Cardioversion in Non-Valvular Atrial Fibrillation
Background: Atrial fibrillation is the most common type of cardiac arrhythmia and is associated with elevated rates of stroke, heart failure, hospital admission, and death. Its prevalence in the overall population is 1.5% to 2%. To convert atrial fibrillation to sinus rhythm, cardioversion is needed.
Methods: This review is based on pertinent articles published from 2004 to December 2014 that were retrieved by a selective PubMed search employing the terms “atrial fibrillation” and “cardioversion.”
Results: In electrical cardioversion, a defibrillator is used to pass a pulse of current between two electrodes. In pharmacological cardioversion, antiarrhythmic drugs are given intravenously or orally. Electrical cardioversion results in sinus rhythm in more than 85% of patients; pharmacological cardioversion results in sinus rhythm in about 70% of patients with recent-onset atrial fibrillation. As a rule, cardioversion should be carried out only under effective therapeutic anticoagulation with heparin, a vitamin K antagonist, or a new oral anticoagulant drug. If atrial fibrillation has been present for more than 48 hours, cardioversion must be preceded by transesophageal echocardiography to rule out blood clot in the left atrium, or else the patient is pretreated with an anticoagulant drug for at least 3 weeks. As cardioversion can transiently impair left atrial pumping function, anticoagulation is usually maintained for 4 weeks after the procedure. The decision whether to continue anticoagulation beyond this point is based on the risk of stroke, as assessed with the CHA2DS2-VASc score.
Conclusion: The main risks of cardioversion—thromboembolism and clinically significant hemorrhage—occur in 1% of cases or less (in the first 30 days after treatment) if the procedure is carried out as recommended in therapeutic guidelines. Serious complications still occur, but they are rare.
Atrial fibrillation is the most common of the serious cardiac rhythm disturbances in the adult population. Typically, atrial fibrillation is diagnosed by means of an electrocardiogram (ECG). The prevalence of atrial fibrillation is 1.5 to 2% in the general population. At age 80 years, approximately 10% of the population have atrial fibrillation (1, 2).
About 40% of patients with atrial fibrillation also have valvular heart disease (e1). Most of the large studies on atrial fibrillation focused on non-valvular atrial fibrillation where no serious valvular heart disease is present. Atrial fibrillation is associated with a marked increase in mortality (1.7-fold, [e2]), stroke (4-fold, [e3]) and heart failure (6-fold, [e2]).
The signs and symptoms of atrial fibrillation can vary widely. Common complaints include:
- Dyspnea (49%)
- Fatigue (49%)
- Palpitations (43%)
- Dizziness (37%)
- Angina pectoris (20%)
However, these complaints may also be caused by other concomitant diseases (3).
Atrial fibrillation is classified into five types (4):
- First detected atrial fibrillation
- Paroxysmal atrial fibrillation (maximum duration 1 week)
- Persistent atrial fibrillation (duration 1 week to 1 year)
- Long-standing persistent atrial fibrillation (duration more than 1 year)
- Permanent atrial fibrillation where the constant presence of the arrhythmia is accepted and no further attempt to control the rhythm is made.
To assess the risk for embolism and stroke in patients with atrial fibrillation, the CHA2DS2-VASc score was introduced.
C = congestive heart failure
H = arterial hypertension
A = age
D = diabetes mellitus
S = status post stroke or transient ischemic attack
VA = vascular disease, such as status post myocardial infarction, and
Sc = female sex.
One point is scored for each of the following: C, H, age 65–74 years, D, VA, and Sc.
Two points are scored for each of the following: age >74 years and status post stroke (S2).
The aim of this paper is to present the current state of knowledge on cardioversion in non-valvular atrial fibrillation. Using the key words “atrial fibrillation“ and “cardioversion,“ a literature search was conducted in the PubMed database, covering the last 10 years up to December 2014.
