© 2004 by European Society of Cardiology
REVIEW
Incidence and management of early recurrent atrial fibrillation (ERAF) after transthoracic electrical cardioversion
aMedizinische Universitäts- und Poliklinik, Innere Medizin III, Kardiologie/Angiologie, Universitätskliniken des Saarlandes D-66421 Homburg, Germany; bReinhard-Nieter Krankenhaus Medizinische Klinik I, Städtische Kliniken Wilhelmshaven, D-26389 Wilhelmshaven, Germany
Manuscript submitted 23 August 2002. Accepted after revision 21 September 2003.
*Corresponding author. Tel.: +49-6841-1623000; fax: +49-6841-1623369. E-mail address: siaplaouras{at}aol.com (S. Siaplaouras).
 |
Abstract |
|---|
 Top Abstract IntroductionMethodsResultsDiscussionConclusionReferences |
|---|
AIMS: The purpose was to determine the incidence of early recurrent atrial fibrillation (ERAF) after transthoracic cardioversion (CV) of persistent atrial fibrillation (AF) and to evaluate the efficacy of a predefined strategy for its management.
METHODS AND RESULTS: Consecutive patients (n=135) underwent elective CV of AF. CV was performed according to a predefined step-up protocol with rising energy delivery (200 J to 360 J). ERAF was defined as a relapse of AF within 1 min after at least two sinus beats. For proper identification of success of CV, additional endocardial recordings were obtained by an electrode catheter positioned in the high right atrium. In case of ERAF, further CVs were attempted, first with higher energy delivery only, second after intravenous flecainide. If transthoracic CV was ineffective, an internal CV was scheduled. All patients could be converted into sinus rhythm. Sixteen patients (12%) had ERAF. ERAF could be suppressed by further shock delivery in 31% of them. In the remaining 69%, a combination of i.v. flecainide and repeated CV was effective in controlling ERAF. Clinical and echocardiographic parameters were comparable in patients with or without ERAF.
CONCLUSION: (1) In the patient population studied, transthoracic CV of AF was technically highly efficacious, so that an internal CV was not necessary in any of the cases. (2) Clinical success of transthoracic cardioversion was limited by ERAF in 12% of the patients. (3) Using the described protocol, ERAF could be suppressed in all patients.
Key Words: early recurrent atrial fibrillation (ERAF), transthoracic cardioversion, flecainide
|
Introduction |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionConclusionReferences |
|---|
Electrical cardioversion is an effective method to convert atrial fibrillation to sinus rhythm. The success rates reported after external cardioversion are 40–90% [1–
4]. The clinical success of this procedure is limited either by ineffective attempts at cardioversion or by early recurrent atrial fibrillation (ERAF). Differentiating between ERAF during the first few seconds and an unsuccessful cardioversion exclusively based on analysis of the surface electrocardiogram is difficult. Therefore, in clinical practice ERAF can be misinterpreted as an ineffective cardioversion. The discrimination of these two possible results is important, because the therapeutical consequences of ERAF or an unsuccessful cardioversion are substantially different.
The incidence rates reported for ERAF are 13–36% after internal cardioversion [5–9] and 16–26% after external cardioversion [4,10].
A reduction of the early relapse rate by application of antiarrhythmic drugs has been shown in larger study groups for sotalol after internal cardioversion as well as for propafenone and amiodarone after external cardioversion [4,5,10]. In isolated cases this also has been reported for flecainide after internal cardioversion [6]. The effect of flecainide in the management of ERAF after successful transthoracic cardioversion of persistent atrial fibrillation has not yet been systematically studied. The aim of this prospective study was to determine the incidence of ERAF after transthoracic cardioversion of persistent atrial fibrillation and to evaluate the efficacy of a predefined treatment protocol including repeated cardioversion and intravenous administration of flecainide to control ERAF.
|
Methods |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionConclusionReferences |
|---|
Consecutive patients referred to our hospital for elective cardioversion of persistent atrial fibrillation were included.
The inclusion criterion was:
- symptomatic persistent atrial fibrillation following the definition of Gallagher et al. [11].
The exclusion criteria were:
- Age <18 years.
- Left-ventricular ejection fraction < 40%.
- Recent myocardial infarction (during the last three months).
- Significant electrolyte imbalance (potassium < 3.5 or > 5.0 mmol/l).
- Reversible cause of atrial fibrillation (e.g. hyperthyroidism).
- Ineffective anticoagulation during the last four weeks prior to cardioversion (international normalized ratio (INR) target range: 2–3).
- Duration of atrial fibrillation > 1 year.
- Drug intoxication (e.g. with digitalis).
- Left-ventricular ejection fraction < 40%.
