Abstract
Introduction
Acute atrial fibrillation is rapid, irregular, and chaotic atrial activity of recent onset. Various definitions of acute atrial fibrillation have been used in the literature, but for the purposes of this review we have included studies where atrial fibrillation may have occurred up to 7 days previously. Risk factors for acute atrial fibrillation include increasing age, cardiovascular disease, alcohol, diabetes, and lung disease. Acute atrial fibrillation increases the risk of stroke and heart failure. The condition resolves spontaneously within 24 to 48 hours in more than 50% of people; however, many people will require interventions to control heart rate or restore sinus rhythm.
Methods and outcomes
We conducted a systematic review and aimed to answer the following clinical questions: What are the effects of interventions to prevent embolism, for conversion to sinus rhythm, and to control heart rate in people with recent-onset atrial fibrillation (within 7 days) who are haemodynamically stable? We searched: Medline, Embase, The Cochrane Library, and other important databases up to April 2014 (Clinical Evidence reviews are updated periodically; please check our website for the most up-to-date version of this review). We included harms alerts from relevant organisations such as the US Food and Drug Administration (FDA) and the UK Medicines and Healthcare products Regulatory Agency (MHRA).
Results
We found 26 studies that met our inclusion criteria. We performed a GRADE evaluation of the quality of evidence for interventions.
Conclusions
In this systematic review, we present information relating to the effectiveness and safety of the following interventions: amiodarone, antithrombotic treatment before cardioversion, atenolol, bisoprolol, carvedilol, digoxin, diltiazem, direct current cardioversion, flecainide, metoprolol, nebivolol, propafenone, sotalol, timolol, and verapamil.
Key Points
Acute atrial fibrillation is rapid, irregular, and chaotic atrial activity of less than 48 hours' duration. It resolves spontaneously within 24 to 48 hours in more than 50% of people. In this review, we have included studies on patients with onset up to 7 days previously.
Risk factors for acute atrial fibrillation include increasing age, CVD, alcohol abuse, diabetes, and lung disease.
Acute atrial fibrillation increases the risk of stroke and heart failure.
The consensus is that people with haemodynamically unstable atrial fibrillation should have immediate direct current cardioversion. In people who are haemodynamically stable, direct current cardioversion increases reversion to sinus rhythm compared with intravenous propafenone.
There is consensus that antithrombotic treatment with heparin should be given before cardioversion of recent-onset atrial fibrillation to reduce the risk of embolism in people who are haemodynamically stable, but we found no studies to show whether this is beneficial.
Oral or intravenous flecainide, propafenone, or amiodarone increase the likelihood of reversion to sinus rhythm compared with placebo in people with haemodynamically stable acute atrial fibrillation.
CAUTION: Flecainide and propafenone should not be used in people with ischaemic heart disease as they can cause (life-threatening) arrhythmias.
We don't know whether sotalol increases reversion to sinus rhythm in people with haemodynamically stable atrial fibrillation, as few adequate trials have been conducted.
Digoxin does not seem to increase reversion to sinus rhythm compared with placebo. We don't know whether verapamil increases reversion to sinus rhythm compared with placebo.
No one drug has been shown to be more effective at controlling heart rate. However, there is general consensus that intravenous bolus amiodarone is more effective than digoxin.
Treatment with digoxin may control heart rate in people with haemodynamically stable atrial fibrillation, despite its being unlikely to restore sinus rhythm.
We don't know whether diltiazem, timolol, and verapamil are effective at controlling heart rate, but they are unlikely to restore sinus rhythm.
We don't know whether sotalol, bisoprolol, metoprolol, atenolol, nebivolol, or carvedilol are effective at controlling heart rate in people with acute atrial fibrillation who are haemodynamically stable. However, sotalol may cause arrhythmias at high doses.
Clinical context
About this condition
Definition
Acute atrial fibrillation is rapid, irregular, and chaotic atrial activity of recent onset. Various definitions of acute atrial fibrillation have been used in the literature, but for the purposes of this review we have included studies where atrial fibrillation may have occurred up to 7 days previously. Acute atrial fibrillation includes both the first symptomatic onset of chronic or persistent atrial fibrillation and episodes of paroxysmal atrial fibrillation. It is sometimes difficult to distinguish new-onset atrial fibrillation from previously undiagnosed long-standing atrial fibrillation. By contrast, chronic atrial fibrillation is more sustained and can be described as paroxysmal (with spontaneous termination and sinus rhythm between recurrences), persistent, or permanent atrial fibrillation. This review deals with people with acute and recent-onset atrial fibrillation who are haemodynamically stable. The consensus is that people who are not haemodynamically stable should be treated with immediate direct current cardioversion. We have excluded studies in people with atrial fibrillation arising during or soon after cardiac surgery. Diagnosis Acute atrial fibrillation should be suspected in people presenting with dizziness, syncope, dyspnoea, or palpitations. Moreover, atrial fibrillation can contribute to a large number of other non-specific symptoms. Palpation of an irregular pulse is generally only considered sufficient to raise suspicion of atrial fibrillation; diagnosis requires confirmation with ECG. However, in those with paroxysmal atrial fibrillation, ambulatory monitoring may be required.
