Secondary Logo

Management of Atrial Fibrillation

Ganz, Leonard I. MD

Critical Pathways in Cardiology: A Journal of Evidence-Based Medicine: March 2002 - Volume 1 - Issue 1 - p 3–11
Articles
Free

From the Department of Cardiac Electrophysiology, University of Pittsburgh Medical Center, and the Department of Medicine, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania.

Address for correspondence: Dr. Leonard I. Ganz, University of Pittsburgh Medical Center, Cardiovascular Institute, PUH B535, 200 Lothrop Street, Pittsburgh, PA 15213-2582. E-mail: ganzl@msx.upmc.edu

Atrial fibrillation (AF) is an extremely common medical problem and the most common arrhythmia encountered in clinical practice. Atrial fibrillation increases in frequency with age and in association with other cardiovascular diseases. Joint practice guidelines from the American College of Cardiology/American Heart Association/European Society of Cardiology were recently published but reflect uncertainty regarding the optimal approach to many aspects of AF care.1,2 Ongoing clinical trials will help shape recommendations. This article outlines strategies for evaluation and management of AF patients; this is the approach of a single electrophysiologist, rather than an accepted clinical pathway.

Back to Top | Article Outline

Diagnosis

The electrocardiographic signature of AF is fibrillatory atrial activity rather than discrete P waves. The ventricular rate is generally irregularly irregular. Multifocal atrial tachycardia is also associated with an irregularly irregular ventricular rate; multifocal atrial tachycardia, however, inscribes discrete P waves of various morphologies, with variable PR intervals.

Atrial fibrillation may have a paroxysmal, persistent, or permanent pattern.3 Patients presenting with paroxysmal palpitations may be evaluated with ambulatory monitoring to correlate a dysrhythmia with symptoms.4 When symptoms are infrequent, event monitoring offers a higher yield than continuous Holter monitoring. Once the arrhythmia is documented electrocardiographically, the proper diagnosis can usually be assigned.

Back to Top | Article Outline

Diagnostic Evaluation

Many cardiovascular and systemic conditions occur in association with AF (Table 1) Often, some other cardiovascular disease process (e.g., hypertension, coronary artery disease, valvular heart disease, and cardiomyopathy) will already be present in patients presenting with AF. Less frequently, AF is the initial manifestation of cardiomyopathy or valvular heart disease. Atrial fibrillation occurring in the absence of structural heart disease or other associated conditions in patients less than 65 years of age is called “lone” or idiopathic AF.5

Table 1

Table 1

Several diagnostic tests are recommended in all patients who present with AF (Table 2 Thyroid testing is reasonable, although rarely is AF the only manifestation of hyperthyroidism, which may trigger AF. An echocardiogram defines left ventricular function, atrial size, and valvular function; the nature and severity of structural heart disease, if present, will determine the therapeutic options for managing AF. Whereas acute pulmonary embolus and acute myocardial infarction may be accompanied by AF, it is extremely unusual for AF to be the only presenting sign or symptom of these diseases. Thus, routine assessment for acute pulmonary embolus and/or myocardial infarction is not recommended in all patients newly diagnosed with AF; evaluation for acute myocardial infarction or pulmonary embolus is only indicated in patients presenting with other suggestive signs or symptoms (e.g., chest pain, dyspnea, hemoptysis).

Table 2

Table 2

Back to Top | Article Outline

Management Strategies

Three treatment objectives should be considered in all AF patients: anticoagulation, ventricular rate control, and rhythm control. Anticoagulation reduces the risk of stroke and other thromboembolic complications in patients with AF, while rate control and rhythm control aim to improve symptoms. Table 3 lists the advantages and disadvantages of the rate and rhythm control strategies.

Table 3

Table 3

Back to Top | Article Outline

Anticoagulation

It is well established that many AF patients are at risk for thromboembolic complications, most importantly stroke (cerebrovascular accident) and transient ischemic attack. Multiple randomized, controlled clinical trials have documented that in most types of patients, anticoagulation with warfarin (target international normalized ratio, 2.5; range, 2.0-3.0) markedly reduces the risk of stroke and other thromboembolic complications. Guidelines for anticoagulation in patients with AF are presented in Table 4.6 In general, anticoagulation recommendations are the same for paroxysmal and persistent AF. Aspirin is recommended to patients less than 65 years of age, without risk factors for thromboembolism; these patients with “lone” AF have a low stroke risk.7 For patients more than 65 years of age or with risk factors for thromboembolism, warfarin is generally recommended. Anticoagulation is not without risk, particularly in elderly patients. Thus, it is important to consider the potential risks of anticoagulation in each patient with AF. In patients for whom warfarin poses a high risk of bleeding, treatment with aspirin confers some protection against thromboembolic complications.

