Treatment Of Atrial Flutter

The goals of treatment in atrial flutter are to control ventricular rate, convert to and maintain sinus rhythm, and prevent thromboembolic complications in patients with prolonged episodes of atrial flutter.

Drugs used for ventricular rate control in atrial flutter include digitalis, verapamil, diltiazem, and beta-blockers. The efficacy of these drugs in preventing 1:1 conduction in atrial flutter is assumed, but has not been proven. Digitalis is a poor single choice for rate control, because circulating catecholamines from daily stressors may easily overwhelm its vagotonic effects on the AV node. Given the typical even-integral (i.e.,

2:1, 4:1, 8:1) ventricular response to atrial flutter, rate control without corresponding bradycardia during sinus rhythm is often difficult to achieve.

The therapeutic options for cardioversion of atrial flutter include electrical or direct current (DC) cardioversion, antiarrhythmic agents (class I and III antiarrhythmics), overdrive pacing, and radiofrequency ablation. Notably, any attempt at acute cardioversion (independent of whether electrical, chemical, pacing or ablative techniques are used) necessitates careful consideration of the risk of thromboembolism.

DC Cardioversion

Direct current (DC) cardioversion was first introduced as a treatment for atrial tachyarrhythmias in 1962 (46). DC cardioversion for atrial flutter is initially successful in 93-100% of patients (47-51). In patients with chronic atrial flutter, recurrence rates are high (52). Traditionally, an initial shock of 50 J has been recommended for atrial flutter, yet more recent evidence reveals a higher rate of first-shock cardioversion, fewer total shocks, and less AF complicating cardioversion when 100 J or higher is used as the initial shock (47,53).

Patients undergoing direct current cardioversion should have an empty stomach, and therefore should not eat for 8 h prior to the procedure. External cardioversion is performed with general anesthesia, typically with a short-acting agent such as propofol. Once the patient is adequately sedated, a synchronized shock at an initial energy of 100 J is successful 85% of the time (53). If the initial shock is unsuccessful, 200-J and 300-J shocks should follow until the patient is in sinus rhythm. In patients refractory to DC cardioversion, the use of a biphasic external defibrillator may be successful. Intracardiac cardioversion is also an option.

Pharmacologic Treatment of Atrial Flutter Acute Cardioversion

Anti-arrhythmic agents used for cardioversion of atrial flutter include class I and class III drugs. Class I agents block sodium channels and slow conduction within the atrium. Theoretically, sufficient slowing of conduction across the isthmus of slow conduction in typical atrial flutter should result in localized conduction block (depressed excitability) and termination of the arrhythmia. Class III agents block potassium channels and prolong refractoriness. In theory, prolonging the refractory period should narrow the excitable gap and/or force the activation pathway to expand beyond the dimensions of the available atrial tissue.

Most of the clinical evidence about antiarrhythmic drug therapy in atrial flutter comes from studies in which atrial flutter is combined with AF (54). Furthermore, most of these studies lack a placebo group for comparison, and therefore the incidence of spontaneous cardioversion was not determined. Studies in which drug effects on atrial flutter have been separated from AF include only a small number of patients. In turn, there is a tremendous lack of information on antiarrhythmic drug efficacy in atrial flutter itself. Cardioversion rates in these studies are disappointing and are in general reported to be less than 40% (55,56).

Ibutilide appears to be more effective than other antiarrhythmic agents in acute cardioversion of atrial flutter. Vos et al. in a double-blind, randomized study of ibutilide vs dZ-sotalol (251 patients with AF and 57 patients with atrial flutter), reported successful cardioversion in 70% of patients with atrial flutter treated with ibutilide (2 mg iv). Only 19% of patients treated with sotalol converted to sinus rhythm. Of the 109 patients treated with 2 mg of iv ibutilide, 8 patients (7.3%) had nonsustained polymorphic ventricular tachycardia (PVT), one patient had nonsustained monomorphic VT, and 1 patient had sustained PVT requiring electrical cardioversion. All proarrhythmic events occurred within 30 min of the infusion of ibutilide (57). Stambler et al. reported a comparison of ibutilide, procainamide, and placebo given for attempted cardioversion in 89 patients with atrial flutter. Ibutilide converted 29 of 45 (64%) patients, procainamide converted 0 of 33 patients, and 0 of 11 patients who received placebo converted to sinus rhythm. Nonsustained PVT was observed in 4% of patients who received ibutilide for atrial flutter (58).

