Atrial Flutter Treatment & Management

General goals for the treatment of symptomatic atrial flutter are similar to those for atrial fibrillation and include the following:

• Control of the ventricular rate
• Restoration of sinus rhythm
• Prevention of recurrent episodes, or decrease in their frequency or duration
• Prevention of thromboembolic complications
• Minimization of adverse effects from therapy

However, these goals can be modified for each patient. In an acute setting with pending hemodynamic collapse, follow the adult advanced cardiac life support algorithms for managing atrial fibrillation and flutter. Consider immediate electrical cardioversion for patients who are hemodynamically unstable.

The main difference between atrial fibrillation and atrial flutter is that most cases of atrial flutter can be cured with radiofrequency ablation. In all available studies, catheter ablation is superior to rate control and rhythm control strategies with antiarrhythmic drugs.

Consider catheter-based ablation as first-line therapy in patients with type I typical atrial flutter if they are reasonable candidates. Ablation is usually done as an elective procedure; however, it can be done when the patient is in atrial flutter as well.

Given the high success rate and low complication rate, radiofrequency ablation is superior to medical therapy. Successful ablation reduces or eliminates the need for long-term anticoagulation and antiarrhythmic medications.

For atrial flutter of less than 48 hours in duration, attempt cardioversion as soon as possible. Postconversion anticoagulation is usually unnecessary, although data from transesophageal echocardiography (TEE) studies indicate that postconversion anticoagulation a reasonable option.

For episodes of atrial flutter of uncertain duration or greater than 48 hours, begin anticoagulation therapy. If cardioversion is needed sooner, anticoagulate patients with intravenous heparin and perform TEE as close to the time of cardioversion as possible. Patients still require anticoagulation for at least 4 weeks after cardioversion. If thrombus is observed or suspected based on TEE findings, delay cardioversion. Rate control and therapeutic anticoagulation is required for a minimum of 4 weeks.

In patients who are not candidates for catheter-based ablation, rate and rhythm control strategies should be considered. The risk of proarrhythmia is probably greatest during the first 24-48 hours after the initiation of antiarrhythmics and drugs such as ibutilide, sotalol, and dofetilide should be initiated in an inpatient setting. Pause-dependent torsades de pointes can occur after conversion to sinus rhythm.

Because data suggest that patients with atrial flutter may be at similar risk for neurologic events as patients with atrial fibrillation, considering anticoagulation in this patient population (at least until sinus rhythm is maintained) is a wise decision. Anticoagulant therapy (ie, heparin and/or warfarin) is indicated, especially when the onset of atrial flutter is of more than 48 hours' duration or is uncertain.

Patients need to maintain a therapeutic international normalized ratio (INR) for 3 weeks prior to conversion and for at least 4 weeks after conversion to sinus rhythm. Long-term anticoagulation is recommended for patients with chronic atrial flutter. Closely monitor the patient's anticoagulation therapy, with a target INR of 2-3. Take special care when additional medications (including antibiotics) are added because they may cause dramatic alterations in INR values.

Preferred medications that slow AV node conduction include beta-blockers (eg, atenolol, metoprolol, propranolol) and calcium channel blockers (eg, verapamil, diltiazem). These medications are used to control ventricular rates. Also use these medications in patients who are taking class IA or IC antiarrhythmic drugs (to prevent rapid ventricular response, which can occur when the atrial rate is slowed).

Antiarrhythmic drugs are indicated for the termination of acute episodes or the prevention of recurrent episodes. For atrial flutter, electrical cardioversion is effective and usually requires less energy than for atrial fibrillation. Catheter ablation is safer than long-term use of an antiarrhythmic agent.

In patients who have atrial flutter and need cardiac surgery, modification of the atrial incision and creation of a cryothermal lesion, similar to the lesion created during radiofrequency catheter ablation, can be curative for atrial flutter and may prevent an incisional reentrant arrhythmia.

Ventricular rate control is a priority because it may alleviate symptoms. Rate control is typically more difficult for atrial flutter than for atrial fibrillation.

Ventricular rate control can be achieved with drugs that block the AV node. Intravenous calcium channel blockers (eg, verapamil, diltiazem) or beta-blockers can be used, followed by initiation of oral agents.

Hypotension and negative inotropic effects are concerns with the use of these medications. A history of Wolff-Parkinson-White syndrome or evidence of ventricular preexcitation should be determined because agents that act exclusively at the level of the AV node may enhance accessory pathway conduction.

The success rate of electrical cardioversion is higher than 95%. Factors to consider include synchronization of shocks to R waves, adequate sedation, and electrode position (apex anterior, apex posterior, anteroposterior). Atrial flutter generally requires less energy for conversion than atrial fibrillation; as few as 50 joules may be necessary.

If cardioversion is not successful with one electrode configuration, switching may improve success. A second set of electrodes can be used with tandem or simultaneous shocks. Biphasic external waveform may be more effective in restoring sinus rhythm.

A few points to remember about the cardioversion technique include a wide electrode separation in the right anterior and left posterior position (sandwiching the atria), although the more traditional location of pad location (anterior and apical) will also work; the application of pressure on paddles or electrodes to reduce thoracic impedance; and the placement of electrode patches under or lateral to the breasts in women.

