic pertains primarily to patients with typical atrial flutter. The pathogenesis of typical atrial flutter makes it highly amendable to curative therapy with RF catheter ablation, though atypical flutters may also be cured with RF ablation. Typical (also called isthmus-dependent) atrial flutter utilizes a large macroreentrant pathway in the right atrium, with the left atrium following passively. (See "Electrocardiographic and electrophysiologic features of atrial flutter".)
The negative deflection of the flutter (F) wave in lead II coincides in time with the impulse activating the low right atrial tissue between the inferior vena cava and the tricuspid valve. Activation then travels anteriorly through the region of the low septum, and superiorly and anteriorly up the medial surface of the right atrium, returning along the lateral wall of the right atrium back to the cavotricuspid isthmus (CTI) [1-6].
The CTI between the inferior vena cava and the tricuspid annulus (IVC-TA isthmus) is an obligatory route for typical flutter, and, as such, is the best anatomic target for ablation (waveform 1A-B) [2-5,7-15].
RISK OF RECURRENT ATRIAL FLUTTER —
The rate of recurrence of atrial flutter is difficult to determine because most published data combine atrial flutter with AF. However, the recurrence rate is substantial. In one report, for example, 50 patients were followed for a mean of 3.5 years after cardioversion for chronic atrial flutter [16]. Prophylactic antiarrhythmic drugs were not given. Sinus rhythm was maintained at six months and five years in 53 and 42 percent of patients, respectively. In a second study of 59 patients with lone atrial flutter, 75 percent developed recurrent or chronic atrial flutter [17].
However, because of the high rate of recurrence in patients without a correctable cause, and because of its high success rate, radiofrequency catheter ablation is generally preferable to long-term pharmacologic therapy in patients with typical atrial flutter. The isthmus between the inferior vena cava and the tricuspid annulus (cavotricuspid isthmus) is an obligatory route for typical flutter, and, as such, is the preferred anatomic target for ablation (figure 1). This applies to the common counterclockwise circuit, as well as the less common clockwise circuit. A meta-analysis of 21 studies demonstrated an ablation success rate for a single procedure of 91.7 percent and for multiple procedures of 97.0 percent [18]. (See "Atrial fibrillation and flutter after cardiac surgery", section on 'Pathogenesis' and "Atrial fibrillation: Catheter ablation", section on 'Arrhythmic complications'.)
In a meta-analysis of 48 studies (between 1996 and 2015) of patients undergoing catheter ablation for typical atrial flutter, who were followed for an average of 2.5 years, those without prior AF had a 23 percent incidence of new AF diagnosis. Not surprisingly, those with prior history of paroxysmal AF undergoing atrial flutter ablation had a much higher recurrence rate of 52 percent, highlighting the need for individualized risk assessment for long-term anticoagulation [19].
RF CATHETER ABLATION —
For patients with typical atrial flutter in whom a decision is made to maintain sinus rhythm, radiofrequency (RF) catheter ablation is usually preferred to pharmacologic therapy.
Technique — The femoral approach is generally used and, under fluoroscopic guidance or using a three-dimensional mapping system, an ablation catheter is placed at the cavotricuspid isthmus (CTI) where a large ventricular and small atrial electrogram are recorded. RF energy is applied, and the catheter is slowly withdrawn to create a line of ablation from the annulus to the inferior vena cava.
The goal is to create a complete ablation line with the absence of electrical conduction across the CTI both medially to laterally and laterally to medially. This is the best marker for long-term success (waveform 1A-B). If the patient presents in typical atrial flutter, CTI block should still be assessed with differential pacing on both sides of the ablation line after termination of atrial flutter, since frequently there can still be conduction across the CTI [20,21]. An infusion of isoproterenol during pacing may help to assess the completeness of isthmus block [22]. Alternatively, adenosine may also be given to assess for block across the line [23].
Another method for ablation is the maximum voltage technique [24]. Coronary sinus ostial pacing is completed and the largest amplitude atrial signal in the CTI is ablated as a point lesion. The next largest signal is then targeted, and the process is repeated until block is seen across the isthmus.
Electroanatomic mapping is used in many cases for identifying the appropriate target area for ablation; it is a nonfluoroscopic three-dimensional mapping system. This system permits reconstruction of cardiac anatomy without the use of fluoroscopy. A study of 50 patients with atrial flutter compared isthmus ablation using conventional fluoroscopy for catheter positioning to positioning with electromagnetic mapping [25]. The success rate for complete isthmus blockade after 20 RF pulses or 25 minutes of fluoroscopy time was greater with electromagnetic mapping (96 versus 67 percent). Electromagnetic mapping significantly reduced the overall fluoroscopic time (4 versus 22 minutes) and the fluoroscopic time needed for isthmus mapping (0.2 versus 17.7 minutes).