Indications for the restoration of sinus rhythm in atrial fibrillation
None of the large studies on cardioversion in atrial fibrillation conducted so far was able to demonstrate improvements in prognosis for the hard endpoints ”death“ and “stroke rate“ (5–9). However, these studies included only very few patients younger than 60 years of age. Cardioversion is thus primarily aimed at improving existing symptoms. The Box shows the indications for cardioversion as recommended in the guidelines (4). In a 2012 survey of 57 electrophysiological centers in Europe, 75% of hospitals reported to perform more than 100 cardioversion procedures annually (10). According to data from a prospective European registry, treatment for maintaining sinus rhythm is provided for approx. 60% of patients with atrial fibrillation (between 48.7% in Italy and 72% in France), with 18.1% of patients receiving electrical cardioversion and 19.5% pharmacological cardioversion (11).
Anticoagulation and/or transesophageal echocardiography before cardioversion
Before cardioversion, anticoagulation therapy for 3–4 weeks or transesophageal echocardiography are recommended to ensure the absence of left atrial thrombi (4, 12). In patients with recent onset of atrial fibrillation, a thrombus is detected in approx. 10 and 0.6% of cases in the left and right atrial appendage, respectively (13). In these patients, cardioversion should only be performed after dissolution of intracardiac thrombi by means of effective anticoagulation.
Anticoagulation in cardioversion of atrial fibrillation
When Lown (14) introduced the method of electrical cardioversion to treat atrial fibrillation, the risk of thromboembolism during the period immediately after the intervention was already known. In 1992, a retrospective analysis of 454 electrical cardioversions of atrial fibrillation found an incidence of embolic events of 1.32%; no patient with thromboembolism was on anticoagulation therapy (15). The timing of thromboembolic events after electrical cardioversion of atrial fibrillation was described based on data from 32 studies conducted between 1966 and 1997 (16). Among a total of 4621 electrical cardioversions, 92 thromboembolic events were identified; almost all these events (except for four cases) occurred within the first seven days after cardioversion. A recently published retrospective analysis of 16 274 first-time electrical cardioversions performed in Denmark between 2000 and 2008 found a more than twofold increase in the risk of thromboembolic events during the first 30 days after the intervention among patients receiving no anticoagulation therapy during and after cardioversion (17). The thromboembolic incidence rate was 4 and 10.33 per 100 patient-years for the group with and without prior oral anticoagulant therapy, respectively. The risk of thromboembolism then fell within 360 days to 1.84 and 3.18 per 100 patient-years with and without anticoagulation, respectively.
The CHA2DS2-VASc score had no impact on the occurrence of thromboembolic events with and without anticoagulation within 30 days after cardioversion. For a CHA2DS2-VASc score of 0 and 1, the risk of thromboembolism after cardioversion without anticoagulation versus with anticoagulation was 2.21-fold increased, while a 2.4-fold increase was noted for CHA2DS2-VASc scores above 2. Aspirin did not significantly reduce the risk of cardioversion-related thromboembolism. The retrospective analysis of this study does not allow to draw conclusions as to why the anticoagulant therapy received by the patients was so variable. The risk of cardioversion-related thromboembolic events is lower in patients with atrial fibrillation of <48 h duration without risk factors; therefore, only heparin anticoagulation at the time of cardioversion is recommended and no subsequent anticoagulant therapy (4). In patients with risk factors for thromboembolism, oral anticoagulant therapy is required over a period of at least four weeks after cardioversion. This recommendation is backed by a recent retrospective Finnish study evaluating the incidence of thromboembolic events after 5116 cardioversions (88% electrical) within 30 days in 2481 patients with atrial fibrillation <48 h duration without anticoagulation (18). Altogether 38 thromboembolic events were noted (0.7% of the cardioversions). In 10 of these cases, the CHA2DS2-VASc score was 0–1. The thromboembolic events occurred between day 1 and day 27 (median: day 2). The highest risk for thromboembolism was observed in patients with heart failure, diabetes mellitus and age >60 years. The lowest risk of thromboembolism was found in non-heart-failure patients <60 years (0.2%).