Risius et al found that in external electrical cardioversion of atrial flutter, anterior-lateral electrode positioning yields results superior to those achieved with anterior-posterior positioning. In this randomized trial, 96 patients (72 of them men), received sequential biphasic waveform shocks using a step-up protocol consisting of 50, 75, 100, 150, or 200 J.

Compared with anterior-posterior positioning, anterior-lateral positioning resulted in successful cardioversion with less mean energy (65±13 vs 77±13 J) and fewer mean shocks (1.48±1.01 vs 1.96 ±1.00). In addition, cardioversion occurred with the first 50 J shock in 73% of patients when anterior-lateral positioning was used, versus 36% with the anterior-posterior electrode position.^[6]

Flecainide^[7] is effective in only approximately 10% of patients. Dofetilide^[8] is effective in 70-80% of patients. This drug should be initiated in an inpatient setting.

Ibutilide^{[9, 10, 11, 12]} is effective, converting recent-onset atrial flutter to sinus rhythm in 63% of patients with a single infusion. This is the only agent available intravenously in the United States that can be used for cardioversion. This drug must be given in a monitored setting due to risk of QT prolongation and torsade de pointes. The patient should be monitored with continuous ECG monitoring for at least 4 hours after the infusion.

Large single oral doses of type IC antiarrhythmic agents, such as propafenone (450-600 mg) or flecainide (200-300 mg), have also been shown to be effective in converting recent-onset atrial fibrillation to sinus rhythm. Their use in atrial flutter can be assumed to have at least equal success.

Antiarrhythmic medication prior to electrical cardioversion has been shown to improve the rate of conversion to sinus rhythm.

Radiofrequency ablation is often used as first-line therapy to permanently restore sinus rhythm. This procedure is often performed electively, rather than in the acute setting.

For patients with recurrent symptomatic atrial flutter that is proven to be isthmus-dependent in the electrophysiologic laboratory, expect a success rate of higher than 95% with current technology.

Catheter ablation has been shown to significantly improve the quality of life in patients with atrial flutter. The frequency of hospital admissions and emergency department visits and the number of antiarrhythmic drugs administered are decreased significantly after ablation. Activity capacity significantly improves in patients with preexisting LV dysfunction.

Ablation for type I atrial flutter

Catheter ablation is typically an outpatient procedure in patients with type I atrial flutter (tricuspid valve isthmus dependent). The procedure involves moderate sedation and accessing the femoral veins for catheter insertion. The diagnosis of atrial flutter is confirmed using pacing maneuvers and ablation is performed typically at 6:00 on the tricuspid valve isthmus.

A line of conduction block is required to interrupt the circuit (see the image below). Postablation pacing maneuvers can confirm that the substrate required for the circuit has been modified.

Recurrence is less than 5%. Postprocedure anticoagulation with warfarin is usually continued for 4-6 weeks.

Ablation for type II atrial flutter

Type II atrial flutter (non—isthmus dependent) circuits are amenable to catheter ablation, especially in centers with advanced mapping systems. The ablation procedure is similar but may involve additional mapping of the left atrium (via a trans-septal puncture).

Success depends on localizing the circuit and creating a line of block that includes an electrically inert anatomic structure (ie, the mitral valve annulus). While success should approach 95%, recurrence is more common and may also require the use of antiarrhythmic agents for suppression.

After the initial episode is terminated and the underlying disease is treated, the patient may not need any further intervention except avoidance of the precipitating factor (eg, alcohol, caffeine). For atrial fibrillation, approximately 30% of patients remain in sinus rhythm at 1 year without antiarrhythmic therapy.

Antiarrhythmic agents

Data on the use of antiarrhythmic agents specifically for atrial flutter are limited. Most studies of antiarrhythmics agents and atrial fibrillation include some patients with atrial flutter (10-20%). (For more information on the use of antiarrhythmic agents, see Atrial Fibrillation.)

In general, the use of antiarrhythmic drugs in atrial flutter is similar to that of atrial fibrillation; however, with a high success rate and low complication rate, the use of radiofrequency ablation in atrial flutter makes this procedure a favorable option compared with lifelong antiarrhythmic drug therapy because fatal proarrhythmic events (even in healthy hearts) and organ toxicity may occur.

In general, antiarrhythmics used to treat atrial fibrillation have been shown effective in fibrillation or flutter during a 6- to 12-month follow-up. Considering the characteristic adverse effects of each antiarrhythmic agent, the choice of medication should take into account the underlying cardiac pathology, as follows:

• No structural heart disease - class IC agents can be used safely
• Left ventricular hypertrophy without ischemia or conduction delay - class III agents, specifically amiodarone, can be used
• Ischemic heart disease - sotalol or amiodarone can be used; avoid class IC agents
• Significant systolic dysfunction - amiodarone or dofetilide may be used; avoid class IC agents

Patients with atrial flutter are at increased risk of thromboembolic complications compared with the general population. The anticoagulation strategy used for atrial fibrillation is also recommended for atrial flutter. In general, when atrial flutter persists for more than 48 hours, 4 weeks of adequate anticoagulation or TEE is needed before attempting cardioversion to sinus rhythm. Postconversion anticoagulation is recommended for a minimum of 4 weeks, as thromboembolic complications occur spontaneously after cardioversion or ablation.

