Long term treatment of atrial flutter

Recent improvements in the efficacy of catheter ablation techniques and the long recognised difficulty in achieving adequate chronic suppression of atrial flutter with drug treatment have significantly affected the approach to long term treatment of atrial flutter. In short, if atrial flutter is an important clinical problem in any patient, characterisation of the mech-

Acute treatment of atrial flutter

• Depends on clinical presentation

- need for prompt restoration of sinus rhythm: DC cardioversion

- elective restoration of sinus rhythm: antiarrhythmic drug treatment (ibutilide or class IC agent), DC cardioversion or rapid atrial pacing

- ventricular rate control: often required (P blocker or calcium channel blocker), especially with use of class IC antiarrhythmic agent anism of atrial flutter followed by catheter ablation as treatment of choice (cure) is now recommended.

Catheter ablation treatment Two types of catheter ablation are available for the treatment of chronic or recurrent atrial flutter, one curative and one palliative. Appropriate application of radiofrequency energy via an electrode catheter can be used to cure atrial flutter. Advances in both electrophysiologic mapping and radiofrequency catheter ablation techniques have improved the efficacy of this therapeutic approach to about a 95% cure rate for patients with typical or reverse typical atrial flutter,7 19 making it the treatment of choice in most patients in whom the arrhythmia is clinically important. The technique involves elec-trophysiologic study of the atria during atrial flutter to identify the location of the re-entrant circuit and then to confirm that the re-entrant circuit includes a critical isthmus between the inferior vena cava-Eustachian ridge-coronary sinus ostium and the tricuspid valve (fig 24.5). When this latter area is identified, radiofre-

Figure 24.5. Targets for typical or reverse typical atrial flutter ablation. The schematic drawing shows the atria in an anterior view. The endocardium, inside the tricuspid (left) and mitral (right) rings, is shaded. The openings of the inferior vena cava (IVC), coronary sinus (CS), and left pulmonary veins (PV) are shown in black. Long arrows show activation sequence in common atrial flutter. The striped areas (large open arrows) mark ablation targets: 1, IVC-tricuspid valve isthmus; 2, CS-tricuspid valve isthmus; 3, CS-IVC isthmus. SVC, superior vena cava. Reproduced with permission from Cosío et al.19

Figure 24.5. Targets for typical or reverse typical atrial flutter ablation. The schematic drawing shows the atria in an anterior view. The endocardium, inside the tricuspid (left) and mitral (right) rings, is shaded. The openings of the inferior vena cava (IVC), coronary sinus (CS), and left pulmonary veins (PV) are shown in black. Long arrows show activation sequence in common atrial flutter. The striped areas (large open arrows) mark ablation targets: 1, IVC-tricuspid valve isthmus; 2, CS-tricuspid valve isthmus; 3, CS-IVC isthmus. SVC, superior vena cava. Reproduced with permission from Cosío et al.19

quency energy is delivered through the electrode catheter to create a bidirectional line of block across it. This isthmus may be difficult to ablate completely,7 19 but combined entrain-ment pacing and mapping techniques have now evolved which permit both the reliable demonstration that this isthmus is a part of the re-entrant circuit, and that application of radio-frequency energy has produced complete bidirectional conduction block in this isthmus. When the latter is demonstrated, successful ablation of atrial flutter has been accomplished.

Similarly, when incisional re-entrant atrial flutter is identified by electrophysiological mapping techniques, a vulnerable isthmus usually can be identified and successfully ablated using radiofrequency catheter ablation techniques.9 There is insufficient information available to discuss the likely efficacy of successful radiofrequency ablation techniques to cure left atrial flutter or atypical atrial flutter, although contemporary electrophysiological mapping techniques are capable of identifying the location of the re-entrant circuits associated with these types of atrial flutter, making effective ablation treatment a possibility.

AV nodal-His bundle ablation to create high degree AV block (generally third degree AV block) can be used palliatively to eliminate the rapid ventricular response rate to atrial flutter. It does not prevent the atrial flutter, and requires placement of a pacemaker system. For patients in whom catheter ablation of atrial flutter is unsuccessful and in whom anti-arrhythmic drug treatment is either ineffective or is not tolerated, or in whom atrial flutter with a clinically unacceptable rapid ventricular response rate recurs despite drug treatment, producing third degree AV block or a high degree of AV block provides a successful form of therapy. Selection of a pacemaker in such circumstances should be tailored to the needs of the patient, and may include a single chamber, rate responsive, ventricular pacemaker or a dual chamber pacemaker with mode switching capability.