Table 4

Table 4

Few data exist regarding the use of anticoagulants and antithrombotics other than warfarin and aspirin in patients with AF. Intravenous unfractionated heparin, dosed to an activated partial thromboplastin time about two times control, is frequently used as a bridge until a therapeutic international normalized ratio is achieved with warfarin. Enoxaparin, a low molecular weight heparin, is being compared with standard unfractionated intravenous heparin as a bridge to warfarin after transesophageal echocardiogram-expedited cardioversion in the ACUTE 2 trial.

There are specific recommendations for anticoagulation related to cardioversion, whether electrical or pharmacologic (Table 5). In patients with AF known to be of 24 to 36 hours duration or less, cardioversion can generally be performed without anticoagulation. If AF is of longer or unknown duration, even in lone AF patients in whom chronic anticoagulation is not generally required, one of two anticoagulation strategies should be undertaken. The traditional approach requires therapeutic anticoagulation for at least 3 weeks before, and for at least 4 weeks after, cardioversion. Alternatively, the expedited approach calls for initiation of therapeutic anticoagulation with warfarin or heparin, and then performance of a transesophageal echocardiogram. If there is no evidence of atrial thrombus on transesophageal echocardiogram, cardioversion is then performed. When the international normalized ratio is therapeutic, heparin is discontinued; anticoagulation with warfarin is continued for at least 4 weeks after restoration of sinus rhythm. In the ACUTE trial the incidence of cerebrovascular accident and transient ischemic attack did not differ significantly in patients randomized to the two strategies. Overall, the risk of cerebrovascular thromboembolism was 0.6% among the 1222 patients in the study.8

Table 5

Table 5

Anticoagulation is recommended for at least 4 weeks after cardioversion, presuming sinus rhythm is maintained. Because of the high risk of recurrent AF, warfarin is frequently continued for longer periods, or even indefinitely, in patients with AF. Even when antiarrhythmic drug therapy appears effective in suppressing AF recurrences, many electrophysiologists favor indefinite anticoagulation.

Back to Top | Article Outline

Ventricular Rate Control

Pharmacologic atrioventricular (AV) nodal blocking therapy to slow the ventricular rate is generally prescribed to improve symptoms and hemodynamic parameters in AF patients.9 Even in patients who are asymptomatic, persistently elevated ventricular rates can lead to a tachycardia-induced cardiomyopathy. Table 6 summarizes AV nodal blocking agents and dosing information, for both acute therapy and chronic administration.

Table 6

Table 6

The efficacy of rate control is frequently overestimated. The ventricular rate should be assessed both at rest and during daily activities and exertion, with a formal exercise test, Holter recording, or informal exercise in the physician's office. Digoxin is rarely effective when given as monotherapy in young or active patients. Beta-blockers or nonhydropyridine cal-cium-channel blockers (e.g., verapamil, diltiazem) are generally more effective; frequently, combination AV nodal blocking therapy is necessary.10 Radiofrequency catheter ablation of the A-V junction with implantation of a permanent pacemaker, a nonpharmacologic method of achieving rate control, is discussed below.

Back to Top | Article Outline

Rhythm Control (Restoration and Maintenance of Sinus Rhythm)

Sinus rhythm may be restored spontaneously, pharmacologically, or with direct current cardioversion (DCCV). The majority of AF episodes of short duration will convert spontaneously to sinus rhythm.11 In patients who are not chronically anticoagulated, cardioversion should be considered if AF persists for 12 to 24 hours, so that the need for anticoagulation before and after cardioversion can be obviated.

Historically, DCCV has been effective in restoring sinus rhythm in approximately 80% of patients. Just as biphasic waveforms improve the efficacy of implantable cardioverter defibrillators, recently available biphasic external defibrillators markedly increase the success rate of DCCV.12 Pretreatment with ibutilide has also been shown to increase the efficacy of DCCV,13 although this is rarely necessary in the presence of a biphasic defibrillator. Predictors of failure of external cardioversion include chronicity of AF, marked left atrial enlargement, and body habitus (morbid obesity, barrel chest, etc.). Internal cardioversion can also be undertaken in refractory patients. Now that biphasic defibrillators and internal cardioversion permit restoration of sinus rhythm in a higher percentage of patients, immediate or early recurrence of AF is noted more commonly.