Etiology of thromboembolism after cardioversion
Atrial stunning is considered to be the primary cause of thromboembolism after cardioversion (19). While in the presence of atrial fibrillation no atrial contractions occur, there is still some degree of movement of blood in the left atrium and atrial appendage. Restoration of sinus rhythm by means of cardioversion can initially cause a deterioration of blood flow in the left atrium and the left atrial appendage (19), promoting local blood clot formation. Atrial stunning has been observed after transthoracic electrical, internal electrical, pharmacological, and spontaneous cardioversion (19). The longer the period of atrial fibrillation before cardioversion, the longer atrial stunning may persist (20). Typically, left atrial function returns to normal within one week after cardioversion; however, in patients with long-standing atrial fibrillation the process of normalization may take a month (20).
Anticoagulants in cardioversion
Heparins, vitamin K antagonists or novel oral anticoagulants can be used to ensure effective anticoagulation at the time of cardioversion, while aspirin does not offer adequate protection. With unfractionated heparin, an initial intravenous bolus of 60–80 units/kg body weight (BW) is followed by intravenous therapy aimed at extending the activated partial thromboplastin time to about 50–70 seconds (21). Adequate anticoagulation for cardioversion can also be achieved with enoxaparin at a dose of 1 mg/kg BW subcutaneously twice daily (22). Certoparin is another low molecular weight heparin which has been used (23). Effective anticoagulation using a vitamin K antagonist (e.g. warfarin, phenprocoumon) is thought to be achieved at international normalized ratio (INR) values in the range of 2 to 3 (21). With cardioversion, an INR >2.5 appears to better prevent thromboembolic events (24). Rivaroxaban is the first novel oral anticoagulant to be compared with vitamin K antagonists in a prospective study on cardioversion (mostly electrical). About 1000 patients received rivaroxaban in a dose of 20 mg/d (creatinine clearance >50 mL/min) or 15 mg/d (creatinine clearance 30–49 mL/min) in two strategies (long or short pre-treatment) or a vitamin K antagonist (25). Rivaroxaban was administered orally between three weeks and, at the latest, four hours before cardioversion. Two strokes (0.2%) and one fatal hemorrhage were observed. No significant differences between rivaroxaban and vitamin K antagonists were found for the endpoints of this study. Post-hoc subgroup analyses of the large pivotal studies on novel oral anticoagulants indicate that dabigatran (26) and apixaban (27) may also be effective anticoagulants in a cardioversion setting. As yet, no prospective data on these agents are available.
Practice of electrical cardioversion for atrial fibrillation
Electrical cardioversion is typically performed under continuous ECG monitoring and intravenous procedural anesthesia (10); given the risk of ventricular fibrillation and asystole, provisions for resuscitation measures should be made. The electrodes of the defibrillator/cardioverter can be placed in the anterior–left lateral (apical) or anterior–posterior position so that the heart is located between the two electrodes. The most effective way to position the electrodes with older monophasic defibrillators was the anterior–posterior arrangement (28). Using biphasic defibrillators, higher cardioversion rates are achieved today at lower energy levels (29). With this technology, electrode positioning and the geometry of energy transfer are of minor importance (30). In patients with implanted pacemakers or defibrillators, the electrodes should ideally be placed at a distance >8 cm from the unit in an anterior–posterior arrangement (31). The electrical discharge of the defibrillator is synchronized with the R wave in the electrocardiogram (14, 32). Using a biphasic defibrillator, it is advisable to start with a shock energy of 100 J in patients with atrial fibrillation of less than 48-hour duration and 150 J in patients with longer-standing atrial fibrillation (33). According to a large prospective registry study, sinus rhythm is initially restored by electrical cardioversion in approximately 88% of cases (34). Predictors of successful cardioversion include the absence of chronic obstructive pulmonary disease, paroxysmal atrial fibrillation, and a short history of atrial fibrillation. If sinus rhythm cannot be achieved even with the use of maximum energy, a new attempt can be made about 3 minutes after the last shock application as body resistance is lower at that time (32). Another way to improve the chance of successful electrical cardioversion is the oral administration of amiodarone (35) or propafenone (36) before the procedure. In individual difficult cases (e.g. patients with significant obesity), internal cardioversion may be considered (32). In patients with atrial fibrillation and implantable cardioverter-defibrillator (ICD), the ICD can be used for internal cardioversion. However, with approximately 30% the success rate is lower than with external cardioversion (37).