Antiarrhythmic drug treatment Atrial flutter is quite difficult to suppress completely with drug treatment. In fact, based on available long term data, drug treatment offers a limited ability to maintain sinus rhythm without occasional to frequent recurrences of atrial flutter, even when multiple agents are used. This is among the reasons why this form of therapy is no longer the long term treatment of choice in most patients with atrial flutter. For patients in whom drug treatment is selected, an important measure of efficacy should be the frequency of recurrence of atrial flutter rather than a single recurrent episode. For instance, recurrence only at long intervals—for example, once or twice per year—probably should be classified as a treatment success rather than a failure.

In the past, standard antiarrhythmic drug treatment consisted of administration of a class IA agent (quinidine, procainamide, or diso-pyramide) in an effort to prevent recurrence. However, recent studies indicate that the type

IC antiarrhythmic agents flecainide and propafenone are as effective, if not more effective, are generally better tolerated, and have less organ toxicity than class IA agents. Principally because of their serious adverse effects demonstrated in the cardiac arrhythmia suppression trial (CAST I), it is widely accepted that class IC agents should not be used in the presence of underlying ischaemic heart disease. In fact, this approach has generally been extrapolated to include the presence of underlying structural heart disease. Nevertheless, class IC agents are recommended for long term suppression of atrial flutter in the absence of structural heart disease.

Moricizine, a class I drug with A, B, and C properties, also may be effective in the treatment of atrial flutter. The long term data from CAST II, in which moricizine and placebo were no different in terms of mortality, suggests that moricizine may be a good choice for patients with atrial flutter and coronary artery disease late (> 3 months) after a myocardial infarction. However, more data are required to establish moricizine's efficacy and safety in this clinical setting.

In addition, the class III antiarrhythmic agents amiodarone, sotalol, and dofetilide also may be quite effective. When using sotalol or dofetilide, care must be taken to avoid Q-Tc interval prolongation much beyond 500 ms in order to avoid precipitation of torsades de pointes. Amiodarone appears to be quite effective, but its potential toxicity is a well recognised concern, making widespread use of this drug to treat atrial flutter problematic.20 Thus, the use of amiodarone as the drug of first choice to treat atrial flutter probably should be limited to patients with notably depressed left ventricular function. Since atrial flutter tends to recur despite antiarrhythmic drug treatment, it is important to remember that on a class IA (quinidine, procainamide, disopyra-mide) or especially a class IC or IC-like (flecainide, propafenone, moricizine) agent, the atrial flutter rate may be much slower (for example, 180-220 bpm) than in the absence of one of these drugs. Therefore, it is very important that adequate block of AV nodal conduction be present, usually with concurrent use of a P blocker or a calcium channel blocker, alone or in combination with digoxin.

Anticoagulant treatment

Although one study found neither atrial clot formation nor stroke associated with atrial flutter in a relatively small cohort of patients after open heart surgery, the association of the potential risk of stroke with atrial flutter has now been established.14 15 Other data support this association. Thus, atrial flutter and atrial fibrillation often co-exist in patients. Additionally, using transoesophageal echocardiography, a high incidence of spontaneous echo contrast and atrial thrombi have been documented, as were striking abnormalities in the left atrial appendage in patients with atrial flutter. In short, in patients with atrial flutter, daily warfarin treatment to achieve an international normalised ratio (INR) of 2 to 3 is recom-

Long term treatment of clinically important atrial flutter

• Treatment of choice: radiofrequency catheter ablation to achieve cure

• Alternative treatment (warfarin therapy usually required)

- drug treatment (class IC, III or IA antiarrhythmics plus an AV nodal blocking drug)

- device implantation (antitachycardia pacemaker or low energy atrial defibrillator)

- His bundle ablation plus pacemaker implantation mended using the same criteria as for atrial fibrillation. Also, the same criteria apply for cardioversion. Thus, if the patient has had atrial flutter for greater than 48 hours and the INR is not therapeutic (INR > 2), warfarin treatment should be either initiated or adjusted, and after achieving a therapeutic INR for three consecutive weeks, cardioversion may be attempted. Following cardioversion, the patient should remain on warfarin with a therapeutic INR for four weeks.