Incidence/ Prevalence
We found limited evidence on the incidence or prevalence of acute atrial fibrillation. Extrapolation from the Framingham study suggests an incidence in men of 3/1000 person-years at age 55 years, rising to 38/1000 person-years at age 94 years. In women, the incidence was 2/1000 person-years at age 55 years and 32.5/1000 person-years at age 94 years. The prevalence of atrial fibrillation ranged from 0.5% for people aged 50 to 59 years to 9% in people aged 80 to 89 years. Among acute emergency medical admissions in the UK, 3% to 6% had atrial fibrillation, and about 40% of these were newly diagnosed. Among acute hospital admissions in New Zealand, 10% (95% CI 9% to 12%) had documented atrial fibrillation.
Aetiology/ Risk factors
Common precipitants of acute atrial fibrillation are acute MI and the acute effects of alcohol. Age increases the risk of developing acute atrial fibrillation. Men are more likely than women to develop atrial fibrillation (38 years' follow-up from the Framingham Study; RR, after adjustment for age and known predisposing conditions, 1.5). Atrial fibrillation can occur in association with underlying disease (both cardiac and non-cardiac) or can arise in the absence of any other condition. Epidemiological surveys found that risk factors for the development of acute atrial fibrillation include ischaemic heart disease, hypertension, heart failure, valve disease, diabetes, alcohol abuse, thyroid disorders, and disorders of the lung and pleura. In a British survey of acute hospital admissions of people with atrial fibrillation, a history of ischaemic heart disease was present in 33%, heart failure in 24%, hypertension in 26%, and rheumatic heart disease in 7%. In some populations, the acute effects of alcohol explain a large proportion of the incidence of acute atrial fibrillation. Paroxysms of atrial fibrillation are more common in athletes.
Prognosis
Spontaneous reversion: observational studies and placebo arms of RCTs found that more than 50% of people with acute atrial fibrillation revert spontaneously within 24 to 48 hours, especially if atrial fibrillation is associated with an identifiable precipitant such as alcohol or MI. Progression to chronic atrial fibrillation: we found no evidence about the proportion of people with acute atrial fibrillation who develop more chronic forms of atrial fibrillation (e.g., paroxysmal, persistent, or permanent atrial fibrillation). Mortality: we found little evidence about the effects on mortality of acute atrial fibrillation where no underlying cause is found. Acute atrial fibrillation during MI is an independent predictor of both short- and long-term mortality. Heart failure: onset of atrial fibrillation reduces cardiac output by 10% to 20%, irrespective of the underlying ventricular rate, and can contribute to heart failure. People with acute atrial fibrillation who present with heart failure have worse prognoses. Stroke: acute atrial fibrillation is associated with a risk of imminent stroke. One case series using transoesophageal echocardiography in people who had developed acute atrial fibrillation within the preceding 48 hours found that 15% had atrial thrombi. An ischaemic stroke associated with atrial fibrillation is more likely to be fatal, have a recurrence, or leave a serious functional deficit among survivors than a stroke not associated with atrial fibrillation.
Aims of intervention
To reduce symptoms, morbidity, and mortality with minimum adverse effects.
Outcomes
Major outcomes include: thromboembolism, stroke or transient ischaemic attack, major bleeding, mortality, and adverse effects of treatment. Proxy measures include heart rhythm, ventricular rate, and time to restoration of sinus rhythm. The following outcomes are reported in this review: for the question on interventions to prevent embolism: thromboembolic events (thromboembolism, stroke, TIA); for the question on interventions for conversion to sinus rhythm: conversion to sinus rhythm; for the question on interventions to control heart rate: control of heart rate; for all questions: mortality, adverse effects. Frequent spontaneous reversion to sinus rhythm makes it difficult to interpret short-term studies of rhythm; treatments may accelerate restoration of sinus rhythm without increasing the proportion of people who eventually convert. The clinical importance of changes in mean heart rate is also unclear.