In clinical practice, it is easier to attempt pharmacological cardioversion as it does not require anesthesia. The European guidelines for the management of atrial fibrillation (4) list as drugs recommended for pharmacological cardioversion amiodarone, flecainide, ibutilide, propafenone, and vernakalant; however, ibutilide is not available in Germany and vernakalant was granted limited marketing authorization (Table 1).
Besides intravenous administration, amiodarone can also be given orally in high doses (30 mg/kg) for cardioversion in recent-onset atrial fibrillation (38). With the “pill in the pocket” approach, oral propafenone or flecainide is used for cardioversion in patients with atrial fibrillation <48 h duration without or with only minor structural heart disease under ECG monitoring. Patients who underwent the supervised treatment without problems can repeat it independently outside the hospital, should arterial fibrillation recur.
Success rates of electrical and pharmacological cardioversion
Two large prospective registry studies provide a very good overview on cardioversion in Europe (34, 39). According to these studies, pharmacological cardioversion is typically performed in patients with new-onset or paroxysmal atrial fibrillation (median duration of present atrial fibrillation episode: 0.5–2 days ) and electrical cardioversion in patients with persistent atrial fibrillation (median duration of present atrial fibrillation episode: 30 days ). Electrical cardioversion was successfully performed in 88% of 712 patients (34) and 90% of 1946 patients (39), respectively. Sinus rhythm was pharmacologically restored in 71% of 1089 patients (34) und 69% of 1026 patients (39). After one year, in 70% of patients with successful cardioversion sinus rhythm was observed in the electrocardiogram (34). No randomized study comparing the success rates achieved with electrical versus pharmacological cardioversion was found in the literature.
Complications after cardioversion of atrial fibrillation
In Table 2, the main complications of cardioversion reported in studies with more than 1000 patients are listed, primarily related to thromboembolic events, bleeding and arrhythmia. Complication rates are typically <1% of patients treated; however, individual patients may experience serious adverse events.
What thromboembolic risk is associated with cardioversion despite anticoagulation?
Thromboembolic complications occur within 30 days after cardioversion despite adequate anticoagulation with a probability between 0% (27) and 1.6% (22). The Randomized Evaluation of Long-Term Anticoagulation Therapy (RE-LY) compared the novel oral anticoagulant dabigatran in doses of 150 mg (D150) twice daily and 110 mg (D110) twice daily with the oral vitamin K antagonist warfarin (W) in 18 113 patients with atrial fibrillation (40). The annual rate of stroke or systemic embolism was 1.53% (D110), 1.11% (D150) and 1.69% (W), respectively. In this prospective study, 1270 patients underwent 1983 cardioversions, analyzed post-hoc as a subgroup (26). Stroke and systemic embolism occurred within 30 days after cardioversion in 0.77% (D110: 5 of 647), 0.3% (D150: 2 of 672) and 0.6% (W: 4 of 664) of cardioversions. By calculating the annual thromboembolism rates in the three treatment groups of the total study based on a period of 30 days and then comparing them with the thromboembolism rates within 30 days after cardioversion, it is revealed that thromboembolic events occurred 3-times (D150), 4-times (W) and 6-times (D110), respectively, more frequently in the month after cardioversion compared with the remaining months of the study. If the thromboembolism rates after cardioversion were based on patients rather than cardioversions performed, the calculated risk of thromboembolic events associated with cardioversion would even be greater. This is supported by the very large retrospective study on cardioversion from Denmark (17) which found that even with anticoagulation the risk of thromboembolism within the first 30 days after cardioversion was more than twice as high compared with the remaining follow-up period. As these are very large, trustworthy studies, it is reasonable to assume that cardioversion increases the overall small risk of systemic embolism, including stroke, despite anticoagulation. The current guidelines recommend that a patient with a CHA2DS2-VASc score of 0 should receive effective anticoagulation for medically performed cardioversion, while this is not required for a patient with atrial fibrillation or spontaneous cardioversions (4). Based on the information available after the publication of the large retrospective 2015 cardioversion study from Denmark, it is clear that even patients with a CHA2DS2-VASc score of 0 undergoing medically performed cardioversion should receive effective anticoagulation which is in line with the guideline recommendations (4) that were not previously supported by evidence from studies.