The incidence of pro-arrhythmia in these two trials is consistent with other published data. The overall incidence of PVT in a report of 586 patients who received ibutilide in clinical trials was 4.4%. The incidence of sustained PVT was 1.7% (59). Although ibutilide appears to be efficacious in the acute termination of atrial flutter, there is a significant risk of proarrhythmia, and patients should be closely monitored until resolution of drug-induced QT prolongation (minimum of 60 min after the iv infusion is complete).

Chronic Maintenance of Sinus Rhythm

Data on the efficacy of long-term maintenance of sinus rhythm with pharmacologic therapy of atrial flutter is lacking, again because of the inclusion of patients with AF in most trials. A potential danger with antiarrhythmic therapy is that it may cause sufficient slowing of the flutter rate to allow the AV node to conduct 1:1 in the absence of sufficient AV-nodal blocking agents. This may result in hemodynamic instability, myocardial ischemia, or sudden death. It is important that patients treated with antiarrhythmic therapy (for AF or atrial flutter) are placed on medications that will sufficiently slow AV conduction, such as beta-blockers or calcium-channel blockers.

Treatment of Atrial Flutter with Atrial Pacing

When atrial pacing is readily available (as in the presence of a DDD pacemaker or an atrial lead inserted after cardiac surgery), rapid atrial pacing may be utilized to terminate atrial flutter. This procedure is performed by pacing at a slightly faster rate than the flutter rate. When an atrial lead is available, this method is attractive because it causes little discomfort to the patient and does not require anesthesia.

Clinical trials of antitachycardia pacing for atrial flutter have yielded modest results for pacing alone (60-66). Atrial pacing may be complicated by the induction of AF, which may occur in up to 70% of patients after rapid pacing of atrial flutter (62,63,65). Improvement in pace termination rates with significant reduction in the induction of AF can be achieved with the addition of class IA (procainamide, disopyramide) agents prior to atrial overdrive pacing. The efficacy of combination therapy is reported to be 70-100% (61-63,66,67). Class IA agents prolong the cycle length to a greater extent than the effective refractory period, and significantly increase the excitable gap in atrial flutter (66). These agents appear to exert their effect by decreasing the conduction velocity and widening the excitable gap, and therefore facilitating the penetration of the pacing stimulus into the atrial flutter circuit.

Ibutilide, a class III agent, appears as efficacious as procainamide in aiding the success of overdrive pacing for atrial flutter. Stambler et al. (67) reported conversion of atrial flutter in 2 of 11 (18%) patients with pacing alone, 13 of 15 (87%) patients who received iv ibutilide and overdrive pacing, and 29 of 33 (88%) patients who received iv procainamide and overdrive pacing.

Treatment of Atrial Flutter with Radiofrequency Ablation

Radiofrequency catheter ablation has revolutionized the treatment of supraventricular tachyarrhythmias. Understanding the anatomic barriers that confine the macroentry circuit of typical atrial flutter has allowed electrophysiologists to focus treatment on the narrow isthmus between the IVC and tricuspid annulus (23,68,69) (see Fig. 6). A linear lesion is applied with radiofrequency energy within the isthmus to the end point of bidirectional conduction block, demonstrated with pacing and multi-electrode catheter recordings (see Fig. 7). The acute success rate is greater than 95% (23,68,70-72) and when bidirectional block is demonstrated within the isthmus, the recurrence rate is 6-9% (71,73). The procedure is performed anatomically, and can therefore be performed with the patient in sinus rhythm (72,75). Radiofrequency ablation of atrial flutter is safe, with relatively few reported complications, and is effective. Success rates in excess of 95% have been reported; recurrence rates are less than 10% with current techniques.

