Direct current cardioversion is one of the most effective means of converting atrial fibrillation into sinus rhythm. Medical cardioversion is one alternative. However, direct current cardioversion has the highest overall success rate. (1,2) In all, patients who require cardioversion will often undergo direct current cardioversion rather than pharmacologic conversion because of its:
- Shorter overall procedure duration
- Higher success rate
- Lower risk of proarrhythmia
Direct current cardioversion is indicated in patients who are:
- Hemodynamically unstable
- Stable, but in whom spontaneous reversion that would follow correction of an underlying disease is not likely
Direct current cardioversion success rates vary from 75% to 93%. They are inversely related to the atrial fibrillation duration, chest wall impedance, and left atrial size. (3-7) Indeed, success rates vary according to the point in time that success is defined. In one series of 1,838 direct current cardioversions, success rates were 84%, 78%, 77%, and 66%, respectively, (8) when the duration of AF was <30, 30 to 90, 90 to 180, and >180 days. When atrial fibrillation has been present for more than five years, success rates are only approximately 50%. (9)
I - External cardioversion
Cardioversion should be performed with the patient in a fasting state under adequate general anaesthesia. The anaesthetic agent must 1) provide analgesia and sedation, and 2) cause the least cardiovascular compromise while allowing for rapid recovery. (10-12) Oxygen saturation and electrolytes should be normal and anticoagulation status monitored. Drug levels, such as digoxin and antiarrhythmic agents, should be within the therapeutic range. Digoxin shouldn't be withheld unless there is a suggestion of digitalis excess or toxicity. (11) A baseline 12-lead electrocardiogram should be recorded and venous cannulation should be secured. A pacing catheter may be placed prophylactically in the right ventricle if sick sinus syndrome is suspected. For backup, external pacing pads may be used for both cardioversion and for prophylaxis should asystole or bradycardia ensue. Overnight hospitalisation is seldom required. (10)
Biphasic waveforms superior to monophasic waveforms
Whether cardioversion will succeed depends on whether delivery of current flow through the heart is adequate or not. (13) The major determinants of current delivery are: 1) the nature of the shock waveform (mono or biphasic) 2) level of delivered energy. In terms of shock waveform, both monophasic and biphasic waveforms are used. Currently, most evidence favors the use of biphasic, external defibrillators due to their categorically lower energy requirements and greater efficacy. (14,15) Indeed, in a study of 912 patients with AF and atrial flutter, restoration of sinus rhythm was higher in patients who had received biphasic waveforms (94% versus 84% for monophasic waveforms) and with lower cumulative energy (199 J versus 554 J). (16) Biphasic waveforms may be of special interest in patients who have failed to revert with the use of monophasic waveforms. (17) Furthermore, fewer shocks are required, thereby potentially reducing procedure times and, thus, requirements for intravenous sedation. A lower incidence of skin burns (18) and less skeletal muscle damage (19) have also been reported. Additionally, biphasic waveforms result in fewer postshock arrhythmias, and a shorter period of myocardial stunning. (20)
The amount of energy needed for initial attempts of DCC has been controversial. Once satisfactory synchronisation is obtained, sedation or anaesthesia is initiated, and a shock is delivered. After shock delivery, if conversion is unsuccessful, higher energy, repeat, direct current cardioversion is attempted. This can be repeated until the arrhythmia terminates or the decision is made to abandon direct current cardioversion. Using a monophasic waveform, the energy required will often be >200 joules, (21) with possibly more being required in obese patients and long-standing atrial fibrillation. (22,23) However, biphasic devices have been shown to be more effective in two randomised clinical trials and to require less energy delivery than monophasic devices. (19,24) Higher biphasic energies might be recommended as a first direct cardioversion shock for patients who are overweight or have a higher transthoracic impedance. The Best-AF Trial demonstrated that when biphasic waveforms were used there was a significant increase in the first-shock success for direct current cardioversion if the initial energy selected was 200 J rather than 100 J. (25) In patients who were overweight or obese, first-shock success was significantly greater if a higher-energy shock was selected. However, in patients with a normal or low body mass index, there was no difference in the first-shock success regardless of whether 100 J or 200 J was used. The initial energy may be lower for cardioversion of atrial flutter. (25) In a review including 985 cardioversions in 840 patients with atrial flutter, the median energy level for successful cardioversion was 50 joules with a biphasic defibrillator and 200 joules with a monophasic defibrillator. (26)