Historically, intravenous procainamide has been used to restore sinus rhythm, although data supporting this practice are few. Newer, more effective dosing regimens for effecting pharmacologic conversion of AF to sinus rhythm are summarized in Table 6. Loading oral doses of the class IC agents flecainide and propafenone are frequently effective. Pretreatment with a beta-blocker or calcium-channel blocker reduces the proarrhythmic risk of atrial flutter with 1:1 A-V conduction. The IC agents are contraindicated in coronary artery disease patients. Ibutilide, a class III agent available intravenously for acute conversion to sinus rhythm, is more effective in terminating atrial flutter than AF. Like other class III agents, ibutilide carries with it a risk of inducing torsade de pointes ventricular tachycardia.14 Risk factors for torsade with ibutilide include bradycardia, low ejection fraction, female gender, and history of congestive heart failure. After ibutilide infusion, patients should be monitored for at least 4 hours, or until the QT interval returns to baseline.

Because antiarrhythmic drugs pose a risk of potentially life-threatening proarrhythmia, the role of chronic antiarrhythmic therapy in patients with AF remains uncertain. The ongoing AFFIRM trial compares the rate control and rhythm control strategies in AF patients.15 In patients with symptoms related to AF despite adequate ventricular rate control, treatment with an antiarrhythmic drug in an effort to maintain sinus rhythm is certainly reasonable.16 Dosing information for the various antiarrhythmic drugs used for AF are summarized in Table 6. On average, the likelihood of maintaining sinus rhythm is similar among the different agents, except perhaps for amiodarone, which appears to be the most effective agent. A careful evaluation of the patient's cardiac substrate and potential proarrhythmic risk will lead to the best antiarrhythmic choice. Table 7 summarizes reasonable initial choices for antiarrhythmic drug therapy for various patient groups. Complete suppression of AF is rarely achieved; rather, a significant reduction in the frequency and duration of AF episodes should be considered successful therapy.

Table 7

Table 7

Most patients should be admitted for continuous cardiac monitoring during initiation or dose titration of antiarrhythmic drugs.17 Patients started on QT prolonging drugs, such as quinidine, procainamide, disopyramide, sotalol, and dofetilide, should be admitted for drug initiation. Patients with structurally normal hearts can frequently be initiated on propafenone or flecainide as outpatients. These agents should always be used in conjunction with AV nodal blocking agents. Event monitoring to detect proarrhythmia may facilitate outpatient initiation of these drugs in appropriate patients. Exercise testing to exclude exercise-induced proarrhythmia is reasonable once a steady state dose has been achieved. With amiodarone, ventricular proarrhythmia is rare. Thus, amiodarone can frequently be initiated in outpatients if the risk of significant bradycardia is not thought to be excessive. Baseline pulmonary, liver, and thyroid function should be assessed before initiating amiodarone therapy; a screening ophthalmologic examination is also reasonable.

Patients treated chronically with antiarrhythmic drugs should be monitored extremely carefully to reduce the risk of proarrhythmia and other potential complications. With amiodarone the risk of extracardiac toxicity appears to be related to the cumulative dose. Potential adverse effects of antiarrhythmic drugs and recommendations for follow-up testing are listed in Table 8.

Table 8

Table 8

Back to Top | Article Outline

Approach to the Patient With a First Episode of Atrial Fibrillation

Many physicians think that at least one attempt at restoring sinus rhythm is reasonable in most patients. Hence, if a first AF episode does not revert spontaneously to sinus rhythm, pharmacologic or DCCV should generally be performed after appropriate anticoagulation, if necessary (Figure 1). Beta-blockers may facilitate conversion by attenuating sympathetic tone, which is frequently elevated at the onset of an AF episode. After cardioversion it is reasonable to follow the patient without longitudinal antiarrhythmic drug therapy, while monitoring to see if AF recurs. Treatment with a beta-blocker, verapamil, or diltiazem after cardioversion may provide two benefits. First, these AV nodal blockers may attenuate the ventricular rate should AF recur. Furthermore, intriguing experimental data suggest that these agents may reduce the frequency of AF recurrences by reversing atrial electrophysiologic remodeling that accompanies and promotes recurrent AF.18 If anticoagulation is necessary pericardioversion, continuing warfarin for 1 month or more is reasonable, with discontinuation of warfarin if sinus rhythm persists.