Methods
Clinical Evidence search April 2014. The following databases were used to identify studies for this systematic review: Medline 1966 to April 2014, Embase 1980 to April 2014, and The Cochrane Database of Systematic Reviews 2014, issue 4 (1966 to date of issue). Additional searches were carried out in the Database of Abstracts of Reviews of Effects (DARE) and the Health Technology Assessment (HTA) database. We also searched for retractions of studies included in the review. Titles and abstracts of the studies retrieved from the initial search, run by an information specialist, were first assessed against predefined criteria by an evidence scanner. Full texts for potentially relevant studies were discussed with an expert contributor. All data relevant to the review were then extracted by an evidence analyst. Study design criteria for inclusion in this review were: published RCTs and systematic reviews of RCTs in the English language, at least single-blinded, and containing at least 20 individuals (at least 10 per arm), of whom at least 80% were followed up. There was no minimum length of follow-up required to include studies. We excluded all studies described as 'open', 'open label', or not blinded unless blinding was impossible. We included RCTs and systematic reviews of RCTs where harms of an included intervention were studied, applying the same study design criteria for inclusion as we did for benefits. In addition, we use a regular surveillance protocol to capture harms alerts from organisations such as the FDA and the MHRA, which are added to the reviews as required. To aid readability of the numerical data in our reviews, we round many percentages to the nearest whole number. Readers should be aware of this when relating percentages to summary statistics such as relative risks (RRs) and odds ratios (ORs). We have performed a GRADE evaluation of the quality of evidence for interventions included in this review (see table). The categorisation of the quality of the evidence (high, moderate, low, or very low) reflects the quality of evidence available for our chosen outcomes in our defined populations of interest. These categorisations are not necessarily a reflection of the overall methodological quality of any individual study, because the Clinical Evidence population and outcome of choice may represent only a small subset of the total outcomes reported, and population included, in any individual trial. For further details of how we perform the GRADE evaluation and the scoring system we use, please see our website (www.clinicalevidence.com).
Table.
GRADE Evaluation of interventions for Atrial fibrillation (acute onset).
| Important outcomes | Control of heart rate, Conversion to sinus rhythm, Mortality | ||||||||
| Studies (Participants) | Outcome | Comparison | Type of evidence | Quality | Consistency | Directness | Effect size | GRADE | Comment |
| What are the effects of interventions for conversion to sinus rhythm in people with recent-onset atrial fibrillation who are haemodynamically stable? | |||||||||
| 5 (1031) | Conversion to sinus rhythm | Flecainide versus placebo | 4 | –1 | 0 | 0 | 0 | Moderate | Quality point deducted for incomplete reporting of results |
| 4 (727) | Conversion to sinus rhythm | Flecainide versus amiodarone | 4 | –1 | 0 | –1 | 0 | Low | Quality point deducted for incomplete reporting of results; directness point deducted for inclusion of different regimens |
| 3 (919) | Conversion to sinus rhythm | Flecainide versus propafenone | 4 | –1 | –1 | –1 | 0 | Very low | Quality point deducted for incomplete reporting of results; consistency point deducted for conflicting results; directness point deducted for inclusion of different regimens |
| 10 (1226) | Conversion to sinus rhythm | Propafenone versus placebo | 4 | 0 | 0 | 0 | 0 | High | |
| 1 (123) | Conversion to sinus rhythm | Propafenone versus digoxin | 4 | –2 | 0 | 0 | 0 | Low | Quality points deducted for sparse data and short follow-up |
| 4 (at least 500) | Conversion to sinus rhythm | Propafenone versus amiodarone | 4 | 0 | –1 | –1 | 0 | Low | Consistency point deducted for conflicting results; directness point deducted for differences in endpoints and regimens |
| 6 (at least 600) | Conversion to sinus rhythm | Amiodarone versus placebo | 4 | –1 | –1 | –1 | 0 | Very low | Quality point deducted for incomplete reporting of results; consistency point deducted for conflicting results; directness point deducted for difference in regimens |
| 6 (399) | Conversion to sinus rhythm | Amiodarone versus digoxin | 4 | –1 | –1 | 0 | 0 | Low | Quality point deducted for incomplete reporting of results; consistency point deducted for conflicting results |
| 1 (140) | Conversion to sinus rhythm | Amiodarone versus sotalol | 4 | –2 | 0 | 0 | 0 | Low | Quality points deducted for sparse data and incomplete reporting of results |
| 1 (24) | Conversion to sinus rhythm | Amiodarone versus verapamil | 4 | –2 | 0 | 0 | +1 | Moderate | Quality points deducted for sparse data and short follow-up; effect size point added for relative risk (RR) >2 |
| 1 (247) | Conversion to sinus rhythm | Direct current cardioversion versus chemical cardioversion | 4 | 0 | 0 | 0 | 0 | High | |
| 4 (396) | Conversion to sinus rhythm | Digoxin versus placebo | 4 | 0 | 0 | –2 | 0 | Low | Directness points deducted for wide inclusion criteria and for use of different regimens |
| What are the effects of interventions to control heart rate in people with recent-onset atrial fibrillation who are haemodynamically stable? | |||||||||
| 1 (100) | Control of heart rate | Amiodarone versus digoxin | 4 | –2 | –1 | 0 | 0 | Very low | Quality points deducted for sparse data and incomplete reporting of results; consistency point deducted for different results at different endpoints |
| 2 (333) | Control of heart rate | Digoxin versus placebo | 4 | 0 | 0 | –1 | 0 | Moderate | Directness point deducted for wide inclusion criteria |
We initially allocate 4 points to evidence from RCTs, and 2 points to evidence from observational studies. To attain the final GRADE score for a given comparison, points are deducted or added from this initial score based on preset criteria relating to the categories of quality, directness, consistency, and effect size. Quality: based on issues affecting methodological rigour (e.g., incomplete reporting of results, quasi-randomisation, sparse data [<200 people in the analysis]). Consistency: based on similarity of results across studies. Directness: based on generalisability of population or outcomes. Effect size: based on magnitude of effect as measured by statistics such as relative risk, odds ratio, or hazard ratio.