All patients gave written informed consent to the study protocol.
Administration of the established chronic antiarrhythmic therapy was not interrupted for the procedure. All patients had venous access. Blood pressure, ECG and oxygen saturation were monitored continuously throughout the procedure and at least for 3 h after cardioversion. For proper identification of a successful transthoracic cardioversion and for back-up pacing in case of severe bradycardia following cardioversion, a 6 French quadripolar electrode catheter (Bard Electrophysiology, Lowell, MA, USA) was positioned transvenously in the high right atrium. The catheter was inserted in the right medial cubital vein or in the right femoral vein if the first approach was unsuccessful. Under fluoroscopic control, an optimized position of the cardioversion paddles for anterior–posterior cardioversion was achieved as reported elsewhere [12]. The optimal position was defined as the position in which as much as possible of the fluoroscopic shadow of the atria was covered by the fluoroscopic shadow of the posterior paddle in order to obtain a high current density in the atrial myocardium. The procedure was performed under deep sedation using intravenous (i.v.) midazolam (5 mg initially with rising dosage, if necessary additionally with fentanyl 0.05–0.1 mg i.v.). R-wave synchronized electrical cardioversion with a conventional monophasic waveform using an external defibrillator (Lifepak 9, Physio-Control Corporation, Redmond, Washington, USA) was performed according to the predefined step-up protocol (Fig. 1) with active pressure on the hand-held anterior paddle. Endocardial recordings obtained from the high right atrium were monitored during the whole procedure. ERAF was defined as relapse of atrial fibrillation within 1 min after at least two consecutive sinus beats. If necessary, flecainide (1.5 mg per kg bodyweight) was infused over 5 min. The next cardioversion was attempted 5 min after drug delivery. If transthoracic cardioversion was ineffective, an internal cardioversion was scheduled.
|
Statistics
All data are presented as mean (standard deviation, SD). To compare continuous variables of groups, Student's t-test was used. The chi-square and Fisher's exact test were used to compare categorical variables. A value of p<0.05 was considered statistically significant.
|
Results |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionConclusionReferences |
|---|
One hundred and thirty-five patients, who fulfilled the above-mentioned criteria, were included. All patients could be converted by transthoracic cardioversion into sinus rhythm at least for two sinus beats with a mean of 1.5±0.8 cardioversion attempts. Therefore, an internal cardioversion was not necessary in any of the cases. Patients with ERAF needed significantly more attempts than patients without ERAF (3.1±1.1 vs. 1.2±0.5, p<0.001).
Sixteen patients (12%) had a total of 24 episodes of ERAF after a mean duration of 30±19 s (25±18 s until the first relapse, in patients with more than one episode the mean duration until the second relapse was 42±16 s).
ERAF always was initialized by an atrial premature beat with a mean coupling interval of 442±169 ms during sinus rhythm with a mean cycle length of 903±280 ms.
ERAF could be suppressed by further shock delivery in five of 16 cases (31%). In the remaining 11 patients (69%) the combination of i.v. flecainide and a further cardioversion attempt was effective in controlling ERAF (Fig. 2). None of the patients without ERAF needed administration of the antiarrhythmic drug (p<0.0001 vs. patients with ERAF).
|
Mean energy delivered was significantly higher in patients with ERAF (965±392 vs. 282±172 J, p<0.0001).
By using the described protocol all patients, with or without ERAF, could be converted into stable sinus rhythm, documented until discharge.
There was no clinical predictor for ERAF. Age, structural cardiac disease, duration of atrial fibrillation (first manifestation and the present episode), left-ventricular function and atrial diameter were comparable in patients with and without ERAF (Table 1). There were no significant differences between the two patient groups concerning chronic antiarrhythmic treatment with class I and class III antiarrhythmic drugs or digitalis when entering the study. However, patients with ERAF were on betablocker therapy more often when included in the study compared with patients without ERAF.
|
During the complete study, no procedure-related complication occurred.
|
Discussion |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionConclusionReferences |
|---|
Reestablishing stable sinus rhythm can be the goal in patients with symptomatic persistent atrial fibrillation. The rationale is to eliminate arrhythmia dependent symptoms and to improve the exercise capacity. Transthoracic electrical cardioversion of persistent atrial fibrillation is a generally accepted and efficacious method for restoration of sinus rhythm [1
–4]. Its clinical success is limited either by ineffective attempts at cardioversion or by ERAF. In clinical practice, ERAF after transthoracic cardioversion during the first few seconds is often difficult to distinguish from an ineffective cardioversion because of disturbance of the surface electrocardiogram. But its discrimination is of clinical relevance for the individual patient, because there are fundamentally different treatment strategies for ERAF and for ineffective cardioversion. In case of ERAF, the aim must be to avoid the relapse. This is possible with antiarrhythmic drugs [4,5,10] or, as recently reported by Tse et al. [13] in some cases, by atrial pacing immediately after cardioversion. After technically ineffective cardioversion using a transthoracic current, the next therapeutic step can be either an internal cardioversion attempt or no further attempts at conversion but only control of heart rate [14].