Ablation guided by intracardiac echocardiography can also be used, and may be helpful to assess for pouches and ridges in the CTI during difficult cases or repeat procedures [10].
Outcome — The initial success rate for RF catheter ablation of typical atrial flutter has ranged from 65 to 100 percent [26,27]. A meta-analysis of a 21 studies examining atrial flutter success rate suggested a single procedure success of 92 percent and multiple procedure success rate of 97 percent [18].
Recurrent atrial flutter or fibrillation — Between 7 and 44 percent of patients who undergo flutter ablation have recurrent atrial arrhythmia, though the recurrent arrhythmia is usually AF [26,27]. Thus, some patients should undergo surveillance for recurrent atrial flutter or AF. Our approach to surveillance for recurrent arrhythmia is as follows. For patients who were initially symptomatic and who did not develop a tachycardia mediated cardiomyopathy, we perform testing to document recurrent arrhythmia only for symptoms. If the patient was initially asymptomatic, we perform periodic examinations (every 12 months) at which time we obtain an electrocardiogram, Holter, or event monitor. For those patients who developed tachycardia-mediated cardiomyopathy, standard heart failure therapy is still indicated unless otherwise contraindicated. Follow-up assessment of left ventricular function by imaging techniques such as echocardiography is warranted. We obtain a repeat echocardiogram three to six months after initiation of therapy.
The rate of recurrent AF appears to depend upon the presence or absence of AF before the procedure. In a study of 100 patients, 29 of whom had documented AF before the procedure, AF occurred in 36.4 percent of those with complete follow-up after a mean of almost 15 months [28]. However, in another study of approximately 100 patients without pre-existent AF, new onset AF developed in only 12.9 percent during a mean follow-up of 19 months [29]. Most patients (92 percent) who develop AF after flutter ablation do so within six months. The risk may be as low as 10 percent (mean follow-up of 20 months) in those with no prior AF and a left ventricular ejection fraction >50 percent [30]. The likely reasons for the difference in the rates of recurrence likely has to do with differing populations being studied (eg, symptomatic versus asymptomatic patients) and the intensity of follow-up.
In a study of 363 patients who underwent RF ablation for typical atrial flutter, 82 percent developed drug refractory AF during a follow-up period of 39 (+/- 11) months [31]. Elimination of atrial flutter may delay, but does not prevent AF and the two may share common triggers. Therefore, patients may derive a better long-term benefit from additional anatomical ablative treatment, lifestyle modifications, and/or pharmacological therapy of AF. (See 'Patients with atrial fibrillation' below.)
Improvement in left ventricular function — Persistent atrial flutter can result in a tachycardia-mediated left ventricular cardiomyopathy, similar to what has been seen with AF and other arrhythmias. On the other hand, reversal of the arrhythmia can result in improvement in left ventricular ejection fraction and, in 6 of 11 patients in one report, restoration of normal function [32]. (See "Hemodynamic consequences of atrial fibrillation and cardioversion to sinus rhythm" and "Arrhythmia-induced cardiomyopathy", section on 'Atrial fibrillation and atrial flutter'.)
Quality of life — RF ablation improves the quality of life and reduces symptoms in patients with atrial flutter, particularly if there is no associated AF [27,33]. Other benefits include a reduced frequency of hospitalizations, emergency department visits, need for cardioversion, and the need for antiarrhythmic drugs [34].
Safety — RF catheter ablation of atrial flutter is significantly safer than that for AF, in part because the left atrium is not entered and because the procedure is generally shorter due to the fact that ablation in a very limited area that is not adjacent to vulnerable structures such as the esophagus and pulmonary veins [35]. (See "Atrial fibrillation: Catheter ablation", section on 'Complications'.)
Pericardial effusion, AV block, and vascular access complications occur infrequently [36]. Procedure-related mortality is very rare and was 0 percent in a meta-analysis of 12 studies [18].
RF ablation versus pharmacologic therapy — With the high success rate of RF catheter ablation for treating atrial flutter and its low complication rate, pharmacologic therapy is increasingly being replaced by ablation as the preferred strategy in most patients.