Lown et al. recommended an anteroposterior electrode configuration over anteroanterior positioning. (27,28) However, the two current conventional orientations that are commonly used for electrode placement are anteroposterior and anterolateral. A number of studies have examined the effect of one over the other and showed that less energy is required and higher success rates are achieved when using the anteroposterior position. (20-32) Some reports, nevertheless, have failed to confirm these findings. (33,34) In some patients, one position and not the other may be effective. Thus, it has been suggested that if initial shocks are unsuccessful in terminating the arrhythmia, the electrodes should be relocated and cardioversion repeated. (31) Thus, when cardioversion fails, shocks can be repeated at highest energy until the arrhythmia terminates or a decision is made to abandon direct current cardioversion. Repositioning the paddles should also be done in case of failure. Furthermore, the double-paddle technique is another alternative as well as pharmacologic facilitation of cardioversion. In one study, patients who had AF and had failed 360-J monophasic cardioversion were loaded orally with amiodarone. If repeat 360-J monophasic cardioversion persisted in failing, the patients underwent the double-paddle technique: two monophasic defibrillators were used with two sets of paddles for each patient. Each defibrillator was set for a synchronous shock at the maximum output of 360 J; they then were discharged simultaneously, resulting in successful conversion of 13 out of 15 patients. (35)
II - Internal cardioversion
Internal cardioversion is performed with the patient under conscious sedation or general anaesthesia. Due to the potential risk of bleeding, warfarin therapy is usually withheld in view of the procedure and resumed afterward. Temporary anticoagulation before and after the procedure can be accomplished with heparin. Internal cardioversion is indicated:
- After failure of conventional external cardioversion
- In patients with a high transthoracic impedance and/or contraindications to general anaesthesia, (40) due to the procedure being more effective, yet as safe as external cardioversion (36-40)
Despite such significant advantages, the spread of this new methodology in clinical practice has been limited by the need of a laboratory of electrophysiology with fluoroscopy and of specific technical competence for lead positioning, either in the coronary sinus or in the left pulmonary artery. Simplification of the procedure is obviously very important for the future of internal cardioversion, particularly because of the recent improvement in success rates of external cardioversion using biphasic shocks, higher energy shocks or pretreatment with drugs before cardioversion. (24,42,43)
The 2010 ESC guidelines state that internal cardioversion may be helpful in specific situations where a patient will undergo an invasive procedure and cardioversion catheters can be positioned without adding vascular access. However, the guidelines go on to state that this procedure has been largely abandoned as a means for cardioversion, except where implanted defibrillation devices are present. (2)
III - Other considerations
Despite its widespread clinical use, controversy surrounds the electrophysiologic mechanisms by which direct current cardioversion terminates atrial fibrillation involving multiple microreentrant circuits. Most investigators agree that defibrillation occurs when a certain amount of current density reaches the myocardium. However, it is unclear what amount of current density is needed and what energy setting is necessary to achieve homogeneous current density. Complications associated with direct current cardioversion are mainly risks related to general anaesthesia, thromboembolic events and postcardioversion arrhythmias. Overall however, risk is low in patients who are selected adequately (44) - only a 1–2% risk of thromboembolic events. (45-47) Thromboembolic events, nevertheless, are more likely to occur in patients with atrial fibrillation who have not been anticoagulated prior to cardioversion. Patients with a previous embolism do not have an increased risk of embolisation if anticoagulation is adequate. (48) The estimated incidence of thromboembolism varies, but in a large nonrandomised series that included 437 patients, embolism occurred in 5.3 % of nonanticoagulated patients, compared with 0.8% of those receiving anticoagulation. (49) Many kinds of arrhythmias, especially ventricular and supraventricular premature beats, bradycardia, and sinus arrest, may arise following cardioversion and commonly subside spontaneously. (50) More dangerous arrhythmias, such as ventricular tachycardia and fibrillation, may arise in the face of hypokalemia, digitalis intoxication, or inadequate synchronisation. (51,52)
Patients with implantable devices
Patients who have implanted permanent pacemakers or cardioverter-defibrillators can undergo external cardioversion with minimal risk to their devices and themselves, provided appropriate precautions are taken. Devices are typically implanted anteriorly, so the electrode paddle should be at least 8 cm from the pacemaker battery; an anteroposterior paddle position is recommended. (2,53,54) Elective cardioversion should be begun with low energies in order to avoid damage to the pacemaker circuitry and the electrode-myocardial interface. After cardioversion, the pacemaker should be interrogated and evaluated to ensure normal pacemaker function. (2)
Pretreatment with antiarrhythmic drugs
Pretreatment or repeat treatment with antiarrhythmic drugs such as ibutilide, amiodarone, sotalol, propafenone or flecainide increases the likelihood of restoration of sinus rhythm and helps prevent recurrent atrial fibrillation. (2)
Enhanced efficacy may involve decreasing the energy required to achieve cardioversion, prolonging atrial refractory periods, and suppressing atrial ectopy that may cause early recurrence of atrial fibrillation. (55-55) Antiarrhythmic medications may be initiated out of hospital or in hospital immediately prior to direct-current cardioversion.