Natale et al. prospectively studied outcomes of patients with atrial flutter who were randomly assigned to initial antiarrhythmic therapy vs primary radiofrequency ablation (74). Of 61 patients, 30 were assigned to drug therapy and 31 were assigned to radiofrequency ablation therapy. After a mean follow-up of 21 ± 11 mo, only 11 of 30 (36%) patients treated with antiarrhythmics were in sinus rhythm, vs 25 of 31 (80%) who received radiofrequency ablation (p < 0.01). Furthermore, 63% of patients who were treated with antiarrhythmics required one or more hospitalizations after initiation of therapy vs 22% of patients post-radiofrequency ablation. Importantly, a quality-of-life and symptom questionnaire (Endicott Quality of Life Enjoyment and Satisfaction Questionnaire) was administered at the beginning of the study and 6 and 12 mo thereafter. Sense of well-being and function in daily life improved significantly after ablation (2.0 ± 3 pre radiofrequency vs 3.8 ± 0.5 post-radiofrequency, p < 0.01); 2.3 ± 0.4 pre-radiofrequency vs 3.6 ± 0.6 post-radiofrequency, p <0.01 respectively). These parameters did not change significantly in patients treated with drugs (74). Interestingly, 53% patients treated with antiarrhythmic medication in this study developed AF vs 29% of patients who were treated with radiofrequency ablation (p < 0.05). This finding casts further doubts into the efficacy of antiarrhythmic therapy.

AF following radiofrequency ablation for typical atrial flutter occurs in approx 25% of patients. Philippon et al. reported an incidence of 26.4% (14 patients) in 53 consecutive patients during a mean follow-up of 13 mo after radiofrequency ablation (76). Paydak reported a rate of 25% (28 patients) in 110 consecutive patients treated with ablation during a mean follow-up of 20 mo (77). Patients with structural heart disease and a history of AF are at greatest risk (76,77). In the absence of structural heart disease, patients with this complication can be treated safely with class I antiarrhythmic drugs (see section on Hybrid therapy). Patients with AF and structural heart disease should be treated on an individual basis with either anticoagulation and rate control or anti-arrhythmic therapy (such as amiodarone or dofetilide).

The efficacy of radiofrequency ablation in true atypical atrial flutter is not as well defined. Experience with ablation of true atypical atrial flutter with fixed anatomic

Atrial Flutter Ablation

Fig. 6. Fluoroscopic images of catheters within the right atrium. (A) Left anterior oblique 30° projection. The halo catheter encircles the tricuspid annulus and has 10 bipolar electrodes (from distal to proximal, labeled T1-T10). The His catheter sits immediately on the atrial side of the tricuspid annulus over the bundle of His. The coronary sinus (CS) catheter is placed within the coronary sinus. In counterclockwise typical atrial flutter, activation around the Halo follows the direction of the arrow. (B) Right anterior oblique 60° projection of the same catheters, now including the ablation (ABL) catheter. During ablation of typical atrial flutter, a lesion is created in the isthmus between the tricuspid annulus and the IVC. This is usually between the CS catheter and T1 on the Halo catheter.

Fig. 6. Fluoroscopic images of catheters within the right atrium. (A) Left anterior oblique 30° projection. The halo catheter encircles the tricuspid annulus and has 10 bipolar electrodes (from distal to proximal, labeled T1-T10). The His catheter sits immediately on the atrial side of the tricuspid annulus over the bundle of His. The coronary sinus (CS) catheter is placed within the coronary sinus. In counterclockwise typical atrial flutter, activation around the Halo follows the direction of the arrow. (B) Right anterior oblique 60° projection of the same catheters, now including the ablation (ABL) catheter. During ablation of typical atrial flutter, a lesion is created in the isthmus between the tricuspid annulus and the IVC. This is usually between the CS catheter and T1 on the Halo catheter.

Atrial Flutter Halo Catheter

Fig. 7. Diagram of right atrial activation and intracardiac electrograms from His, Coronary sinus ostium (CS), Halo catheter electrodes. (A) Activation sequence prior to ablation of typical atrial flutter. Schematic diagram (left) represents position of electrodes in relation to anatomic structures within the right atrium. The critical isthmus lies between the inferior vena cava (IVC) and the tricuspid annulus (TA). Pacing from the CS os starts a wavefront that conducts in both directions through the atrium, the impulse proceeds "colliding" at approx T7. This is seen clearly in the intracardiac electrograms on the right. (B) Activation sequence after successful ablation of isthmus. The paced impulse blocks at the site of the lesion, but proceeds superiorly on the atrial septum (CS to His), across the roof of the atrium, and then inferiorly on the atrial free wall (T10 to T1). The T1 electrode is now the latest electrode site activated, despite its proximity to the CS pacing site. Bidirectional block is demonstrated by a similar discontinuous conduction pattern during pacing from the low lateral right atrium (T3 position). When this site is paced, the CS os electrode site should be the latest in the sequence with successful ablation.