Improved outcomes with ablation, compared to drug therapy, were illustrated in a randomized trial of 61 patients with at least two episodes of symptomatic atrial flutter within a four-month period [37]. The patients were assigned to conventional antiarrhythmic drug therapy or catheter ablation as a first line treatment. After a mean follow-up of 21 months, the following significant benefits were noted in the patients undergoing ablation:
●More were in sinus rhythm (80 versus 36 percent with drugs; P<0.01)
●Fewer required rehospitalization (22 versus 63 percent)
●Fewer developed AF (29 versus 53 percent)
●Sense of well-being and function during daily life activities improved with ablation but did not change with drugs
PHARMACOLOGIC THERAPY —
For most patients with atrial flutter, pharmacologic therapy is not chosen for the long-term maintenance of sinus rhythm. The success rate at one year has been estimated at only 20 to 30 percent, with the risk of recurrence highest in the patient with an enlarged right atrium who is in heart failure. Good prognostic signs for maintaining sinus rhythm are normal atrial size, recent onset, little or no heart failure, and an underlying reversible disorder such as hyperthyroidism, myocardial infarction, or pulmonary embolism. For patients in whom an attempt will be made to maintain sinus rhythm with antiarrhythmic drug therapy, we use the following drugs (with suggested starting doses): dronedarone 400 mg twice daily; flecainide 50 to 100 mg twice daily with an AV nodal agent; sotalol 80 mg twice daily; dofetilide 500 microgram twice daily; or amiodarone. Our reviewers have differing preferences as to the order in which these are tried.
The drugs that are most likely to maintain sinus rhythm are the same as those used for rhythm control in AF (algorithm 1). They act by suppressing triggering beats and arrhythmias and affecting atrial electrophysiologic properties. In a meta-analysis that included 36 patients, flecainide was 50 percent effective in the maintenance of sinus rhythm over variable follow-up [38]. Flecainide can also slow down the atrial flutter rate; thus, AV nodal agents should always be used in conjunction to prevent one-to-one atrial flutter. (See "Antiarrhythmic drugs to maintain sinus rhythm in patients with atrial fibrillation: Recommendations", section on 'Selecting an antiarrhythmic drug'.)
Oral dofetilide, a class III antiarrhythmic drug available for use in the United States, may be more effective than other agents for maintaining sinus rhythm. In the SAFIRE-D trial, which included 48 patients with atrial flutter, the probability of maintaining sinus rhythm at one year with dofetilide at a dose of 125, 250, or 500 mcg twice daily was 0.40, 0.37, and 0.58 versus 0.25 for placebo [39].
Dronedarone has been studied for the use of atrial flutter, though the major studies all included patients with AF also. In a trial of 2327 patients with AF or atrial flutter who were randomly assigned to either dronedarone 400 mg twice daily or placebo, dronedarone reduced the chances of recurrent AF or flutter by 25 percent and prolonged the time to first recurrence from 498 to 737 days [40]. In those with atrial flutter who had a recurrence, the mean heart rate was reduced by six beats/min, reflecting its rate control properties also.
PATIENTS WITH ATRIAL FIBRILLATION —
Many patients with atrial flutter also have episodes of AF. For many of these patients who have chosen ablation, we recommend AF (with or without atrial flutter ablation) ablation rather than atrial flutter ablation alone. The electrophysiologic substrates of AF and atrial flutter are different, and the addition of atrial flutter ablation to AF ablation adds very little risk. However, in some cases, we believe it is reasonable to perform atrial flutter ablation alone, particularly if atrial flutter is the predominant rhythm and if the rate in flutter is difficult and causing most symptoms. (See "Atrial fibrillation: Catheter ablation".)
The optimal approach to ablation in patients with both atrial flutter and AF was evaluated in the single-blind APPROVAL trial, which randomly assigned 360 patients to ablation of AF (with or without atrial flutter ablation) or ablation of flutter alone [41]. Among patients in the first group, 124 received AF ablation only and 58 had both ablation procedures. At nearly 22 months of follow-up, patients assigned to the group that received AF ablation (with or without atrial flutter ablation) had a higher rate of primary end point of freedom from arrhythmia off antiarrhythmic drug therapy during follow-up (64 versus 19 percent). This outcome was similar for the two subpopulations in the first group (AF ablation with or without atrial flutter ablation). Patients in group one had significant improvement in scores on most quality-of-life measures, whereas those in group two did not.
The finding in APPROVAL of similar outcomes between patients who received both AF and atrial flutter ablation and those who received AF ablation alone was noted in an earlier study of 108 patients with both AF and typical atrial flutter who were randomly assigned to either a dual ablative procedure (pulmonary vein isolation [PVI] and cavotricuspid isthmus ablation, 49 patients) or PVI alone (59 patients) [42].
These findings suggest that pulmonary vein triggers appear to initiate atrial flutter as well as AF. This conclusion is consistent with evidence that atrial flutter commonly starts after a transitional rhythm of variable duration, usually AF [43,44]. (See "Electrocardiographic and electrophysiologic features of atrial flutter".)