- Amiodarone: A study of 92 patients found that pretreatment with oral amiodarone for one month before cardioversion improved the reversion rate: 88% versus 56-65 % without pretreatment. (58) In another study, in-hospital treatment with oral propafenone started two days before direct current decreased early recurrence of atrial fibrillation after shock.
- Propafenone: Compared with placebo, propafenone did not influence either the mean defibrillation threshold or the rate of conversion (shock efficacy 84% vs. 82%, respectively) but suppressed immediate recurrences (within 10 minutes), and 74% versus 53% of patients were in sinus rhythm after two days. (59) In-hospital treatment with oral propafenone started two days before direct current cardioversion decreased early recurrence of AF aftershock, thus allowing more patients to be discharged from the hospital with a sinus rhythm. Compared to placebo, propafenone did not influence either the mean defibrillation threshold or the success rate. However, it suppressed immediate recurrences, and 74% versus 53% of patients were in sinus rhythm after two days. (59)
- Sotalol: Pretreatment with antiarrhythmic drugs may also reduce the energy requirement for cardioversion. Consistent with this hypothesis is the observation in a report of 18 patients with atrial fibrillation of more than three months duration in which intravenous sotalol (1.5 mg/kg) reduced the energy requirements in 10 patients from 263 to 163 joules. (60) Intermittent verapamil, when given in combination with continuous propafenone for three days before and three months after cardioversion, reduced the incidence of recurrence to 6%, compared with 10% if given for three days prior and three days after, or 30% if propafenone was given alone. (61)
- Verapamil: given around the time of electrical cardioversion, verapamil also works with other antiarrhythmic drugs. Use of an angiotensin receptor blocker with amiodarone also has been reported to lessen the likelihood of early recurrence, compared with amiodarone alone. (62)
Direct current cardioversion is an effective means of restoring sinus rhythm in patients with atrial fibrillation - improving patient outcomes is, thus, usually in our hands. Attention to proper technique for direct current cardioversion has the power to optimise efficacy.
- Success rates are higher with the use of biphasic waveforms.
- Internal cardioversion may be helpful in special situations.
- Pretreatment with antiarrhythythmic drugs increases the likelihood of restoration of sinus rhythm.
- Complications are usually self-limiting or relatively benign.
However after cardioversion, potential life-threatening complications, such as arrhythmias and thromboembolism, remain a possibility.
1. Electrical conversion of atrial fibrillation: immediate and long-term results and selection of patients.
Morris J. J. Jr., Peter R. H., & McIntosh H. D. Ann Intern Med., 1966. 65: 216–231.
2. Guidelines for the management of atrial fibrillation: the Task Force for the Management of Atrial Fibrillation of the European Society of Cardiology. Camm A. J., Kirchhof P., Lip G. Y., Schotten U., Savelieva I., Ernst S,. Van Gelder I. C., Al-Attar N., Hindricks G., Prendergast B., Heidbuchel H., Alfieri O., Angelini A., Atar D., Colonna P., De Caterina R., De Sutter J., Goette A., Gorenek B., Heldal M., Hohloser S. H., Kolh P., Le Heuzey J. Y., Ponikowski P., & Rutten F. H. Eur Heart J., 2010. 31: 2369-429.
3. Initial energy sitting, outcome and efficiency in direct current cardioversion of atrial fibrillation.
Gallagher M. M., Guo X. H., Poloniecki J. D., Guan Yap Y., Ward D., & Camm A. J. J Am Coll Cardiol, 2001. 38: 1498-504.
4. Chronic atrial fibrillation: long term results of direct current cardioversion. Lundstrom T., & Ryden L. Acta Med Scand, 1988. 223: 53-9.
5. Electrical reversion of cardiac arrhythmias. Lown B. Br Heart J, 1967. 29: 469-89.
6. Factors determining success and energy requirement for cardioversion of atrial fibrillation.
Dalzell G. W., Anderson J., & Adgey A. A. Q J Med, 1990. 76: 903-13.