Should patients with interventional or surgical closure of the left atrial appendage receive anticoagulation for cardioversion?
With no pertinent studies available, this question cannot be answered. In case no anticoagulation therapy is initiated, it should at least be ensured that the left atrial appendage is completely closed (e4) and no thrombi are present in the left atrium.
Conflict of interest statement
The authors declare that no conflict of interest exists.
Manuscript received on 23 March 2015; revised version accepted on 1 June 2015
Translated from the original German by Ralf Thoene, MD.
Prof. Dr. med. Hermann H. Klein
Medizinische Klinik II, Helios Klinikum Warburg
Langwiesen Straße 13, 55743 Idar-Oberstein, Germany
Fot eReferences please refer to:
|1.||Kannel WB, Wolf PA, Benjamin EJ, Levy D: Prevalence, incidence, prognosis, and predisposing conditions for atrial fibrillation: population-based estimates. Am J Cardiol1998; 82: 2N–9N CrossRef|
|2.||Trappe JH: Atrial fibrillation: Established and innovative methods of evaluation and treatment. Dtsch Arztebl Int 2012; 109: 1–7 VOLLTEXT|
|3.||Meinertz T, Kirch W, Rosin L, Pittrow D, Willich SN, Kirchhof P, ATRIUM investigatorsr: Management of atrial fibrillation by primary care physicians in Germany: baseline results of the ATRIUM registry. Clin Res Cardiol 2011; 100: 897–905 CrossRef MEDLINE PubMed Central|
|4.||Camm AJ, Kirchhof P, Lip GYH, et al.: Guidelines for the management of atrial fibrillation. Eur Heart J 2010; 31: 2369–429 CrossRef MEDLINE|
|5.||The Atrial Fibrillation Follow-Up Investigation of Rhythm Management (AFFIRM) Investigators: A comparison of rate control and rhythm control in patients with atrial fibrillation. New Engl J Med 2002; 347: 1825–33 CrossRef MEDLINE|
|6.||Van Gelder IC, Hagens VE, Bosker HA, et al.: A comparison of rate control and rhythm control in patients with recurrend persistent atrial fibrillation. N Engl J Med 2002; 347: 1834–40 CrossRef MEDLINE|
|7.||Roy D, Talajic M, Nattel S, et al.: Rhythm control versus rate control for atrial fibrillation and heart failure. N Engl J Med 2008; 358: 2667–77 CrossRef MEDLINE|
|8.||AI-Khatib SM, Allen LaPointe NM, Chatterjee R, et al.: Rate- and rhythm-control therapies in patients with atrial fibrillation: a systemic review. Ann Intern Med 2014; 160: 760–73 CrossRef MEDLINE|
|9.||Shariff N, Desai RV, Patel K, et al.: Rate-control versus rhythm-control strategies and outcome in septuagenarians with atrial fibrillation. Am J Med 2013; 126: 887–93 CrossRef MEDLINE PubMed Central|
|10.||Hernandez-Madrid A, Svendsen JH, Lip GYH, van Gelder IC, Dobreanu D, Blomstrom-Lundqvist C: Cardioversion for atrial fibrillation in current European practice: results of the European Heart Rhythm Association survey. Europace 2013; 15: 915–8 CrossRef MEDLINE|
|11.||Kirchhof P, Ammentorp B, Darius H, et al.: Management of atrial fibrillation in seven European countries after publication of the 2010 ESC guidelines on atrial fibrillation: primary results of the PREvention oF thromboemolic events-European Registry in Atrial Fibrillation (PREFER in AF). Europace 2014; 16: 6–14 CrossRef MEDLINE PubMed Central|
|12.||Schuchert A, Gulba D, Horstkotte DH, Meinertz T, Tebbe U: Kommentar zu den ACC/AHA/ESC-Leitlinien 2001 zur Prävention arterieller Thromboembolien bei Patienten mit Vorhofflimmern. Z Kardiol 2003; 92: 694–703 CrossRef|