ANTICOAGULATION —
The discussion of anticoagulation below focuses on patients who undergo radiofrequency (RF) catheter ablation. However, similar issues apply to patients with atrial flutter (and AF) in whom antiarrhythmic drug therapy is to be started. Any therapy that causes conversion of atrial flutter (or fibrillation) to sinus rhythm leads to a measurable increase in the short-term risk of embolization unless proper anticoagulation is in place. (See "Prevention of embolization prior to and after restoration of sinus rhythm in atrial fibrillation".)
Anticoagulation before RF catheter ablation — For patients in atrial flutter scheduled to under RF ablation, anticoagulation is handled, broadly speaking, in a manner similar to that for patients with AF who undergo cardioversion. Most of these patients require at least three to four weeks of adequate anticoagulation before the procedure. (See "Atrial flutter: Restoration of sinus rhythm", section on 'Anticoagulation' and "Atrial flutter: Risk of thromboembolism and role of anticoagulation", section on 'Catheter ablation'.)
For those patients with atrial flutter of less than 48 hours duration, there is disagreement whether a transesophageal echocardiogram (TEE) is necessary to exclude the presence of a left atrial thrombus, as there is not good quality evidence available. If a TEE is performed and no thrombus is found, RF catheter ablation may be performed without prior anticoagulation. For low-risk patients with atrial flutter of less than 48 hours, it may be reasonable to proceed with ablation without a TEE. (See "Prevention of embolization prior to and after restoration of sinus rhythm in atrial fibrillation", section on 'AF duration less than 48 hours'.)
If the patient is not in atrial flutter at the time of the ablation, therapeutic anticoagulation is not necessary and a TEE is not usually performed.
Anticoagulation after RF catheter ablation — Anticoagulation for the prevention of embolic events may be necessary, at least on a temporary basis, after flutter ablation due to the potential for the development of recurrent atrial flutter or AF within six months. However, there are limited data to support this approach [45]. We use the following approach (algorithm 2):
●Initial postablation anticoagulation
•For right atrial ablation site – This is the location for cavotricuspid isthmus (CTI) ablations (as well as some non-CTI ablations).
-Atrial flutter at time of the ablation – Patients are treated with oral anticoagulation for at least four weeks after ablation.
-Sinus rhythm at the time of the ablation – If there is history of AF, the CHA2DS2-VASc score is assessed to determine whether oral anticoagulation is indicated, as discussed separately. (See "Atrial fibrillation in adults: Selection of candidates for anticoagulation".)
•For left atrial ablation site – This is the location for some non-CTI ablations. Patients are treated with oral anticoagulation for at least two to three months after ablation.
●Subsequent anticoagulation – For patients who were treated with an initial course (four weeks or two to three months) of postablation anticoagulation, next steps are based upon whether there is a history of AF.
•History of atrial fibrillation – If there is history of AF, the CHA2DS2-VASc score is assessed to determine whether oral anticoagulation is indicated, as discussed separately. (See "Atrial fibrillation in adults: Selection of candidates for anticoagulation".)
•No atrial fibrillation – If there is no history of AF, anticoagulation is stopped and the patient's symptoms and rhythm are monitored to assess for new AF or recurrent atrial flutter, which would prompt assessment of CHA2DS2-VASc score to determine need for ongoing anticoagulation. (See "Atrial fibrillation in adults: Selection of candidates for anticoagulation" and "Atrial flutter: Risk of thromboembolism and role of anticoagulation".)
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".)
SUMMARY AND RECOMMENDATIONS
●Indications – We attempt to maintain sinus rhythm in most patients with recurrent atrial flutter to decrease symptoms and prevent complications. Unlike atrial fibrillation (AF), the alternative strategy of rate control is usually unsuccessful. (See 'Indications' above.)
●Radio frequency ablation – For most patients with typical atrial flutter in whom a rhythm control strategy is desired, we recommend radiofrequency (RF) catheter ablation rather than a pharmacologic approach (Grade 1B). (See 'RF catheter ablation' above and 'RF ablation versus pharmacologic therapy' above.)
For patients with both atrial flutter and fibrillation, we recommend RF catheter ablation of the AF and flutter rather than ablation of atrial flutter alone (Grade 1B). (See 'Patients with atrial fibrillation' above.)
For those patients in whom atrial flutter is the predominant rhythm, atrial flutter ablation alone is a reasonable strategy.
●Importance of anticoagulation – Anticoagulation around the time of RF catheter ablation or pharmacologic cardioversion is handled in a manner similar to that for patients with atrial flutter or fibrillation scheduled to undergo cardioversion. Most patients will require effective anticoagulation both before and after the procedure. (See 'Anticoagulation' above.)
ACKNOWLEDGMENT —
The UpToDate editorial staff acknowledges Jie Cheng, MD, PhD, FACC, who contributed to earlier versions of this topic review.