In our study the incidence of ERAF was 12%. Compared with other reported incidences (13–36%) [4–6,9], it was low. The reason for this could be the smaller numbers in these reports (11–64 patients) or different characteristics of the studied populations. Sra and coworkers [9] selectively investigated patients who could be successfully converted by internal cardioversion. Additionally, six of the 11 patients were in sinus rhythm when included in the study. Atrial fibrillation had to be induced first in these patients. The data of Tse et al. [5] comprising 64 patients after internal cardioversion were completely retrospectively collected. The study groups of Timmermans et al. [6] and Yu et al. [4] were comparable with ours. As in ours, consecutive patients referred for elective cardioversion were included. The incidence of ERAF documented by Timmermans et al. [6] was 13% and similar to this study. Yu et al. [4] reported a much higher incidence of ERAF (26%). An explanation could be the considerably longer mean duration of atrial fibrillation in their patients (71±54 months vs. 3.2±3.3 months in our patients). Electrical remodelling of the atrial myocardium could have occurred over a longer time period in their patients. This factor might have influenced the incidence of ERAF. Further investigation concerning this is needed.
The mean duration until the relapse in our study was 30.2 s and was comparable with the documented time in the studies of Yu et al. [4] and Timmermans et al. [6] (19 and 26 s, respectively), but much longer than that reported by Sra et al. [9] (8.2 s). A reason for this could be the different handling of the chronic medical treatment (Yu et al. [4] discontinued all antiarrhythmic drugs five half-lives before cardioversion, Sra et al. [9] in some patients, Timmermans et al. [6] continued the established therapy) as well as the already mentioned differences in the studied populations and research methods.
Corresponding with other published data [4–6], we did not find a significant difference between the patient groups with or without ERAF concerning clinical characteristics, the duration of atrial fibrillation and echocardiographic parameters such as left-ventricular function or atrial diameter. Additionally, the chronic antiarrhythmic therapy with class I and class III antiarrhythmic drugs or digitalis was comparable in our two study groups. Remarkably, a greater proportion of patients with ERAF were on betablocker therapy than patients without ERAF. This could be due to the small number of patients with ERAF. However, only one patient with sinus bradycardia who developed ERAF was on betablocker therapy, so that an increased incidence of ERAF, caused by the betablocker inducing sinus bradycardia, cannot be excluded, but seems to be unlikely.
In our study using the described optimized technique (fluoroscopic paddle control, active pressure on the paddle, etc.), all patients could be converted successfully for at least two sinus beats by external cardioversion. Additionally, those with ERAF could be converted into stable sinus rhythm following the predefined protocol. This emphasizes the necessity of a careful interpretation of the electrocardiogram immediately after electrical cardioversion. With a better identification of patients with ERAF, otherwise falsely classified as ineffective cardioversion, the number of the invasive and, therefore, more cost- and time-consuming internal cardioversions could be further reduced.
In published studies sotalol, propafenone and amiodarone were able to suppress ERAF effectively after internal or external cardioversion [4,5,10]. Flecainide also positively influenced the early relapse rate in at least two patients in the study of Timmermans et al. [6] after internal cardioversion. We could show in a larger patient population that intravenous flecainide effectively prevents early recurrence of atrial fibrillation after transthoracic cardioversion. Eleven of 16 patients with ERAF (69%) needed the administration of flecainide and all could be converted into stable sinus rhythm by a further attempt at cardioversion.
With the described therapy protocol, an effective suppression of ERAF in all patients could be achieved by only a combination of higher shock energy with the administration of flecainide. Sra and coworkers [9] did not need an additional antiarrhythmic drug in their small study group with, in part, induced atrial fibrillation. Our results are confirmatory of other studies in which control of ERAF in 83%–100% of the cases was only possible by using higher energy amounts together with the administration of an antiarrhythmic drug [4–6].
It remains unclear whether further shocks at the same energy level would be as efficacious as the investigated protocol with higher energy levels for the second shock. To investigate this, it would be necessary to compare further shocks after ERAF either with the same or with higher energy levels in a random fashion. That was not an aim of this study and, therefore, was not investigated. That could be the subject of further investigations.
By obtaining intracardiac recordings using a transvenous electrode catheter, discrimination of ERAF and ineffective cardioversion was highly efficacious. Of course, due to its invasive character it is limited to studies and is not a method suitable for routine use in cardioversion.