Glossary
- Atrial flutter
A similar arrhythmia to atrial fibrillation, but the atrial electrical activity is less chaotic and has a characteristic saw-tooth appearance on an electrocardiogram.
- Chronic atrial fibrillation
Refers to more sustained or recurrent forms of atrial fibrillation, which can be subdivided into paroxysmal, persistent, or permanent atrial fibrillation.
- High-quality evidence
Further research is very unlikely to change our confidence in the estimate of effect.
- Low-quality evidence
Further research is very likely to have an important impact on our confidence in the estimate of effect and is likely to change the estimate.
- Moderate-quality evidence
Further research is likely to have an important impact on our confidence in the estimate of effect and may change the estimate.
- Paroxysmal atrial fibrillation
If the atrial fibrillation recurs intermittently with sinus rhythm, with spontaneous recurrences or termination, it is designated as 'paroxysmal', and the objective of management is suppression of paroxysms and maintenance of sinus rhythm.
- Permanent atrial fibrillation
If cardioversion is inappropriate, and has not been indicated or attempted, atrial fibrillation is designated as 'permanent', where the objective of management is rate control and antithrombotic treatment.
- Persistent atrial fibrillation
When atrial fibrillation is more sustained than paroxysmal, atrial fibrillation is designated "persistent" and needs termination with pharmacological treatment or electrical cardioversion.
- Very low-quality evidence
Any estimate of effect is very uncertain.
- Wolff–Parkinson–White syndrome
Occurs when an additional electrical pathway exists between the atria and ventricles as a result of anomalous embryonic development. The extra pathway may cause rapid arrhythmias. Worldwide, it affects about 0.2% of the general population. In people with Wolff–Parkinson–White syndrome, beta-blockers, calcium channel blockers, and digoxin can increase the ventricular rate and cause ventricular arrhythmias.
Disclaimer
The information contained in this publication is intended for medical professionals. Categories presented in Clinical Evidence indicate a judgement about the strength of the evidence available to our contributors prior to publication and the relevant importance of benefit and harms. We rely on our contributors to confirm the accuracy of the information presented and to adhere to describe accepted practices. Readers should be aware that professionals in the field may have different opinions. Because of this and regular advances in medical research we strongly recommend that readers' independently verify specified treatments and drugs including manufacturers' guidance. Also, the categories do not indicate whether a particular treatment is generally appropriate or whether it is suitable for a particular individual. Ultimately it is the readers' responsibility to make their own professional judgements, so to appropriately advise and treat their patients. To the fullest extent permitted by law, BMJ Publishing Group Limited and its editors are not responsible for any losses, injury or damage caused to any person or property (including under contract, by negligence, products liability or otherwise) whether they be direct or indirect, special, incidental or consequential, resulting from the application of the information in this publication.
Contributor Information
Gregory Y. H. Lip, University of Birmingham Centre for Cardiovascular Sciences, City Hospital, Birmingham, UK.
Stavros Apostolakis, University of Birmingham Centre for Cardiovascular Sciences, City Hospital, Birmingham, UK.