7. Echocardiographic and clinical predictors for outcome of elective cardioversion of atrial fibrillation.
Dittrich H. C., Erikson J. S., Schneideman T., Blacky A. R., Savides T., & Nicod P. H. Am J Cardiol, 1989. 63: 193-7.
8. Initial energy setting, outcome and efficiency in direct current cardioversion of atrial fibrillation and flutter.
Gallagher M. M., Guo X. H., Poloniecki J. D. et al. J Am Coll Cardiol, 2001. 38: 1498.
9. Electrical reversion of cardiac arrhythmias. Lown, B. Br Heart J, 1967. 29: 469.
10. Safety and efficacy of in-office cardioversion for treatment of supraventricular arrhythmias.
Lesser M. F. Am J Cardiol, 1990. 66: 1267–8.
11. Absence of cardioversion-induced ventricular arrhythmias in patients with therapeutic digoxin levels.
Mann D. L., Maisel A. S., Atwood J. E. et al. J Am Coll Cardiol, 1985. 5: 882.
12. Stoneham M. D. Anaesthesia for cardioversion. Anaesthesia, 1996. 51: 565-7
13. Epicardial mapping of ventricular defibrillation with monophasic and biphasic shocks in dogs.
Zhou X., Daubert J. P., Wolf P. D. et al. Circ Res, 1993. 72: 145–60
14. Prediction of uneventful cardioversion and maintenance of sinus rhythm from direct current electrical cardioversion of chronic atrial fibrillation and flutter. Van Gelder I. C., Crijns H. J., Van Gilst W. H. et al. Am J Cardiol, 1991. 68: 41.
15. Early recurrences of atrial fibrillation after electrical cardioversion: A result of fibrillation-induced electrical remodeling of the atria. Tieleman R. G., Van Gelder I. C., Crijns H. J. G. M. et al. J Am Coll Cardiol, 1998. 31: 167.
16. Comparative efficacy of monophasic and biphasic waveforms for transthoracic cardioversion of atrial fibrillation and atrial flutter. Gurevitz O. T., Ammash N. M., Malouf J. F., Chandrasekaran K., Rosales A. G., Ballman K. V., Hammill S. C., White R. D., Gersh B. J., & Friedman P.A. Am Heart J, 2005. 149: 316-21.
17. Biphasic versus monophasic cardioversion in shock-resistant atrial fibrillation.
Khaykin Y., Newman D., Kowalewski M., Korley V., & Dorian P. Cardiovasc Electrophysiol, 2003. 14: 868-72.
18. BiCard Investigators. Biphasic versus monophasic shock waveform for conversion of atrial fibrillation.
Page R. L., Kerber R. E., Russell J. K. et al. J Am Coll Cardiol, 2002. 39: 1956–63.
19. Efficacy and impact of monophasic versus biphasic countershocks for transthoracic cardioversion of persistent atrial fibrillation. Marinsek M., Larkin G. L., Zohar P. et al. Am J Cardiol, 2003. 92: 988–91.
20. Post-shock myocardial stunning: a prospective randomized double-blind comparison of monophasic and biphasic waveforms. Ambler J. J. Resuscitation, 2006. 68: 329–33.
21. Prospective assessment of the minimum energy needed for external cardioversion of atrial fibrillation.
Ricard P., Levy S., Trigano J. et al. Am J Cardiol, 1997. 79: 815-6.
22. Initial energy sitting, outcome and efficiency in direct current cardioversion of atrial fibrillation.
Gallagher M. M., Guo X. H., Poloniecki J. D., Guan Yap Y., Ward D., & Camm A. J. J Am Coll Cardiol, 2001. 38: 1498-504.
23. A new algorithm for transthoracic cardioversion of atrial fibrillation based on body weight.
Rashba E. J., Bouhouch R., Koshy S. et al. Am J Cardiol, 2001. 88: 1043-5.
24. Transthoracic cardioversion of atrial fibrillation. Comparison of rectilinear versus damped sine wave monophasic shocks. Mittal S., Ayati S., Stein K. M. et al. Circulation, 2000. 101: 1282-7.
25. Biphasic energy selection for transthoracic cardioversion of atrial fibrillation. Glover B. Mm, Walsh S. J., McCann C. J., Moore M. J., Manoharan G., Dalzell G. W., McAllister A., McClements B., McEneaney D. J., Trouton T. G., Mathew T. P., & Adgey A. A. The BEST AF Trial. Heart, 2008. 94: 884-7.
