Am Fam Physician. 2004 May 1;69(9):2173-2176.
This clinical content conforms to AAFP criteria for evidence-based continuing medical education (EB CME). EB CME is clinical content presented with practice recommendations supported by evidence that has been systematically reviewed by an AAFP-approved source. The practice recommendations in this activity are available at http://www.clinicalevidence.com/ceweb/conditions/cvd/0210/0210.jsp.
What are the effects of interventions to prevent embolism?
Antithrombotic Treatment Before Cardioversion
We found no randomized controlled trials (RCTs) of aspirin, heparin, or warfarin as thromboprophylaxis before attempted cardioversion in acute atrial fibrillation.
What are the effects of interventions for conversion to sinus rhythm?
TRADE OFF BETWEEN BENEFITS AND HARMS
One RCT found that compared with placebo, intravenous flecainide increased the proportion of people who reverted to sinus rhythm within one hour and in whom the sinus rhythm was maintained after six hours. Flecainide has been associated with serious adverse events such as severe hypotension and torsades de pointes. Two RCTs found that compared with intravenous amiodarone, oral flecainide increased the proportion of people who reverted to sinus rhythm within eight hours. We found insufficient evidence to draw any conclusions about comparisons between intravenous flecainide and intravenous amiodarone and flecainide versus quinidine. Two RCTs found no significant difference between flecainide and propafenone. Flecainide and propafenone are not used in people with known or suspected ischemic heart disease caused by possible proarrhythmic effects.
One systematic review and subsequent RCTs have found that compared with placebo, propafenone increased the proportion of people converting to sinus rhythm within one to four hours. One RCT found no significant difference between intravenous propafenone and amiodarone in the proportion of people converting to sinus rhythm within one hour in people with onset of atrial fibrillation of less than 48 hours. Another RCT found that compared with amiodarone, a higher proportion of people converted to sinus rhythm with oral propafenone within two and one-half hours, but the difference did not remain significant at 24 hours in people with onset of atrial fibrillation of less than two weeks. Two RCTs found no significant difference between flecainide and propafenone. Propafenone and flecainide are not used in people with known or suspected ischemic heart disease caused by possible proarrhythmic effects.
We found insufficient evidence from three RCTs about the effects of amiodarone as a single agent compared with placebo for conversion to sinus rhythm in people with acute atrial fibrillation. Four small RCTs have found no significant difference between amiodarone versus digoxin in rate of conversion to sinus rhythm at 24 to 48 hours, although the studies may have lacked power to exclude clinically important differences. We found insufficient evidence from one small RCT to compare amiodarone with verapamil. We found no RCTs comparing amiodarone with direct current (DC) cardioversion or diltiazem.
We found no RCTs of DC cardioversion in acute atrial fibrillation. It may be unethical to conduct RCTs in people with acute atrial fibrillation and hemodynamic compromise.
We found no RCTs comparing quinidine with placebo. One small RCT in people with onset of atrial fibrillation of less than 48 hours found that compared with sotalol, quinidine plus digoxin increased the proportion of people converting to sinus rhythm within 12 hours.
We found no systematic review or RCTs comparing sotalol with placebo. One small RCT in people with onset of atrial fibrillation of less than 48 hours found that compared with sotalol, quinidine plus digoxin increased the proportion of people converting to sinus rhythm within 12 hours.
UNLIKELY TO BE BENEFICIAL
Three RCTs found no significant difference in conversion to sinus rhythm with digoxin versus placebo in people with atrial fibrillation of up to seven days’ duration. Four small RCTs found no significant difference between amiodarone versus digoxin for conversion to sinus rhythm in people with acute atrial fibrillation, although the trials might have lacked power to exclude clinically important differences.
What are the effects of interventions to control heart rate?
LIKELY TO BE BENEFICIAL
We found no RCTs in people with only acute atrial fibrillation. Two RCTs found that digoxin versus placebo significantly reduced ventricular rate within two hours in people with atrial fibrillation of up to seven days’ duration.