References
- 1.Lip GY, Tello-Montoliu A. Management of atrial fibrillation. Heart 2006;92:1177–1182. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 2.Camm AJ, Kirchhof P, Lip GY, et al; European Heart Rhythm Association, European Association for Cardio-Thoracic Surgery, ESC Committee for Practice Guidelines. Guidelines for the management of atrial fibrillation: the Task Force for the Management of Atrial Fibrillation of the European Society of Cardiology (ESC). Europace 2010;12:1360–1420. [DOI] [PubMed] [Google Scholar]
- 3.Freestone B, Lip GYH. Epidemiology and costs of cardiac arrhythmias. In: Lip GYH, Godtfredsen J, eds. Cardiac arrhythmias: a clinical approach. Edinburgh, UK: Mosby, 2003:3–24. [Google Scholar]
- 4.Lip GYH, Tean KN, Dunn FG. Treatment of atrial fibrillation in a district general hospital. Br Heart J 1994;71:92–95. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 5.Zarifis J, Beevers DG, Lip GYH. Acute admissions with atrial fibrillation in a British multiracial hospital population. Br J Clin Pract 1997;51:91–96. [PubMed] [Google Scholar]
- 6.Stewart FM, Singh Y, Persson S, et al. Atrial fibrillation: prevalence and management in an acute general medical unit. Aust N Z J Med 1999;29:51–58. [DOI] [PubMed] [Google Scholar]
- 7.Kannel WB, Wolf PA, Benjamin EJ, et al. Prevalence, incidence, prognosis, and predisposing conditions for atrial fibrillation: population-based estimates. Am J Cardiol 1998;82:2N–9N. [DOI] [PubMed] [Google Scholar]
- 8.Furlanello F, Bertoldi A, Dallago M, et al. Atrial fibrillation in elite athletes. J Cardiovasc Electrophysiol 1998;9(8 suppl):S63–S68. [PubMed] [Google Scholar]
- 9.Pedersen OD, Bagger H, Kober L, et al. The occurrence and prognostic significance of atrial fibrillation/flutter following acute myocardial infarction. TRACE Study group. TRAndolapril Cardiac Evaluation. Eur Heart J 1999;20:748–754. [DOI] [PubMed] [Google Scholar]
- 10.Clark DM, Plumb VJ, Epstein AE, et al. Hemodynamic effects of an irregular sequence of ventricular cycle lengths during atrial fibrillation. J Am Coll Cardiol 1997;30:1039–1045. [DOI] [PubMed] [Google Scholar]
- 11.Schumacher B, Luderitz B. Rate issues in atrial fibrillation: consequences of tachycardia and therapy for rate control. Am J Cardiol 1998;82:29N–36N. [DOI] [PubMed] [Google Scholar]
- 12.Petersen P, Godtfredsen J. Embolic complications in paroxysmal atrial fibrillation. Stroke 1986;17:622–626. [DOI] [PubMed] [Google Scholar]
- 13.Sherman DG, Goldman L, Whiting RB, et al. Thromboembolism in patients with atrial fibrillation. Arch Neurol 1984;41:708–710. [DOI] [PubMed] [Google Scholar]
- 14.Wolf PA, Kannel WB, McGee DL, et al. Duration of atrial fibrillation and imminence of stroke: the Framingham study. Stroke 1983;14:664–667. [DOI] [PubMed] [Google Scholar]
- 15.Corbalan R, Arriagada D, Braun S, et al. Risk factors for systemic embolism in patients with paroxysmal atrial fibrillation. Am Heart J 1992;124:149–153. [DOI] [PubMed] [Google Scholar]
- 16.Stoddard MF, Dawkins PR, Prince CR, et al. Left atrial appendage thrombus is not uncommon in patients with acute atrial fibrillation and a recent embolic event: a transesophageal echocardiographic study. J Am Coll Cardiol 1995;25:452–459. [DOI] [PubMed] [Google Scholar]
- 17.Lin HJ, Wolf PA, Kelly-Hayes M, et al. Stroke severity in atrial fibrillation. The Framingham Study. Stroke 1996;27:1760–1764. [DOI] [PubMed] [Google Scholar]
- 18.Klein AL, Jasper SE, Katz WE, et al. The use of enoxaparin compared with unfractionated heparin for short-term antithrombotic therapy in atrial fibrillation patients undergoing transoesophageal echocardiography-guided cardioversion: assessment of Cardioversion Using Transoesophageal Echocardiography (ACUTE) II randomized multicentre study. Eur Heart J 2006;27:2858–2865. [DOI] [PubMed] [Google Scholar]