|13.||Cresti A, Garcia-Fernandez A, Miracapillo G, et al.: Frequency and significance of right atrial appendage thrombi in patients with persistent atrial fibrillation or atrial flutter. J Am Soc Echocardiogr 2014; 27: 1200–7 CrossRef MEDLINE|
|14.||Lown B, Perlroth M, Kaidbey S, Abe T, Harken DE: „Cardioversion“ of atrial fibrillation. A report on the treatment of 65 episodes in 50 patients. N Engl J Med 1963; 269: 325–31 CrossRef MEDLINE|
|15.||Arnold AZ, Mick MJ, Mazurek RP, Loop FD, Trohman RG: Role of prophylactic anticoagulation for direct current cardioversion in patients with atrial fibrillation or atrial flutter. J Am Coll Cardiol 1992; 19: 851–5 CrossRef|
|16.||Berger M, Schweitzer P: Timing of thromboembolic events after electrical cardioversion of atrial fibrillation or flutter: a retrospective analysis. Am J Cardiol 1998; 82: 1545–7 CrossRef|
|17.||Hansen ML, Jepsen RMHG, Olesen JB, et al.: Thromboembolic risk in 16274 atrial fibrillation patients undergoing direct current cardioversion with and without oral anticoagulant therapy. Europace 2015; 17: 18–23 CrossRef MEDLINE|
|18.||Airaksinen KEJ, Grönberg T, Nuotio I, et al.: Thromboembolic complications after cardioversion of acute atrial fibrillation. J Am Coll Cardiol 2013; 62: 1187–92 CrossRef MEDLINE|
|19.||Khan IA: Atrial stunning: basic and clinical considerations. Int J Cardiol 2003; 92: 113–28 CrossRef|
|20.||Manning WJ, Silverman DI, Katz SE, et al.: Impaired left atrial mechanical function after cardioversion: relation to the duration of atrial fibrillation. J Am Coll Cardiol 1994; 23: 1535–40 CrossRef|
|21.||Alquwaizani M, Buckley L, Adams C, Fanikon J: Anticoagulants: A review of the pharmacology, dosing and complications. Curr Emerg Hosp Med Rep 2013; 1: 83–97 CrossRef MEDLINE PubMed Central|
|22.||Stellbrink C, Nixdorf U, Hofmann T, et al.: 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. Circulation 2004; 109: 997–1003 CrossRef MEDLINE|
|23.||Tebbe U, Oeckinghaus R, Appel KF, et al.: AFFECT: a prospective, open-label, multicenter trial to evaluate the feasibility and safety of a short-term treatment with subcutaneous certoparin in patients with persistent non-valvular atrial fibrillation. Clin Res Cardiol 2008; 97: 389–96 CrossRef MEDLINE|
|24.||Gallagher MM, Hennessey BJ, Edvardsson N, et al.: Embolic complications of direct current cardioversion of atrial arrhythmias: association with low intensity of anticoagulation at the time of cardioversion. J Am Coll Cardiol 2002; 40: 926–33 CrossRef|
|25.||Cappato R, Ezekowitz MD, Klein AL, et al.: Rivaroxaban vs. vitamin K antagonists for cardioversion in atrial fibrillation. Eur Heart J 2014; 35: 3346–55 CrossRef MEDLINE|
|26.||Nagarakanti R, Ezekowitz MD, Oldgren J, et al.: Dabigatran versus warfarin in patients with atrial fibrillation: An analysis of patients undergoing cardioversion. Circulation 2011; 123: 131–6 CrossRef MEDLINE|
|27.||Flaker G, Lopes RD, Al-Khatib SM, et al.: Efficacy and safety of apixaban in patients after cardioversion for atrial fibrillation. J Am Coll Cardiol 2014; 63: 1082–7 CrossRef MEDLINE|
|28.||Adgey AAJ, Walsh SJ: Theory and practice of defibrillation: (1) Atrial fibrillation and DC conversion. Heart 2004; 90: 1493–8 CrossRef MEDLINE PubMed Central|