Use long-term anticoagulation for patients with persistent or paroxysmal atrial flutter. As with atrial fibrillation, keep the international normalized ratio (INR) at 2-3 to optimize the therapeutic effect and minimize the risk of bleeding.

Unlike atrial fibrillation, atrial flutter has a regular pattern of atrial contraction. TEE data have demonstrated an organized sawtooth pattern of the left atrial appendage flow with alternating filling and emptying wavelets. No difference in the left atrial appendage function is observed compared with patients in sinus rhythm. Patients with both atrial flutter and atrial fibrillation have significantly decreased left atrial appendage function, more spontaneous echo contrast, and larger left atria and accompanying appendages.

Other reports have demonstrated thrombus in the left atrium appendage of patients with atrial flutter (as many as 43%). Most studies of non–anticoagulated patients with atrial flutter report a rate of 10-15% for patients with thrombus in the left atrium or left atrial appendage. Spontaneous echo contrast associated with increased risk of thromboembolism was found in 6-43% of patients with atrial flutter.

Patients with atrial flutter and episodes of atrial fibrillation are at higher risk of thromboembolic events; however, determining whether episodes of atrial fibrillation are associated with episodes of atrial flutter is difficult.

A large retrospective review of patients in chronic atrial flutter revealed a 14% occurrence rate of thromboembolic events over 4.5 years, with half of these events being ischemic stroke. In another large cohort of patients with atrial flutter, the occurrence rate of embolic complications in patients with chronic or recurrent atrial flutter was 12%.

For stroke, this risk is estimated at approximately one third of patients with nonrheumatic atrial fibrillation. Males with hypertension, structural heart disease, left ventricular dysfunction, and diabetes may be at higher risk of thromboembolic complications. Interestingly, associated atrial fibrillation did not significantly increase the risk of the embolic complications.

The CHA2DS2-VASc score includes the following risk factors:

• Congestive heart failure
• Hypertension
• Age 65-74 years
• Diabetes
• Previous stroke
• Vascular disease
• Sex

This score has been shown to perform well at predicting whether a patient is at high or low risk for thromboembolism.^[13]

Postcardioversion thromboembolic events can complicate as many as 7.3% of procedures in patients who are not anticoagulated. These events occur within 3 days after the cardioversion; almost all occur within 10 days after the cardioversion^[14] .

In atrial fibrillation, postcardioversion stunning of the left atrial appendage is thought to contribute to thrombogenicity.^[15] This phenomenon may last as long as 4 weeks in patients with atrial fibrillation and may be related to how long patients have been in the arrhythmia.

Stunning of the left atrial appendage also occurs following conversion from atrial flutter to sinus rhythm (electrical or spontaneous), although to a lesser degree. Left atrial and left atrial appendage function decrease immediately after conversion, and, in one study, spontaneous echo contrast was noted to develop within 5 minutes after conversion in 43% of patients. This is thought to be the source of emboli in patients whose TEE findings revealed no evidence of thrombus but who had a thromboembolic event after cardioversion.

In a study comparing left atrial appendage function before and after catheter ablation (immediate, 1 d, 1 wk, and 6 wk) of persistent atrial flutter, a significant increase in atrial standstill, decrease in left atrial appendage function, and new spontaneous echo contrast occurred after ablation. One patient formed a new left atrial appendage thrombus after ablation. Evidence of atrial stunning significantly improved after 1 week. Anticoagulation for at least 1 week is advocated after ablation of an atrial flutter that persists for more than 2 days.

Adequate anticoagulation, as recommend by the American College of Chest Physicians, has been shown to decrease thromboembolic complications in patients with chronic atrial flutter and in patients undergoing cardioversion.

Termination of long-standing atrial flutter with a rapid ventricular response has been reported to improve left ventricular systolic function in patients without other known causes of dilated cardiomyopathy.

Because atrial flutter is a nonfatal arrhythmia, carefully assess the risks and benefits of drug therapy, especially with antiarrhythmic agents. Always consider catheter-based ablation as first-line therapy prior to starting an antiarrhythmic agent. A few points to remember that will help minimize the adverse effects include the following:

• Avoidance of precipitating factor(s) or therapy of the underlying problem may be all that is needed to prevent recurrent episodes
• Of antiarrhythmic agents, amiodarone is effective and is associated with a low proarrhythmic risk but may adversely affect multiple organs, including the skin, liver, lungs, and thyroid; thus, sotalol would seem a reasonable choice of antiarrhythmic drug therapy for atrial flutter; per guidelines, sotalol should be initiated in the inpatient setting.
• Radiofrequency ablation is currently the preferred therapeutic choice; although many patients who were treated with radiofrequency ablation subsequently developed atrial fibrillation after long-term follow-up (56% in one study), this procedure still represents a safe alternative to antiarrhythmic agents