- 19.Fuster V, Ryden LE, Asinger RW, et al. ACC/AHA/ESC guidelines for the management of patients with atrial fibrillation: executive summary. Circulation 2006;114:e257–e354. [DOI] [PubMed] [Google Scholar]
- 20.Capucci A, Lenzi T, Boriani G, et al. Effectiveness of loading oral flecainide for converting recent onset atrial fibrillation to sinus rhythm in patients without organic heart disease or with only systemic hypertension. Am J Cardiol 1992;70:69–72. [DOI] [PubMed] [Google Scholar]
- 21.Donovan KD, Power BM, Hockings BE, et al. Intravenous flecainide versus amiodarone for recent-onset atrial fibrillation. Am J Cardiol 1995;75:693–697. [DOI] [PubMed] [Google Scholar]
- 22.Donovan KD, Dobb GJ, Coombs LJ, et al. Efficacy of flecainide for the reversion of acute onset atrial fibrillation. Am J Cardiol 1992;70:50A–55A. [DOI] [PubMed] [Google Scholar]
- 23.Boriani G, Biffi M, Capucci A, et al. Conversion of recent-onset atrial fibrillation to sinus rhythm: effects of different drug protocols. Pacing Clin Electrophysiol 1998;21:2470–2474. [DOI] [PubMed] [Google Scholar]
- 24.Romano S, Fattore L, Toscano G, et al. Effectiveness and side effects of the treatment with propafenone and flecainide for recent-onset atrial fibrillation. Ital Heart J Suppl 2001;2:41–45. [In Italian] [PubMed] [Google Scholar]
- 25.Martinez-Marcos FJ, Garcia-Garmendia JL, Ortega-Carpio A, et al. Comparison of intravenous flecainide, propafenone, and amiodarone for conversion of acute atrial fibrillation to sinus rhythm. Am J Cardiol 2000;86:950–953. [DOI] [PubMed] [Google Scholar]
- 26.Akiyama T, Pawitan Y, Greenberg H, et al. Increased risk of death and cardiac arrest from encainide and flecainide in patients after non-Q-wave acute myocardial infarction in the Cardiac Arrhythmia Suppression Trial. CAST Investigators. Am J Cardiol 1991;68:1551–1555. [DOI] [PubMed] [Google Scholar]
- 27.National Institute for Health and Care Excellence. Atrial fibrillation: the management of atrial fibrillation. June 2014. Available at Atrial fibrillation: the management of atrial fibrillation (last accessed 24 November 2014). [Google Scholar]
- 28.Bianconi L, Mennuni M. Comparison between propafenone and digoxin administered intravenously to patients with acute atrial fibrillation. PAFIT-3 Investigators. The Propafenone in Atrial Fibrillation Italian Trial. Am J Cardiol 1998;82:584–588. [DOI] [PubMed] [Google Scholar]
- 29.Boriani G, Biffi M, Capucci A, et al. Oral propafenone to convert recent-onset atrial fibrillation in patients with and without underlying heart disease. A randomized, controlled trial. Ann Intern Med 1997;126:621–625. [DOI] [PubMed] [Google Scholar]
- 30.Azpitarte J, Alverez M, Baun O, et al. Value of a single oral loading dose of propafenone in converting recent-onset atrial fibrillation. Results of a randomized, double-blind controlled study. Eur Heart J 1997;18:1649–1654. [DOI] [PubMed] [Google Scholar]
- 31.Ganau G, Lenzi T. Intravenous propafenone for converting recent onset atrial fibrillation in emergency departments: a randomized placebo-controlled multicentre trial. FAPS Investigators Study Group. J Emerg Med 1998;16:383–387. [DOI] [PubMed] [Google Scholar]
- 32.Botto GL, Bonini W, Broffoni T, et al. Randomized, crossover comparison of oral loading versus intravenous infusion of propafenone in recent-onset atrial fibrillation. Pacing Clin Electrophysiol 1998;21:2480–2484. [DOI] [PubMed] [Google Scholar]
- 33.Kochiadakis GE, Igoumenidis NE, Simantirakis EN, et al. Intravenous propafenone versus intravenous amiodarone in the management of atrial fibrillation of recent onset: a placebo-controlled study. Pacing Clin Electrophysiol 1998;21:2475–2479. [DOI] [PubMed] [Google Scholar]
- 34.Fresco C, Proclemer A, Pavan A, et al. Intravenous propafenone in paroxysmal atrial fibrillation: a randomized, placebo-controlled, double-blind multicenter clinical trial. Paroxysmal Atrial Fibrillation Italian Trial (PAFIT)-2 Investigators. Clin Cardiol 1996;19:409–412. [DOI] [PubMed] [Google Scholar]
