January 1, 2011 ◆ Volume 83, Number 1
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American Family Physician 61
Atrial Fibrillation: Diagnosis and Treatment
CECILIA GUTIERREZ, MD, and DANIEL G. BLANCHARD, MD, University of California, San Diego, La Jolla, California
younger than 60 years and about 8 per-
cent of patients older than 80 years.3 Atrial
fibrillation is defined as a supraventricular
tachyarrhythmia characterized by uncoor-
dinated atrial activation with consequent
deterioration of mechanical atrial func-
tion.4 Electrocardiographic findings include
the replacement of the normal consistent
P waves (which represent synchronous atrial
activation) with oscillatory or fibrillatory
waves of different sizes, amplitudes, and
timing (Figure 1). The QRS complex remains
narrow unless other conduction abnormali-
ties exist (e.g., bundle branch block, acces-
sory pathways). The ventricular response is
often rapid, between 90 and 170 beats per
Atrial fibrillation is a source of significant
morbidity and mortality because it impairs
cardiac function and increases the risk of
stroke. Its most important clinical impli-
cations are shown in Figure 2. The cost of
caring for patients with atrial fibrillation
is about five times greater than caring for
patients without it.5 Atrial fibrillation is an
trial fibrillation is the most common
cardiac arrhythmia, and its inci-
dence increases with age.1,2 It
affects about 1 percent of patients
independent risk factor for mortality 6,7; it
can also lead to or worsen heart failure and
increase mortality rates in patients who have
had myocardial infarction.8,9
Two mechanisms have been identified in
triggering and maintaining atrial fibrilla-
tion: enhanced automaticity in one or more
depolarizing foci, and reentry involving one
or more aberrant circuits. If it persists, atrial
fibrillation can cause atrial remodeling,
which is characterized by patchy fibrosis;
abnormal and excessive deposition of colla-
gen; fatty infiltration of the sinoatrial node;
molecular changes in ion channels; changes
in depolarization pattern and cellular energy
use; and apoptosis.10,11 Chronic remodeling
leads to irreversible atrial enlargement. The
longer the heart remains in atrial fibrillation,
the more difficult it is to restore normal sinus
rhythm. After a critical point is reached, par-
oxysmal atrial fibrillation self-perpetuates
and becomes persistent.10,11
Different types of atrial fibrillation have dif-
ferent prognoses, morbidity rates, mortal-
ity rates, and treatment options (Table 1).4
Atrial fibrillation is the most common cardiac arrhythmia. It impairs cardiac function and increases the risk of stroke.
The incidence of atrial fibrillation increases with age. Key treatment issues include deciding when to restore normal
sinus rhythm, when to control rate only, and how to prevent thromboembolism. Rate control is the preferred manage-
ment option in most patients. Rhythm control is an option for patients in whom rate control cannot be achieved or who
have persistent symptoms despite rate control. The current recommendation for strict rate control is a resting heart
rate of less than 80 beats per minute. However, one study has shown that more lenient rate control of less than 110 beats
per minute while at rest was not inferior to strict rate control in preventing cardiac death, heart failure, stroke, and life-
threatening arrhythmias. Anticoagulation therapy is needed with rate control and rhythm control to prevent stroke.
Warfarin is superior to aspirin and clopidogrel in preventing stroke despite its narrow therapeutic range and increased
risk of bleeding. Tools that predict the risk of stroke (e.g., CHADS2) and the risk of bleeding (e.g., Outpatient Bleed-
ing Risk Index) are helpful in making decisions about anticoagulation therapy. Surgical options for atrial fibrillation
include disruption of abnormal conduction pathways in the atria, and obliteration of the left atrial appendage. Catheter
ablation is an option for restoring normal sinus rhythm in patients with paroxysmal atrial fibrillation and normal left
atrial size. Referral to a cardiologist is warranted in patients who have complex cardiac disease; who are symptomatic
on or unable to tolerate pharmacologic rate control; or who may be candidates for ablation or surgical interventions.
(Am Fam Physician. 2011;83(1):61-68. Copyright © 2011 American Academy of Family Physicians.)
▲ Patient information:
A handout on atrial fibril-
lation, written by the
authors of this article, is
provided on page 71.
Downloaded from the American Family Physician Web site at www.aafp.org/afp. Copyright © 2010 American Academy of Family Physicians. For the private, noncommercial
62 American Family Physician
Volume 83, Number 1 ◆ January 1, 2011
For example, valvular atrial fibrillation, which is caused
by structural changes in the mitral valve or congeni-
tal heart disease, carries the highest risk of stroke (i.e.,
17 times that of the general population and five times
the risk of stroke with nonvalvular atrial fibrillation).6
Secondary atrial fibrillation is caused by an underlying
condition and is reversible if the condition is treated.
The most common underlying conditions are listed in
Table 2. Atrial fibrillation may occur immediately after
cardiac and thoracic surgery. It is usually self-limited,
but should be treated aggressively if it persists because
of the increased risk of stroke. Lone atrial fibrillation
occurs in patients younger than 60 years who have no
underlying cardiac disease and no identifiable cause.
The prognosis is very good in patients with lone atrial
fibrillation. Paroxysmal atrial fibrillation refers to epi-
sodes of intermittent atrial fibrillation that terminate
spontaneously. Chronic atrial fibrillation is continu-
ous and either cannot be converted back
to normal sinus rhythm or a decision has
been made not to attempt cardioversion.
Persistent atrial fibrillation does not self-
terminate, but may be terminated by electri-
cal or pharmacologic cardioversion.