Figure 1

Figure 1

Back to Top | Article Outline

Approach to the Patient With Recurrent Atrial Fibrillation

Unfortunately, AF is frequently a recurrent rather than an isolated problem. The treatment strategy used will depend on the patient's underlying structural heart disease and associated conditions and AF pattern (e.g., the frequency and duration of AF recurrences, severity of symptoms). A general treatment algorithm is presented in Figure 1.

Patients with infrequent, spontaneously reverting, mildly symptomatic AF recurrences may be well served with no long-term therapy other than anticoagulation, if indicated. If recurrences cause significant symptoms or are frequent or of long duration, initial chronic treatment with a rate control agent (beta-blocker or calcium-channel blocker) is reasonable. As described above, these agents may attenuate the symptoms of recurrent episodes by reducing the ventricular rate and may even reduce the frequency of recurrent episodes as well. Appropriate anticoagulation therapy should be initiated in these patients, as well. For patients with symptomatic AF refractory to rate control agents, antiarrhythmic therapy should be considered.

If the primary rhythm disturbance is atrial flutter or some other organized supraventricular tachyarrhythmia, curative radiofrequency catheter ablation should be considered early, given the efficacy of this procedure.19 The macroreentrant right atrial circuit in typical (counterclockwise) atrial flutter includes the tricuspid annulus-inferior vena cava isthmus; radiofrequency ablation results causes of bidirectional block in this isthmus prevents recurrent typical atrial flutter. The acute success rate for this procedure is about 90%; during follow-up, the recurrence rate of artial flutter is approximately 10%. Patients who have both AF and atrial flutter before isthmus ablation may or may not have AF postablation or may respond better to antiarrhythmic drug therapy.20

Back to Top | Article Outline

Indications for Hospital Admission

Potential indications for hospital admission in patients with AF are outlined in Table 9. Patients with significant symptoms and/or signs related to rapid rates should be admitted and treated initially with intravenous rate control agents. All patients with minimally symptomatic AF of uncertain duration do not require admission for initiation of anticoagulation; patients at high risk for thromboembolic complications should certainly be considered for admission, however, for establishment of anticoagulation. Admission is also reasonable for patients with AF of less than 24 hours to facilitate cardioversion without the need for anticoagulation. As described above, most patients should be admitted for continuous cardiac telemetry when antiarrhythmic drug therapy is initiated. Certainly, if AF is secondary to acute process (e.g., acute pulmonary embolus, acute myocardial infarction, cardiac tamponade), admission is warranted for management of the primary problem.

Table 9

Table 9

Back to Top | Article Outline

Indications for Nonpharmacologic Therapy

Nonpharmacologic therapies are being used with increasing frequency in patients with AF. Catheter ablation of the A-V junction with permanent pacemaker implantation (i.e., “ablate and pace”) should be considered in patients who are refractory to aggressive attempts at medical therapy or who develop adverse effects from pharmacologic agents.21 Appropriately selected patients generally feel much better after the procedure. Because most patients are pacemaker dependent after A-V junction ablation, caution should be exercised in recommending this procedure to relatively young patients. It is important to remember that this procedure is palliative, not curative. Atrial fibrillation persists; life-long anticoagulation therefore remains necessary. If AF is chronic, a VVIR pacemaker is implanted, whereas a dual-chamber pacemaker with automatic mode switching is appropriate in paroxysmal AF.

The Maze procedure, developed by James Cox, MD, is extremely effective in preventing recurrent AF.22 At present, this surgery requires a median sternotomy; efforts to develop a less invasive procedure through a limited thoracotomy are underway. At present, because of the attendant surgical mortality and morbidity and newer, catheter-based options, this procedure is best applied to patients who require other cardiac surgical procedures. Less elaborate “Mini-Maze” procedures are performed with increasing frequency in patients undergoing mitral valve and other cardiac surgical procedures.23

Intense efforts have led to the development of increasing successful curative catheter ablative approaches to AF.24–26 Current efforts focus on ablation of focal triggers of AF, which arise primarily from the pulmonary venous ostia or from within the pulmonary veins themselves. This technology is in evolution; important questions involve selection of patients most appropriate for this approach, long-term success rates, and complication rates, including thromboembolism and pulmonary vein stenosis.