- 35.Kochiadakis GE, Igoumenidis NE, Hamilos ME et al. A comparative study of the efficacy and safety of procainamide versus propafenone versus amiodarone for the conversion of recent-onset atrial fibrillation. Am J Cardiol 2007;99:1721–1725. [DOI] [PubMed] [Google Scholar]
- 36.Capucci A, Villani GQ, Aschieri D, et al. Safety of oral propafenone in the conversion of recent onset atrial fibrillation to sinus rhythm: a prospective parallel placebo-controlled multicentre study. Int J Cardiol 1999;68:187–196. [DOI] [PubMed] [Google Scholar]
- 37.Reimold SC, Maisel WH, Antman EM, et al. Propafenone for the treatment of supraventricular tachycardia and atrial fibrillation: a meta-analysis. Am J Cardiol 1998;82:66N–71N. [DOI] [PubMed] [Google Scholar]
- 38.Blanc JJ, Voinov C, Maarek M. Comparison of oral loading dose of propafenone and amiodarone for converting recent-onset atrial fibrillation. PARSIFAL Study Group. Am J Cardiol 1999;84:1029–1032. [DOI] [PubMed] [Google Scholar]
- 39.Podrid PJ, Anderson JL; Propafenone Multicenter Study Group. Safety and tolerability of long term propafenone therapy for supraventricular tachyarrhythmias. Am J Cardiol 1996;78:430–434. [DOI] [PubMed] [Google Scholar]
- 40.Slavik RS, Tisdale JE, Borzak S. Pharmacological conversion of atrial fibrillation: a systematic review of available evidence. Prog Cardiovasc Dis 2001;44:121–152. [DOI] [PubMed] [Google Scholar]
- 41.Hilleman DE, Spinler SA. Conversion of recent onset atrial fibrillation with intravenous amiodarone: a meta-analysis of randomised controlled trials. Pharmacotherapy 2002;22:66–74. [DOI] [PubMed] [Google Scholar]
- 42.Peuhkurinen K, Niemela M, Ylitalo A, et al. Effectiveness of amiodarone as a single oral dose for recent-onset atrial fibrillation. Am J Cardiol 2000;85:462–465. [DOI] [PubMed] [Google Scholar]
- 43.Hofmann R, Steinwender C, Kammler J, et al. Effects of a high dose intravenous bolus amiodarone in patients with atrial fibrillation and a rapid ventricular rate. Int J Cardiol 2006;110:27–32. [DOI] [PubMed] [Google Scholar]
- 44.Thomas SP, Guy D, Wallace E, et al. Rapid loading of sotalol or amiodarone for management of recent onset symptomatic atrial fibrillation: a randomized, digoxin-controlled trial. Am Heart J 2004;147:E3. [DOI] [PubMed] [Google Scholar]
- 45.Hou ZY, Chang MS, Chen CY, et al. Acute treatment of recent-onset atrial fibrillation and flutter with a tailored dosing regimen of intravenous amiodarone. A randomised, digoxin controlled study. Eur Heart J 1995;16:521–528. [DOI] [PubMed] [Google Scholar]
- 46.Cochrane AD, Siddins M, Rosenfeldt FL, et al. A comparison of amiodarone and digoxin for treatment of supraventricular arrhythmias after cardiac surgery. Eur J Cardiothorac Surg 1994;8:194–198. [DOI] [PubMed] [Google Scholar]
- 47.Cowan JC, Gardiner P, Reid DS, et al. A comparison of amiodarone and digoxin in the treatment of atrial fibrillation complicating suspected acute myocardial infarction. J Cardiovasc Pharmacol 1986;8:252–256. [DOI] [PubMed] [Google Scholar]
- 48.Joseph AP, Ward MR. A prospective, randomized controlled trial comparing the efficacy and safety of sotalol, amiodarone, and digoxin for reversion of new-onset atrial fibrillation. Ann Emerg Med 2000;36:1–9. [DOI] [PubMed] [Google Scholar]
- 49.Noc M, Stajer D, Horvat M. Intravenous amiodarone versus verapamil for acute cardioversion of paroxysmal atrial fibrillation to sinus rhythm. Am J Cardiol 1990;65:679–680. [DOI] [PubMed] [Google Scholar]
- 50.Bellone A, Etteri M, Vettorello M, et al. Cardioversion of acute atrial fibrillation in the emergency department: a prospective randomised trial. Emerg Med J 2012;29:188–191. [DOI] [PubMed] [Google Scholar]
- 51.Lown B, Amarasingham R, Neuman J. Landmark article Nov 3, 1962: new method for terminating cardiac arrhythmias. Use of synchronized capacitor discharge. JAMA 1986:256;621–627. [DOI] [PubMed] [Google Scholar]