Permanent antitachycardia pacemaker treatment Although rarely used as treatment, in selected patients consideration should be given to implantation of a permanent antitachycardia pacemaker to interrupt recurrent atrial flutter and restore sinus rhythm. While there is only a small published series of patients treated with such devices, it nevertheless has been shown to be safe and effective. Since precipitation of atrial fibrillation is always a potential problem when using any form of pacing to treat atrial flutter, if any pacing induced episodes of atrial fibrillation are clinically unacceptable, placement of a permanent antitachycardia pacemaker to treat atrial flutter should be avoided. To decrease or eliminate an incidence of inadvertent precipitation of atrial fibrillation as well as to decrease the frequency of atrial flutter episodes, chronic use of an antiarrhythmic drug may be desirable.

Surgical treatment

Presently, there is little if any role for surgical ablation of the atrial flutter. Nevertheless, there is a limited experience. Klein, Guiraudon and colleagues have reported on three operated patients in whom cryoablation of the region between the coronary sinus orifice and the tri-cuspid annulus successfully prevented recurrent atrial flutter in two.2122 However, the third patient had subsequent symptomatic atrial fibrillation. Similarities between these surgical data and the catheter ablation data are apparent. Also, Canavan and colleagues reported the successful surgical interruption of the atrial flutter re-entrant circuit after intraoperative mapping in an adolescent who had an atrial septal defect repair as a child.23 The atrial flutter re-entrant circuit was around the atriotomy.

Most atrial flutter is caused by re-entrant excitation in the right atrium. The 12 lead ECG remains the cornerstone for the clinical diagnosis. Acute treatment entails control of the ventricular response rate and restoration of sinus rhythm. Currently, radiofrequency catheter ablation treatment provides the expectation of cure, although atrial fibrillation may subsequently occur. Alternatively, antiarrhythmic drug treatment to suppress recurrent atrial flutter episodes may be useful, recognising that recurrences are common despite therapy. Use of an antitachycardia pacemaker may be helpful in selected patients to terminate atrial flutter, as may His bundle ablation with placement of an appropriate pacemaker system to control the ventricular response rate. Anticoagulation with warfarin in patients with recurrent or chronic atrial flutter is recommended using criteria applied to patients with atrial fibrillation.

Supported in part by grant RO1 HL38408 from the National Institutes of Health, National Heart, Lung, and Blood Institute, Bethesda, Maryland, USA.

1. Waldo AL. Pathogenesis of atrial flutter. J Cardiovasc Electrophysiol 1998;9:518-25.

• Short review of the pathogenesis of atrial flutter.

Demonstration of an area of slow conduction in human atrial flutter. J Am Coll Cardiol 1990;16:1639-48.

• Mapping studies of typical atrial flutter.

3. Cosío FG, Goicolea A, Lopez-Gil M, et al. Atrial endocardial mapping in the rare form of atrial flutter. Am J Cardiol 1990;66:715-20.

• Mapping studies of reverse typical atrial flutter.

4. Olgin JE, Kalman JM, Fitzpatrick AP, et al. Role of right atrial endocardial structures as barriers to conduction during human type I atrial flutter. Activation and entrainment mapping guided by intracardiac echocardiography. Circulation 1995;92:1839-48.

• Studies defining the boundaries of the typical atrial flutter re-entrant circuit.

5. Kalman JM, Olgin JE, Saxon LA, et al. Activation and entrainment mapping defines the tricuspid annulus as the anterior boundary in atrial flutter. Circulation 1996;94:398-406.

• Studies defining the boundaries of the atrial flutter re-entrant circuit.

6. Nakagawa H, Lazzara R, Khastgir T, et al. Role of the tricuspid annulus and the Eustachian valve/ridge on atrial flutter. Relevance to catheter ablation of the septal isthmus and a new technique for rapid identification of ablation success. Circulation 1996;94:407-24.

• Studies defining the boundaries of the atrial flutter re-entrant circuit.

7. Cosio FG, Arribas F, Lopez-Gil M, et al. Atrial flutter mapping and ablation. I. Studying atrial flutter mechanisms by mapping and entrainment. PACE 1996;19:841-53.

• Electrode catheter mapping studies to identify the vulnerable part of the atrial flutter re-entrant circuit.