Limitations
One limitation of this study might be the lack of follow-up. The predictive value of ERAF concerning the late relapse rate has not been investigated here. In other publications, however, the incidence of ERAF did not correlate with increased risk for relapse during the follow-up [4,6].
|
Conclusion |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionConclusionReferences |
|---|
- 1. Using the optimized technique, transthoracic cardioversion was technically highly effective in restoring sinus rhythm, so that an internal cardioversion was not necessary in any of the cases.
- 2. Clinical success of transthoracic cardioversion was limited by ERAF in 12% of the patients.
- 3. Using the described therapy protocol, the clinical efficacy of transthoracic cardioversion could be improved. All patients could be converted into a stable sinus rhythm, and ERAF could be controlled in all cases.
|
References |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionConclusionReferences |
|---|
[1] Levy S., Lauribe P., Dolla E., Kou W., Kadish A., Calkins H., et al. A randomized comparison of external and internal cardioversion of chronic atrial fibrillation. Circulation 1992; 86: 1415–1420.
[2] Paravolidakis K.E., Kolettis T.M., Theodorakis G.N., Paraskevaidis I.A., Apostolou T.S., Kremastinos D.T. Prospective randomized trial of external versus internal transcatheter cardioversion in patients with chronic atrial fibrillation. J Interv Card Electrophysiol 1998; 2: 249–253.[Medline]
[3] Van Gelder I.C., Crijns H.J., Van Gilst W.H., Verwer R., Lie K.I. Prediction of uneventful cardioversion and maintenance of sinus rhythm from direct-current electrical cardioversion of chronic atrial fibrillation and flutter. Am J Cardiol 1991; 68: 41–46.[Web of Science][Medline]
[4] Yu W.C., Lin Y.K., Tai C.T., Hsieh M.H., Chen C.C., et al. Early recurrence of atrial fibrillation after external cardioversion. Pacing Clin Electrophysiol 1999; 22: 1614–1619.[CrossRef][Medline]
[5] Tse H.F., Lau C.P., Ayers G.M. Incidence and modes of onset of early reinitiation of atrial fibrillation after successful internal cardioversion, and its prevention by intravenous sotalol. Heart 1999; 82: 319–324.
[6] Timmermans C., Rodriguez L.M., Smeets J.L.R.M., Wellens H. Immediate reinitiation of atrial fibrillation following internal atrial defibrillation. J Cardiovasc Electrophysiol 1998; 9: 122–128.[Web of Science][Medline]
[7] Garcia Garcia J., Almendral J., Arenal A., Villacastin J., Osende J., Martinez Sande J.L., et al. Internal cardioversion with low-energy shocks in atrial fibrillation resistant to external electrical cardioversion. Rev Esp Cardiol 1999; 52: 180–187.
[8] Zaqqa M., Afshar H., Khoshnevis G.R., Lopez J.A., Massumi A. Low-energy internal cardioversion: Texas Heart Institute experience and review of the literature. Tex Heart Inst J 1999; 26: 114–119.[Medline]
[9] Sra J., Biehl M., Blanck Z., Dhala A., Jazayeri M.R., Deshpande S., et al. Spontaneous reinitiation of atrial fibrillation following transvenous atrial defibrillation. Pacing Clin Electrophysiol 1998; 21: 1105–1110.[CrossRef][Medline]
[10] Bianconi L., Mennuni M., Vjerica L., Castro A., Chieffi M., Santini M. Effects of oral propafenone administration before electrical cardioversion of chronic atrial fibrillation: a placebo-controlled study. J Am Coll Cardiol 1996; 28: 700–706.[Abstract]
[11] Gallagher M.M. and Camm J. Classification of atrial fibrillation. Pacing Clin Electrophysiol 1997; 20: 1603–1605.[CrossRef][Medline]
[12] Mehdirad A.A., Clem K.L., Love C.J., Nelson S.D., Schaal S.F. Improved clinical efficacy of external cardioversion by fluoroscopic electrode positioning and comparison to internal cardioversion in patients with atrial fibrillation. Pacing Clin Electrophysiol 1999; 22: 233–237.[Medline]
[13] Tse H.F., Lau C.P., Ayers G.M. Atrial pacing for suppression of early reinitiation of atrial fibrillation after successful internal cardioversion. Eur Heart J 2000; 21: 1167–1176.
[14] Sopher S.M., Murgatroyd F.D., Slade A.K., Blankoff I., Rowland E., Ward D.E., et al. Low energy internal cardioversion of atrial fibrillation resistant to transthoracic shocks. Heart 1996; 75: 635–638.
CiteULike 
Connotea 
Del.icio.us What's this?
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||