- 52.McNamara RL, Bass EB, Miller MR, et al. Management of new onset atrial fibrillation. Evidence Report/Technology Assessment No. 12 (prepared by the John Hopkins University Evidence-based Practice Center in Baltimore, MD, under contract no. 290-97-0006). AHRQ publication number 01-E026. Rockville, MD: Agency for Healthcare Research and Quality. January 2001. Search date 1998. [Google Scholar]
- 53.Digitalis in Acute AF (DAAF) Trial Group. Intravenous digoxin in acute atrial fibrillation. Results of a randomized, placebo-controlled multicentre trial in 239 patients. Eur Heart J 1997;18:649–654. [DOI] [PubMed] [Google Scholar]
- 54.Jordaens L, Trouerbach J, Calle P, et al. Conversion of atrial fibrillation to sinus rhythm and rate control by digoxin in comparison to placebo. Eur Heart J 1997;18:643–648. [DOI] [PubMed] [Google Scholar]
- 55.Falk RH, Knowlton AA, Bernard SA, et al. Digoxin for converting recent-onset atrial fibrillation to sinus rhythm. A randomized, double-blinded trial. Ann Intern Med 1987;106:503–506. [DOI] [PubMed] [Google Scholar]
- 56.Schatz I, Ordog GJ, Karody R, et al. Wolff-Parkinson-White syndrome presenting in atrial fibrillation. Ann Emerg Med 1987;16:574–578. [DOI] [PubMed] [Google Scholar]
- 57.Strasberg B, Sagie A, Rechavia E, et al. Deleterious effects of intravenous verapamil in Wolff–Parkinson–White patients and atrial fibrillation. Cardiovasc Drugs Ther 1989;2:801–806. [DOI] [PubMed] [Google Scholar]
- 58.Waxman HL, Myerburg RJ, Appel R, et al. Verapamil for control of ventricular rate in paroxysmal supraventricular tachycardia and atrial fibrillation or flutter: a double-blind randomized cross-over study. Ann Intern Med 1981;94:1–6. [DOI] [PubMed] [Google Scholar]
- 59.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;33:304–310. [DOI] [PubMed] [Google Scholar]
- 60.Klein HO, Pauzner H, Di Segni E, et al. The beneficial effects of verapamil in chronic atrial fibrillation. Arch Intern Med 1979;139:747–749. [PubMed] [Google Scholar]
- 61.Salerno DM, Dias VC, Kleiger RE, et al. Efficacy and safety of intravenous diltiazem for treatment of atrial fibrillation and atrial flutter: the Diltiazem–Atrial Fibrillation/Flutter Study Group. Am J Cardiol 1989;63:1046–1051. [DOI] [PubMed] [Google Scholar]
- 62.Schreck DM, Rivera AR, Tricarico VJ. Emergency management of atrial fibrillation and flutter: intravenous diltiazem versus intravenous digoxin. Ann Emerg Med 1997;29:135–140. [DOI] [PubMed] [Google Scholar]
- 63.Doshan HD, Rosenthal RR, Brown R, et al. Celiprolol, atenolol and propranolol: a comparison of pulmonary effects in asthmatic patients. J Cardiovasc Pharmacol 1986;8(suppl 4):105–108. [PubMed] [Google Scholar]
- 64.Lee TH, Salomon DR, Rayment CM, et al. Hypotension and sinus arrest with exercise-induced hyperkalemia and combined verapamil/propranolol therapy. Am J Med 1986;80:1203–1204. [DOI] [PubMed] [Google Scholar]
- 65.Misra M, Thakur R, Bhandari K. Sinus arrest caused by atenolol–verapamil combination. Clin Cardiol 1987;10:365–367. [DOI] [PubMed] [Google Scholar]
- 66.Yeh SJ, Yamamoto T, Lin FC, et al. Repetitive sinoatrial exit block as the major mechanism of drug-provoked long sinus or atrial pause. J Am Coll Cardiol 1991;18:587–595. [DOI] [PubMed] [Google Scholar]
- 67.Sweany AE, Moncloa F, Vickers FF, et al. Antiarrhythmic effects of intravenous timolol in supraventricular arrhythmias. Clin Pharmacol Ther 1985;37:124–127. [DOI] [PubMed] [Google Scholar]
- 68.Aronow WS, Ferlinz J. Verapamil versus placebo in atrial fibrillation and atrial flutter. Clin Invest Med 1980;3:35–39. [PubMed] [Google Scholar]
- 69.Phillips BG, Gandhi AJ, Sanoski CA, et al. Comparison of intravenous diltiazem and verapamil for the acute treatment of atrial fibrillation and atrial flutter. Pharmacotherapy 1997;17:1238–1245. [PubMed] [Google Scholar]