8. Saoudi N, Cosío F, Chen SA, et al. A new classification of atrial tachycardias based on electrophysiologic mechanisms. Eur J Cardiol In press.

• Explanation and examples of the new classification of atrial flutter.

9. Van Hare GF, Lesh MD, Ross BA, et al. Mapping and radiofrequency ablation of intraatrial reentrant tachycardia after the Senning or Mustard procedure for transposition of the great arteries. Am J Cardiol 1996;77:985-91.

• Studies of patients with chronic atrial flutter caused by incisional re-entry following surgical repair of a congenital heart lesion.

10. Chan DP, Van Hare GF, Mackall JA, et al. Importance of the atrial flutter isthmus in post-operative intra-atrial reentrant tachycardia. Circulation In press.

• Studies of patients with chronic atrial flutter following surgical repair of a congenital heart lesion demonstrating that in 75% of these patients, the atrial flutter re-entrant circuit utilises the atrial flutter isthmus.

Characterization of atrial flutter. Studies in man after open heart surgery using fixed atrial electrodes. Circulation 1979;60:665-73.

• Studies characterising type I and type II atrial flutter in patients.

12. Waldo AL, Cooper TB. Spontaneous onset of type I atrial flutter in patients. JAm Coll Cardiol 1996;28:707-12.

• Studies demonstrating that atrial fibrillation generally precedes the onset of atrial flutter.

13. Matsuo K, Tomita Y, Khrestian CM, et al. A new mechanism of sustained atrial fibrillation: studies in the sterile pericarditis model [abstract]. Circulation 1998;98:I-209.

• Demonstration of the nature of atrial fibrillation generated by a re-entrant circuit of very short cycle length (very rapid rate) which produces fibrillatory conduction.

14. Wood KA, Eisenberg SJ, Kalman JM, et al. Risk of thromboembolism in chronic atrial flutter. Am J Cardiol 1997;79:1043-7.

• Study demonstrating important risk of stroke or systemic embolism in the presence of atrial flutter but in the absence of anticoagulation treatment.

15. Seidl K, Haver B, Schwick NG, et al. Risk of thromboembolic events in patients with atrial flutter. Am J Cardiol 1998;82:580-4.

• Study demonstrating thromboembolic risk associated with atrial flutter.

16. Ellenbogen KA, Clemo HF, Stambler BS, et al.

Efficacy of ibutilide for termination of atrial fibrillation and flutter. Am J Cardiol 1996;78(suppl 8A):42-5.

• Study showing efficacy of ibutilide in conversion of atrial flutter to sinus rhythm.

17. Stambler BS, Wood MA, Ellenbogen KA, et al.

Efficacy and safety of repeated intravenous doses of ibutilide for rapid conversion of atrial flutter or fibrillation. Circulation 1996;94:1613-21.

• Study highlighting risks as well as efficacy of ibutilide therapy of atrial flutter.

18. Suttorp MJ, Kingma JH, Jessuren ER, et al. The value of class IC antiarrhythmic drugs for acute conversion of paroxysmal atrial fibrillation or flutter to sinus rhythm. JAm Coll Cardiol 1990;16:1722-7.

• Study showing efficacy of class IC agents in conversion of atrial flutter to sinus rhythm.

19. Cosío FG, Arribas F, Lopez-Gil M, et al. Atrial flutter mapping and ablation. II. Radiofrequency ablation of atrial flutter circuits. PACE 1996;19:965-75.

• Review of ablation techniques to cure atrial flutter.

20. Podrid PJ. Amiodarone: reevaluation of an old drug. Ann Int Med 1995;122:689-700.

• Good review of use of amiodarone for atrial flutter, including data on adverse effects of this drug.

21. Klein GJ, Guiraudon GM, Sharma AD, et al.

Demonstration of macroreentry and feasibility of operative therapy in the common type of atrial flutter. Am J Cardiol 1986;57:587-91.

22. Guiraudon GM, Klein GJ, Sharma AD, et al. Surgical alternatives for supraventricular tachycardias. Am J Cardiol 1989;64:92J-6J.

23. Canavan TE, Schuessler RB, Cain ME, et al.

Computerized global electrophysiological mapping of the atrium in a patient with multiple supraventricular tachyarrhythmias. Ann Thorac Surg 1988;46:232-5.

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