One RCT in people with atrial fibrillation or atrial flutter found that intravenous diltiazem (a calcium channel blocker) reduced heart rate over 15 minutes compared with placebo. Another RCT in people with acute atrial fibrillation or atrial flutter found that intravenous diltiazem reduced heart rate within five minutes compared with intravenous digoxin.
One small RCT in people with atrial fibrillation of unspecified duration found that intravenous timolol (a beta blocker) significantly reduced ventricular rate within 20 minutes compared with placebo.
Two RCTs found that intravenous verapamil (a calcium channel blocker) reduced heart rate at 10 or 30 minutes compared with placebo in people with atrial fibrillation or atrial flutter. One RCT found no significant difference in rate control or measures of systolic function with intravenous verapamil versus intravenous diltiazem in people with atrial fibrillation or atrial flutter, but verapamil caused hypotension in some people.
We found no RCTs examining effects of amiodarone alone on heart rate in people with acute atrial fibrillation.
We found no systematic review or RCTs comparing sotalol with placebo.
Acute atrial fibrillation is rapid, irregular, and chaotic atrial activity of less that 48 hours’ duration. It includes the first symptomatic onset of persistent atrial fibrillation and episodes of paroxysmal atrial fibrillation. It is sometimes difficult to distinguish episodes of new-onset atrial fibrillation from longstanding atrial fibrillation that was previously undiagnosed. Atrial fibrillation within 72 hours of onset is sometimes called recent-onset atrial fibrillation. By contrast, chronic atrial fibrillation is a more sustained form of atrial fibrillation, which in turn can be described as paroxysmal, persistent, or permanent atrial fibrillation. Intermittent atrial fibrillation, with spontaneous recurrences and termination and with sinus rhythm between recurrences, is known as paroxysmal atrial fibrillation. More sustained atrial fibrillation, which is considered amenable to cardioversion, is called persistent atrial fibrillation. If cardioversion is considered inappropriate, then the atrial fibrillation is known as permanent. In this review, we have excluded episodes of atrial fibrillation that arise during or soon after cardiac surgery, and we have excluded management of chronic atrial fibrillation.
We found limited evidence of the incidence or prevalence of acute atrial fibrillation. Extrapolation from the Framingham study1 suggests an incidence in men of three per 1,000 person-years at 55 years of age, rising to 38 per 1,000 person-years at 94 years of age. In women, the incidence was two per 1,000 person-years at 55 years of age and 32.5 per 1,000 person-years at 94 years of age. The prevalence of atrial fibrillation ranged from 0.5 percent for people 50 to 59 years of age to 9 percent in people 80 to 89 years of age. Among acute emergency medical admissions in the United Kingdom, 3 to 6 percent have atrial fibrillation, and about 40 percent were newly diagnosed.2,3 Among acute hospital admissions in New Zealand, 10 percent (95 percent confidence interval, 9 to 12 percent) had documented atrial fibrillation.4
Paroxysms of atrial fibrillation are more common in athletes.5 Age increases the risk of developing acute atrial fibrillation. Men are more likely to develop atrial fibrillation than women (38 years’ follow-up from the Framingham Study, relative risk after adjustment for age and known predisposing conditions 1.5).6 Atrial fibrillation can occur in association with underlying disease (cardiac and noncardiac) or can arise in the absence of any other condition. Epidemiologic surveys have found that risk factors for the development of acute atrial fibrillation include ischemic heart disease, hypertension, heart failure, valve disease, diabetes, alcohol abuse, thyroid disorders, and disorders of the lung and pleura.1 In a U.K. survey of acute hospital admissions with atrial fibrillation, a history of ischemic heart disease was present in 33 percent, heart failure in 24 percent, hypertension in 26 percent, and rheumatic heart disease in 7 percent.3 In some populations, the acute effects of alcohol explain a large proportion of the incidence of acute 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). Observational studies and placebo arms of RCTs have found that more than 50 percent 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 myocardial infarction. We found little evidence about the effects on mortality and morbidity of acute atrial fibrillation where no underlying cause is found. Acute atrial fibrillation during myocardial infarction is an independent predictor of short-and long-term mortality.7 Onset of atrial fibrillation reduces cardiac output by 10 to 20 percent irrespective of the underlying ventricular rate8,9 and can contribute to heart failure. People with acute atrial fibrillation who present with heart failure have a worse prognosis. Acute atrial fibrillation is associated with a risk of imminent stroke.10–13 One case series used transesophageal echocardiography in people who had developed acute atrial fibrillation within the preceding 48 hours; it found that 15 percent had atrial thrombi.14 An ischemic stroke associated with atrial fibrillation is more likely to be fatal, have a recurrence, and leave a serious functional deficit in survivors, than a stroke not associated with atrial fibrillation.15
Gregory Lip has been reimbursed by various pharmaceutical companies for attending conferences and running educational programs and research projects.