26. Comparison of the rectilinear biphasic waveform with the monophasic damped sine waveform for external cardioversion of atrial fibrillation and flutter. Niebauer M. J., Brewer J. E., Chung M. K., & Tchou P. J. Am J Cardiol, 2004. 15, 93: 1495-9.
27. New method for terminating cardiac arrhythmias: use of sychronized capacitor discharge.
Lown B., Amarasingham R., & Neuman J. JAMA, 1962. 182: 548–55.
28. Cardioversion of atrial fibrillation: a report on the treatment of 65 episodes in 50 patients.
Lown B., Perlroth M. G., Kaidbey S. et al. N Engl J Med, 1963. 269: 325–31.
29. Anterior-posterior versus anterior-lateral electrode positions for external cardioversion of atrial fibrillation.
Kirchhof P., Eckardt L., Loh P. et al. Lancet, 2002. 360: 1275-9.
30. The technique of cardioversion. Lown B., Kleiger R., & Wolff G. Am Heart J, 1964. 67: 282-4.
31. External cardioversion of atrial fibrillation: role of paddle position on technique efficacy and energy requirements. Botto G. L., Politi A., Bonini W., Broffoni T., & Bonatti R. Heart, 1999. 82: 726-30.
32. Electrode positioning for cardioversion of atrial fibrillation. Myerburg R. J., & Castellanos A. Lancet, 2002. 360: 1263-4.
33. Elective cardioversion: influence of paddle-electrode location and size on success rates and energy requirements. Kerber R. E., Jensen S.R., Grayze, J. et al. N Engl J Med, 1981. 305: 658.
34. Randomised comparison of electrode positions for cardioversion of atrial fibrillation. Mathew T. P., Moore A., McIntyre M. et al. Heart, 1999. 81: 576.
35. Simultaneous double external DC shock technique for refractory atrial fibrillation in concomitant heart disease. Kabukcu M., Demircioglu F., Yanik E. et al. Jpn Heart J, 2004. 45: 929–36.
36. High energy transcatheter cardioversion of chronic atrial fibrillation. Levy S., Lacombe P., Cointe R., Bru P., Levy S., Lacombe P., Cointe R., & Bru P.
37. Effects of transcatheter cardioversion on chronic lone atrial fibrillation.
Kumagai K., Yamanouchi Y., Hiroki T., Arakawa K. Pacing Clin Electrophysiol, 1991. Nov 14 (11 Pt 1): 1571-5.
38. Multicenter low energy transvenous atrial defibrillation (XAD) trial results in different subsets of atrial fibrillation
Levy S., Ricard P., Lau C. P., Lok N S., Camm A. J., Murgatroyd F. D., Jordaens L. J., Kappenberger L. J., Brugada P., & Ripley K. L. J Am Coll Cardiol, 1997, Mar 15. 29(4): 750-5.
39. A randomized comparison of external and internal cardioversion of chronic atrial fibrillation
Levy S., Lauribe P., Dolla E., Kou W., Kadish A., Calkins H., Pagannelli F., Moyal C., Bremondy M., Schork A et al. Circulation, 1992 Nov. 86 (5): 1415-20.
40. Internal defibrillation: where we have been and where we should be going
Levy S. J Interv Card Electrophysiol, 2005, Aug. 13. Suppl 1: 61-6.
41. Low energy intracardiac cardioversion of persistent atrial fibrillation
Santini M., Pandozi C., Toscano S. et al. Pacing Clin Electrophysiol, 1998. 21: 2641-50.
42. Higher energy synchronized external direct current cardioversion for refractory atrial fibrillation
Saliba W., Juratli N., Chung M. K., Niebauer M. J., Erdogan O., Trohman R., Wilkoff B. L., Augostini R., Mowrey K. A., Nadzam G. R., & Tchou P. J. J Am Coli Cardio, 1999. 34: 2031-4.
43. Facilitating transthoracic cardioversion of atrial fibrillation with ibutilide pretreatment
Oral H., Souza J. J., Michaud G. F., Knight B. P., Goyal R., Strickberger S. A., & Morady F. N Engl J Med, 1999. 17; 340: 1849-54
44. Safety of electrical cardioversion in patients without digitalis toxicity
Ditchey R. V., & Karliner J. S.. Ann Intern Med, 1981. 95 (6): 676–9.