Implantable device therapy for AF is also evolving.27 At present, dual-chamber pacemakers are frequently implanted in patients with tachycardia-bradycardia syndrome to facilitate pharmacologic therapy of the AF. Atrial-based pacing results in less AF during follow-up compared with ventricular pacing. Preliminary data suggest that more sophisticated pacing algorithms may prevent AF recurrences; alternate pacing sites (e.g., atrial septal pacing, multisite atrial pacing) are also the focus of clinical investigation. In addition, therapies for AF and other atrial tachyarrhythmias have been incorporated into some implantable cardioverter defibrillators. In clinical trials a surprising number of AF episodes have been terminated with high-frequency burst pacing. High voltage (i.e., “shock”) therapy is also available. It remains unclear what fraction of the AF population will find uncomfortable internal shocks an acceptable therapy for AF.

Back to Top | Article Outline

Atrial Fibrillation After Cardiac Surgery

Atrial fibrillation remains an extremely common complication after cardiac surgery. The optimal management strategy remains uncertain. Minimally invasive surgical approaches seem to result in less postoperative AF than standard surgical procedures.28 Beta-blockers reduce the incidence of AF after cardiac surgery.29 Amiodarone, either administered orally for a week before surgery30 or intravenously immediately after surgery,31 also reduces the prevalence of postoperative AF but has been compared only with placebo and not with beta-blockers.

Our usual practice is to initiate beta-blocker therapy postoperatively as soon as possible and titrate the dose up as tolerated. If AF develops and persists for more than 24 hours, anticoagulation with heparin and warfarin is initiated. If AF persists, DCCV is usually performed after 36 to 48 hours. If the AF pattern is paroxysmal, we typically do not cardiovert. The dose of beta-blockers (or calcium blockers) is increased to control the ventricular rate. We tend not to use antiarrhythmic drug therapy unless symptoms persist despite rate control. If antiarrhythmic therapy is necessary, we prefer amiodarone or sotalol. In most patients the ventricular rate is aggressively controlled, and patients are discharged when the international normalized ratio approaches the therapeutic range.

Postoperative patients treated with warfarin must be followed extremely carefully, as they are prone to bleeding complications and overanticoagulation. Patients without a history of AF before cardiac surgery will frequently convert spontaneously to sinus rhythm as they recover from surgery. If sinus rhythm is present at the 6-week follow-up visit and there are no symptoms to suggest recurrent AF, antiarrhythmic therapy, if present, may be discontinued. If the patient has not been treated with antiarrhythmic drug therapy, warfarin may be discontinued at this time. If the patient has been on an antiarrhythmic agent postoperatively, which is discontinued at the 6-week visit, warfarin may be continued for another 4 to 6 weeks, while patients are monitored for recurrent AF. If AF persists to the 6-week follow-up visit, DCCV is scheduled after verification of adequate anticoagulation.