Fig. 7. Diagram of right atrial activation and intracardiac electrograms from His, Coronary sinus ostium (CS), Halo catheter electrodes. (A) Activation sequence prior to ablation of typical atrial flutter. Schematic diagram (left) represents position of electrodes in relation to anatomic structures within the right atrium. The critical isthmus lies between the inferior vena cava (IVC) and the tricuspid annulus (TA). Pacing from the CS os starts a wavefront that conducts in both directions through the atrium, the impulse proceeds "colliding" at approx T7. This is seen clearly in the intracardiac electrograms on the right. (B) Activation sequence after successful ablation of isthmus. The paced impulse blocks at the site of the lesion, but proceeds superiorly on the atrial septum (CS to His), across the roof of the atrium, and then inferiorly on the atrial free wall (T10 to T1). The T1 electrode is now the latest electrode site activated, despite its proximity to the CS pacing site. Bidirectional block is demonstrated by a similar discontinuous conduction pattern during pacing from the low lateral right atrium (T3 position). When this site is paced, the CS os electrode site should be the latest in the sequence with successful ablation.

substrates is limited. Because of the variable anatomic location, detailed mapping and a case-specific approach are necessary.

Ablation of incisional atrial flutter may be achieved by creating a lesion in a critical isthmus of conduction bounded by anatomic barriers. This isthmus can be localized by entrainment mapping. Once the critical isthmus is localized, a line of block is created from the incision to an anatomic barrier (such as the tricuspid annulus, atrial septal patch, IVC, or SVC) (77a). Kalman et al. reported an acute success rate of 83% (15 of 18 patients). During a mean follow-up of 17 mo, clinical improvement was observed in 73% (13 of 18 patients), and 50% (9 of 18 patients) remained asymptomatic without recurrence of atrial flutter (45).

In refractory cases of incisional atrial flutter with a rapid ventricular rate, radio-frequency ablation of the His bundle with the implantation of a single-chamber ventricular pacing (VVIR)-pacemaker may be an alternative option (78-81).

Typical atrial flutter is the most common subtype of atrial flutter seen clinically. Atrial flutter ablation in typical atrial flutter is curative and safe. Atrial flutter ablation results in a lower incidence of AF than pharmacologic treatment, improves quality of life, and may allow cessation of warfarin.

Treatment of Atrial Flutter After Cardiac and Thoracic Surgery

Atrial arrhythmias are common after cardiothoracic surgery. Right atrial enlargement from hemodynamic factors, pericardial irritation, and withdrawal from chronic beta-blocker therapy contribute to promote the occurrence of atrial tachyarrhythmias. The incidence of atrial arrhythmias after cardiac surgery is approximately 30%, with atrial flutter representing up to one-third of these cases (82). The initial management of postoperative atrial flutter is similar to the management of postoperative AF. If the patient is hemodynamically unstable, DC cardioversion or anti-tachycardia pacing is indicated. If the patient is stable, ventricular rate control with a beta-blocker is preferred unless contraindicated. Most patients will spontaneously convert to sinus rhythm without antiarrhythmic therapy. In patients with late (> 3 d postoperative) onset or recurrent atrial flutter after the initiation of beta-blocker therapy, a reasonable approach is treatment with antiarrhythmic drugs (usually procainamide or amiodarone) and warfarin for 4-6 wk. Catheter ablation is not indicated in the acute postoperative setting, because of the usually transient nature of atrial flutter in this setting.

Prevention of Thromboembolic Complications in Atrial Flutter

Until recently, patients with atrial flutter had not been treated with anticoagulation. Several transesophageal echocardiographic studies have demonstrated a significant prevalence of left atrial thrombus and spontaneous echo contrast in patients referred for cardioversion or ablation of atrial flutter (83-85). Recent studies have demonstrated a risk of thromboembolic complications in patients with atrial flutter. Seidl et al. reported a 7% thromboembolic event-rate flutter over a mean follow-up of 26 mo in a prospective study of 191 consecutive patients referred for treatment of atrial flutter (86). Wood et al. found an embolic rate of 14% over a period of 4.5 yr in 86 patients referred for radiofrequency ablation for atrial flutter (87). Lanzarotti et al. retrospectively reviewed thromboembolic events in 100 patients who underwent direct current cardioversion for atrial flutter, and reported a 6% event rate (88). The preliminary evidence for thromboembolic risk in atrial flutter demonstrates a significant risk rate, approaching the risk seen in AF.