45. Safety and efficacy of enoxaparin compared with unfractionated heparin and oral anticoagulants for prevention of thromboembolic complications in cardioversion of nonvalvular atrial fibrillation: the Anticoagulation in Cardioversion using Enoxaparin (ACE) trial
Stellbrink C., Nixdorff U., Hofmann T. et al. ACE (Anticoagulation in Cardioversion using Enoxaparin) Study Group. Circulation, 2004. 109: 997–1003.
46. Embolic complications of direct current cardioversion of atrial arrhythmias: association with low intensity of anticoagulation at the time of cardioversion
Gallagher M. M., Hennessy B. J., Edvardsson N. et al. J Am Coll Cardiol, 2002. 40: 926–33.
47. Assessment of Cardioversion Using Transesophageal Echocardiography Investigators. Use of transesophageal echocardiography to guide cardioversion in patients with atrial fibrillation
Klein A. L., Grimm R. A., Murray R. D. et al. N Engl J Med, 2001. 344: 1411–20.
48. Safety of electrical cardioversion in patients with previous embolic events
Elhendy A., Gentile F., Khandheria B. K., Bailey K. R., Burger K. N., & Seward J. B. Mayo Clin Proc, 2001. 76: 364-8.
49. The efficacy of anticoagulant therapy in preventing embolism related to D.C. electrical conversion of atrial fibrillation
Bjerkelund, C. J., Orning O.M. Am J Cardiol, 1969. 23: 208
50. Complications and limitations of direct current 51
Rabbino M. D., Likoff W., Dreifus L. S. & Lown B. countershock. JAMA, 1964. 190: 417–20
51. Cardioversion and digitalis drugs:changed threshold to electric shock in digitalized animals
Lown B., Kleiger R., & Williams J. Circ Res, 1965. 17: 519–31.
52. Direct current countershock complications
Aberg H., Cullhed I., Acta Med Scand, 1968. 183: 415–21.
53. Pacemaker failure following external defibrillation
Gould L., Patel S., Gomes G. I., & Chokshi A. B. Pacing Clin Electrophysiol, 1981. 4: 575-7.
54. Adverse acute and chronic effects of electrical defibrillation and cardioversion on implanted unipolar cardiac pacing systems
Levine P. A., Barold S. S., Fletcher R. D., & Talbot P. J Am Coll Cardiol, 1983. June 1(6): 1413-22.
55. Immediate reinitiation of atrial fibrillation following internal atrial defibrillation
Timmermans C., Rodriguez L. M., Smeets J. L. et al. J Cardiovasc Electrophysiol, 1998. 9: 122–8
56. Pharmacological prevention of atrial tachycardia induced atrial remodeling as a potential therapeutic strategy
Shinagawa K., Derakhchan K., & Nattel S. Pacing Clin Electrophysiol, 2003. 26: 752–64.
57. Comparison of verapamil and ibutilide for the suppression of immediate recurrences of atrial fibrillation after transthoracic cardioversion
Sticherling C., Ozaydin M., Tada H. et al. J Cardiovasc Pharmacol Ther, 2002. 7: 155–60.
58. Oral amiodarone increases the efficacy of direct-current cardioversion in restoration of sinus rhythm in patients with chronic atrial fibrillation
Capucci A., Villani G. Q., Aschieri D., Rosi A. & Piepoli M. F. Eur Heart J, 2000. 21: 66-73.
59. Oral loading single dose flecainide for pharmacological cardioversion of recent-onset atrial fibrillation
Khan I.A. Int J Cardiol, 2003. 87: 121–8.
60. Intravenous sotalol decreases transthoracic cardioversion energy requirement for chronic atrial fibrillation in humans: assessment of the electrophysiological effects by biatrial basket electrodes
Lai L. P., Lin J. L., Lien W.P., Tseng Y. Z., & Huang S. K. J Am Coll Cardiol, 2000. 35: 1434-41.
61. Pretreatment with verapamil in patients with persistent or chronic atrial fibrillation who underwent electrical cardioversion
De Simone A., Stabile G., Vitale D. F. et al. J Am Coll Cardiol, 1999. 34: 810-4.
62. Verapamil, plus antiarrhythmic drugs reduce atrial fibrillation recurrences after electrical cardioversion (VEPARAF Study)
De Simone A., De Pasquale M., De Matteris C. et al. Eur Heart J, 2003. 24: 1425-9.
Vol. 11, N° 6
Notes to editor
Prof. Bulent-Gorenek, Ankara, Turkey.
Author's disclosures: None declared.
The content of this article reflects the personal opinion of the author/s and is not necessarily the official position of the European Society of Cardiology.