|29.||Mittal S, Stein KM, Markowitz SM, Iwai S: An update on electrical cardioversion of atrial fibrillation. Card Elektrophysiol Rev 2003; 7: 285–9 CrossRef MEDLINE|
|30.||Deakin CD, Conelly S, Wharton R, Yuen HM: A comparison of rectilinear and truncated exponential biphasic waverforms in elective cardioversion of atrial fibrillation: A prospective randomized controlled trial. Resuscitation 2013; 84: 286–91 CrossRef MEDLINE|
|31.||Israel CW, Geller JC, Klingenheben T, et al.: Empfehlungen zur externen Kardioversion bei Patienten mit Herzschrittmacher oder implantiertem Kardioverter/Defibrillator. Kardiologe 2011; 5: 257–63 CrossRef|
|32.||Joglar JA, Kowal RC: Electrical cardioversion of atrial fibrillation. Cardiol Clin 2004; 22: 101–11 CrossRef|
|33.||Reisinger J, Gstrein C, Winter T, et al.: Optimization of initial energy for cardioversion of atrial tachyarrhythmias with biphasic shocks. Am J Emerg Med 2010; 28: 159–65 CrossRef MEDLINE|
|34.||Pisters R, Nieuwlaat R, Prins MH, et al.: Clinical correlates of immediate success and outcome at 1-year follow-up of real world cardioversion of atrial fibrillation: the Euro Heart Survey. Europace 2012; 14: 666–74 CrossRef MEDLINE|
|35.||vanNoord T, van Gelder IC, Schoonderwoerd BA, Crijns HJGM: Immediate reinitiation of atrial fibrillation after electrical cardioversion predicts subsequent pharmacologic and electrical conversion to sinus rhythm on amiodaron. Am J Cardiol 2000; 86: 1384–5 CrossRef|
|36.||Bianconi L, Mennuni M, Lukie V, Castro A, Chieffi M, Sanatini M: Effects of oral propafenone admistration before electrical cardioversion of chronic atrial fibrillation: a placebo controlled study. J Am Coll Cardiol 1996; 28: 700–6 CrossRef CrossRef|
|37.||Limantoro I, Vernooy K, Weijs B, et al.: Low efficacy of cardioversion of persistent atrial fibrillation with the implantable cardioverter-defibrillator. Neth Heart J 2013; 21: 548–53 CrossRef MEDLINE PubMed Central|
|38.||Nadarasa K, Williams MJA: Single high oral dose amiodarone for cardioversion of recent onset atrial fibrillation. Heart, Lung and Circ 2012; 21: 444–8 CrossRef MEDLINE|
|39.||Crijns HJGM, Weijs B, Fairley AM, et al.: Contemporary real life cardioversion of atrial fibrillation: Results from the multinational RHYTHM-AF study. Int J Cardiol 2014; 172: 588–94 CrossRefMEDLINE|
|40.||Connolly SJ, Ezekowitz MD, Yusuf S, et al.: Dabigatran versus Warfarin in patients with atrial fibrillation. N Engl J Med 2009; 361: 1139–51 CrossRef MEDLINE|
|e1.||Nabauer M, Gerth A, Limbourg T, et al.: The registry of the German competence NETwork on atrial fibrillation. Europace 2009; 11: 423–34 CrossRef MEDLINE PubMed Central|
|e2.||Kannel WB, Abbot RD, Savage DD, McNamara PM: Epidemiologic features of chronic atrial fibrillation. The Framingham Study. N Engl J Med 1982; 306: 1018–22 CrossRef MEDLINE|
|e3.||Britton M, Gustafsson C: Non-rheumatic atrial fibrillation as a risk factor for stroke. Stroke 1985; 16: 182–8 CrossRef|
|e4.||Hanazawa K, Brunelli M, Geller JC: Thromboembolic stroke after cardioversion with incomplete left atrial appendage closure. Clin Res Cardiol 2014; 103: 835–7 CrossRef MEDLINE|
|e5.||Grönberg T, Nuoti I, Nikkinen M, et al.: Arrhythmic complications after electrical cardioversion of acute atrial fibrillation: The FinCV study. Europace 2013; 15: 1432–5 CrossRef MEDLINE|