Back to Top | Article Outline

References

1. Fuster V, Ryden LE, Asinger RW, et al. ACC/AHA/ESC guidelines for the management of patients with atrial fibrillation: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines and the European Society of Cardiology Committee for Practice Guidelines and Policy Conferences (Committee to Develop Guidelines for the Management of Patients with Atrial Fibrillation). J Am Coll Cardiol 2001; 38: 1231-65.
2. Falk RH. Atrial fibrillation. N Engl J Med 2001; 344: 1067-78.
3. Gallagher MM, Camm AJ. Classification of atrial fibrillation. Pacing Clin Electrophysiol 1997; 20: 1603-4.
4. Richardson AW, Zimetbaum PJ. The diagnosis of cardiac arrhythmias. In: Ganz LI, ed. Management of Cardiac Arrhythmias. Totowa, NJ: Humana Press, 2002: 9-28.
5. Ganz LI. Idiopathic atrial fibrillation: therapeutic strategies. Arrhythmia Clin 2000: 1-12.
6. Albers G, Dalen J, Laupacis A, et al. Antithrombotic therapy in atrial fibrillation. Chest 1998; 114: 587S.
7. Investigators of five studies. Risk factors for stroke and efficacy of antithrombotic therapy in atrial fibrillation. Arch Intern Med 1994; 154: 1449-57.
8. Klein AL, Grimm RA, Murray RD, et al. Use of transesophageal echocardiography to guide cardioversion in patients with atrial fibrillation. N Engl J Med 2001; 344: 1411-20.
9. Blitzer M, Costeas C, Kassotis J, et al. Rhythm management in atrial fibrillation: with a primary emphasis on pharmacologic therapy: Part 1. Pacing Clin Electrophysiol 1998; 21: 590-602.
10. Farshi R, Kistner D, Sarma JS, et al. Ventricular rate control in chronic atrial fibrillation during daily activity and programmed exercise: a crossover open-label study of five drug regimens. J Am Coll Cardiol 1999; 33: 304-10.
11. Danias PG, Caulfield TA, Weigner MJ, et al. Likelihood of spontaneous conversion of atrial fibrillation to sinus rhythm. J Am Coll Cardiol 1998; 31: 588-92.
12. Mittal S, Ayati S, Stein KM, et al. Transthoracic cardioversion of atrial fibrillation: comparison of rectilinear biphasic versus damped sine wave monophasic shocks. Circulation 2000; 101: 1282-7.
13. Oral H, Souza JJ, Michaud GF, et al. Facilitating transthoracic cardioversion of atrial fibrillation with ibutilide pretreatment. N Engl J Med 1999; 340: 1849-54.
14. 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: Ibutilide Repeat Dose Study Investigators. Circulation 1996; 94: 1613-21.
15. Planning and Steering Committees of the AFFIRM Study for the NHLBI AFFIRM Investigators. Atrial fibrillation follow-up investigation of rhythm management: the AFFIRM study design. Am J Cardiol 1997; 79: 1198-202.
16. Ganz LI, Antman EM. Antiarrhythmic drug therapy in the management of atrial fibrillation. J Cardiovasc Electrophysiol 1997; 8: 1175-89.
17. Maisel WH, Kuntz KM, Reimold SC, et al. Risk of initiating antiarrhythmic drug therapy for atrial fibrillation in patients admitted to a university hospital. Ann Intern Med 1997; 127: 281-4.
18. Tieleman RG, De Langen C, van Gelder IC, et al. Verapamil reduces tachycardia-induced electrical remodeling of the atria. Circulation 1997; 95: 1945-53.
19. Cosio FG, Arribas F, Lopez-Gil M, et al. Radiofrequency ablation of atrial flutter. J Cardiovasc Electrophysiol 1996; 7: 60-70.
20. Anselme F, Saoudi N, Poty H, et al. Radiofrequency catheter ablation of common atrial flutter: significance of palpitations and quality-of-life evaluation in patients with proven isthmus block. Circulation 1999; 99: 534-40.
21. Brignole M, Menozzi C, Gianfranchi L, et al. Assessment of atrioventricular junction ablation and VVIR pacemaker versus pharmacological treatment in patients with heart failure and chronic atrial fibrillation: a randomized, controlled study. Circulation 1998; 98: 953-60.
22. Sundt TMIII, Camillo CJ, Cox JL. The maze procedure for cure of atrial fibrillation. Cardiol Clin 1997; 15: 739-48.
23. Tuinenburg AE, van Gelder IC, Tieleman RG, et al. Mini-maze suffices as adjunct to mitral valve surgery in patients with preoperative atrial fibrillation. J Cardiovasc Electrophysiol 2000; 11: 960-7.
24. Chen S-A, Tai C-T, Tsai C-F, et al. Radiofrequency catheter ablation of atrial fibrillation initiated by pulmonary vein ectopic beats. J Cardiovasc Electrophysiol 2000; 11: 218-27.
25. Pappone C, Oreto G, Rosanio S, et al. Atrial electroanatomic remodeling after circumferential radiofrequency pulmonary vein ablation. Circulation 2001; 104: 2539-44.
26. Shah DC, Haissaguerre M, Jais P. Curative catheter ablation of paroxysmal atrial fibrillation in 200 patients: strategy for presentations ranging from sustained atrial fibrillation to no arrhythmias. Pacing Clin Electrophysiol 2001; 24: 1541-8.
27. Wellens HJ, Lau CP, Luderitz B, et al. Atrioverter: an implantable device for the treatment of atrial fibrillation. Circulation 1998; 98: 1651-6.
28. Ascione R, Caputo M, Calori G, et al. Predictors of atrial fibrillation after conventional and beating heart coronary surgery: a prospective, randomized study. Circulation 2000; 102: 1530-5.
29. Andrews TC, Reimold SC, Berlin JA, et al. Prevention of supraventricular arrhythmias after coronary artery bypass surgery: a meta-analysis of randomized control trials. Circulation 1991; 84(suppl): 236-44.
30. Daoud EG, Strickberger SA, Man KC, et al. Preoperative amiodarone as prophylaxis against atrial fibrillation after heart surgery. N Engl J Med 1997; 337: 1785-91.
31. Guarnieri T, Nolan S, Gottlieb SO, et al. Intravenous amiodarone for the prevention of atrial fibrillation after open heart surgery: the Amiodarone Reduction in Coronary Heart (ARCH) trial. J Am Coll Cardiol 1999; 34: 343-7.
© 2002 Lippincott Williams & Wilkins, Inc.