search date:February 2003
Adapted with permission from Lip GYH, Freestone B. Atrial fibrillation (acute). Clin Evid Concise 2003; 10:13–6.
editor’s note:Intravenous flecainide is not available in the United States.
1. Benjamin EJ, Wolf PA, Kannel WA. The epidemiology of atrial fibrillation. In: Falk RH, Podrid P, eds. Atrial fibrillation: mechanisms and management. 2d ed. Philadelphia: Lippincott-Raven Publishers, 1997:1–22.
2. Lip GYH, Tean KN, Dunn FG. Treatment of atrial fibrillation in a district general hospital. Br Heart J. 1994;71:92–5.
3. Zarifis J, Beevers DG, Lip GYH. Acute admissions with atrial fibrillation in a British multiracial hospital population. Br J Clin Pract. 1997;51:91–6.
4. 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;29:51–8.
5. Furlanello F, Bertoldi A, Dallago M, et al. Atrial fibrillation in elite athletes. J Cardiovasc Electrophysiol. 1998;9(8 suppl):63–8.
6. 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.
7. Pedersen OD, Bagger H, Kober L, et al. The occurrence and prognostic significance of atrial fibrillation/flutter following acute myocardial infarction. TRACE Study group. TRAn-dolapril Cardiac Evaluation. Eur Heart J. 1999;20:748–54.
8. 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;30:1039–45.
9. Schumacher B, Luderitz B. Rate issues in atrial fibrillation: consequences of tachycardia and therapy for rate control. Am J Cardiol. 1998;82:29N–36N.
10. Peterson P, Godfredson J. Embolic complications in paroxysmal atrial fibrillation. Stroke. 1986;17:622–6.
11. Sherman DG, Goldman L, Whiting RB, et al. Thromboembolism in patients with atrial fibrillation. Arch Neurol. 1984;41:708–10.
12. Wolf PA, Kannel WB, McGee DL, et al. Duration of atrial fibrillation and imminence of stroke: the Framingham study. Stroke. 1983;14:664–7.
13. Corbalan R, Arriagada D, Braun S, et al. Risk factors for systemic embolism in patients with paroxysmal atrial fibrillation. Am Heart J. 1992;124:149–53.
14. Stoddard ME, 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;25:452–9.
15. Lin HJ, Wolf PA, Kelly-Hayes M, et al. Stroke severity in atrial fibrillation. The Framingham Study. Stroke. 1996;27:1760–4.
This is one in a series of chapters excerpted from Clinical Evidence Concise, published by the BMJ Publishing Group, Tavistock Square, London, United Kingdom. Clinical Evidence Concise is published in print twice a year and is updated monthly online. Each topic is revised every eight months, and subscribers should view the most up-to-date version at http://www.clinicalevidence.com. If you are interested in contributing to Clinical Evidence, please contact Claire Folkes (email@example.com). This series is part of the AFP’s CME. See “Clinical Quiz” on page 2055.
Want to use this article elsewhere? Get Permissions