With anticoagulation therapy, there is a fine balance between decreasing the risk of thromboembolic events and the increased risk of bleeding. Bleeding complications from anticoagulation therapy can be estimated from the six major trials examining the effectiveness of anticoagulation in the prevention of stroke in patients with atrial AF (AFASAK, SPAF, BAATAF, CAFA, SPINAF, and SPAFII) (89-94). The target INR in these trials varied, with a range between 1.4 and 4.5. The annual incidence of stroke in these trials was approx 4.5% (range 3.0-7.4%). With warfarin therapy, the incidence of stroke was reduced to a mean of 1.4%. The risk of major bleeding in these studies was extremely low, with an incidence of approx 1.3% per yr in the warfarin groups.

Further insights into the risk of bleeding during anticoagulation therapy can be derived from recent studies of anticoagulation for myocardial infarction (MI). In the ASPECT trial, patients were randomized to anticoagulant treatment following an acute MI with a target International Normalized Ratio (INR) of 2.8 to 4.8 (95). Major bleeding in this trial was reported at a rate of 1.5 per 100-patient years of follow-up. The risk of major bleeding increased dramatically as the INR increased over 4.0. The risk of thromboembolic events increased at an INR <2.0.

Based on the available data, patients with atrial flutter of greater than 48 h duration should be anticoagulated with warfarin (target INR 2.0-3.0). A transesophageal echo-cardiogram should be obtained if cardioversion or ablation is planned prior to at least 3 wk of adequate anticoagulation. Anticoagulation should be continued for 4 wk after cardioversion or radiofrequency ablation of atrial flutter. Long-term anticoagulation is recommended for paroxysmal or chronic atrial flutter, except in patients less than 65 yr of age with "lone" or idiopathic atrial flutter. In these patients, the risk of thromboembolic complications is extremely low, and aspirin therapy is typically recommended (96).

Hybrid Therapy for Atrial Fibrillation

Atrial flutter often coexists with AF within the same individual. It has been observed that up to 11% of patients with lone AF treated with antiarrhythmics will develop persistent atrial flutter. Schumacher et al. studied 187 patients with paroxysmal AF who were treated with class (IC) antiarrhythmic agents (96 patients received flecainide, 91 patients received propafenone) (97). Twenty-four patients (12.8%) developed atrial flutter during treatment. Twenty of the 24 patients (10.7%) were found to have typical atrial flutter by electrophysiologic studies. These 20 patients underwent radiofrequency ablation, which was acutely successful in 19 of 20 patients. These patients were followed by ambulatory Holter monitoring and serial questionnaires for a mean follow-up period of 11 ± 4 mo. The incidence of AF episodes were significantly lower in patients with combined therapy (2.7 ± 3.6 per yr) vs patients treated with drugs alone (7.8 ± 9.2 per yr, p < 0.05). During the follow-up period, 7 patients remained symptom-free with no evidence of atrial tachyarrhythmias, and 8 patients had paroxysmal AF but at a significant lower frequency than before combined therapy (2.3 ± 1.6 per yr vs 11.5 ± 1.50 per yr, p < 0.001). In the remaining four patients, no benefit was found (97). Huang et al. reported 13 patients who developed atrial flutter when treated for AF with antiarrhythmic agents. Nine of these patients had typical atrial flutter and underwent successful radiofre-quency ablation. These nine patients were followed by clinic visits, record review, and telephone interviews and during a mean follow-up of 14.3 ± 6.9 mo, 88.9% remained in sinus rhythm (98). Tai et al. reported atrial flutter in 15 of 136 (11%) patients treated for AF with amiodarone (n = 96) or propafenone (n = 40). Atrial flutter occurred in equal frequency in patients treated with amiodarone vs propafenone. Eleven of these 15 patients had counterclockwise typical atrial flutter and four had clockwise typical atrial flutter. All 15 patients underwent successful radiofrequency ablation. During a mean follow-up period of 12.3 ± 4.2 mo, 14 (93%) remained in sinus rhythm (99).

Hybrid pharmacologic and ablative therapy may be a safe and effective means of maintaining sinus rhythm in a subset of patients who develop atrial flutter during antiarrhythmic treatment for AF.

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Responses

  • adelfo
    Is bundle of HIS catheter placed for atrial flutter?
    7 years ago
  • Helvi Almila
    Can I use h2o2 bath therapy with atrial flutter?
    7 years ago
  • hagosa
    Is cardioversion appropriate for a asymptomatic 91 year old in atrial flutter?
    6 years ago

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