Atrial fibrillation has a wide spectrum of
clinical presentations. Some patients may
be asymptomatic. Others may present with
stroke, overt heart failure, or cardiovascu-
lar collapse. Patients most commonly report
palpitations, dyspnea, fatigue, lighthead-
edness, and chest pain. Because symptoms
are nonspecific, they cannot be used to
diagnose and determine the onset of atrial
fibrillation.4 If electrocardiography does not
demonstrate atrial fibrillation and a strong
suspicion persists, a Holter or cardiac event
monitor may be needed to document the
Figure 1. Electrocardiogram showing atrial fibrillation. P waves are absent and replaced by irregular electrical
activity. The ventricular rate is irregular and chaotic.
Clinical Implications of Atrial Fibrillation
Figure 2. Flowchart for clinical implications of atrial fibrillation.
Loss of coordinated atrial contraction
Decreased diastolic fillingBlood stasis and
atrial clot formation
Rapid ventricular response
Shorter diastolic fill time
Reduced coronary circulation
and possible ischemia
Decreased cardiac output
Increased stroke risk
Increased morbidity and mortality
January 1, 2011 ◆ Volume 83, Number 1
American Family Physician 63
The first goal is to determine the patient’s cardiac sta-
bility and provide emergency stabilization if needed. If
the patient is unstable because of hypotension, ongo-
ing ischemia, severe heart failure, or cerebrovascular
events, emergency electrical cardioversion is warranted.
If the patient is clinically stable, the history, physical
examination, and diagnostic testing should focus on
potential causes, triggers, and comorbid conditions. Stan-
dard tests used to evaluate cardiac function and identify
common comorbid conditions include electrocardiog-
raphy, complete blood count, complete metabolic pro-
file, thyroid-stimulating hormone measurement, chest
radiography, and echocardiography (Table 3). Echocar-
diography provides information about heart size, cham-
ber sizes, valvular anatomy and function, wall motion
abnormalities, systolic and diastolic function, and peri-
cardial disease. If there is clinical suspicion of myocardial
ischemia, creatine kinase isoenzyme and troponin levels
should be obtained. Select patients may need additional
tests, such as stress testing and electrophysiology studies.4
Two main strategies have been compared in the treatment
of atrial fibrillation: rhythm control and rate control. Data
show that patients assigned to rhythm control have more
hospitalizations from adverse cardiovascular events, more
serious adverse effects from medications, and the same
rate of thromboembolic events compared with patients
assigned to rate control.12-15 Therefore, rate control is rec-
ommended in most patients. Rhythm control remains an
option when rate control is unsuccessful or when symp-
toms persist despite rate control.4,16 Both strategies require
anticoagulation therapy to prevent stroke.
Table 1. Classification of Atrial Fibrillation
Type of atrial
Continuous atrial fibrillation that
is unresponsive to cardioversion;
cardioversion will not be reattempted
Occurs in persons younger than
60 years and in whom no clinical or
echocardiographic causes are found
Not caused by valvular disease, prosthetic
heart valves, or valve repair
Episodes that terminate spontaneously
Paroxysmal atrial fibrillation sustained for
more than seven days, or atrial fibrillation
that terminates only with cardioversion
Two or more episodes of atrial fibrillation
Caused by a separate underlying condition
or event (e.g., myocardial infarction,
cardiac surgery, pulmonary disease,
Information from reference 4.
Table 2. Secondary Causes of Atrial Fibrillation
Congenital heart disease
Infiltrative disease (e.g., amyloid heart disease)
Table 3. Initial Evaluation of Atrial Fibrillation
Chest radiography Identify possible pulmonary disease
(e.g., pneumonia, vascular
congestion, chronic obstructive
Identify comorbid conditions
(e.g., anemia, infection)
Identify electrolyte abnormalities
that may cause or exacerbate atrial
Assess kidney and liver function and
blood glucose level
Assess heart size and shape; chamber
sizes and pressures; valve structure
and function; presence of pericardial
effusion; wall motion abnormalities;
systolic and diastolic function
Diagnose atrial fibrillation and
identify other arrhythmia (e.g.,
atrial flutter, atrial tachycardia)
Identify other cardiac conditions
(e.g., left ventricular hypertrophy,
ischemia, strain, injury)
64 American Family Physician
Volume 83, Number 1 ◆ January 1, 2011
Cardioversion to restore normal sinus rhythm can be
achieved electrically or pharmacologically. Antico-
agulation therapy, before and after cardioversion, is
recommended with either strategy to prevent thrombo-
embolism. Guidelines recommend initiating anticoagu-
lation therapy three weeks before and four weeks after
cardioversion, because thrombi may form as soon as
48 hours after the onset of atrial fibrillation (Figure 3),
and atrial function does not return to normal immedi-
ately after cardioversion to normal sinus rhythm.4 The
atria are often “stunned,” and the risk of stroke is high
for several weeks if warfarin (Coumadin) is not used.17,18
Pharmacologic cardioversion and maintenance of
normal sinus rhythm are difficult to achieve because
of the limited long-term effectiveness of medications,
the risk of triggering ventricular arrhythmias, and the
risk of long-term adverse effects from medication use.
Medications commonly used for cardioversion include
ibutilide (Corvert), flecainide (Tambocor), dofetilide
(Tikosyn), sotalol (Betapace), propafenone (Rythmol),
and amiodarone (Cordarone).4 Older agents such as
quinidine, procainamide, and disopyramide (Norpace)
are rarely used because of adverse effects. Dronedarone
(Multaq), which is a noniodinated derivative of amioda-
rone, has been shown to reduce atrial fibrillation with-
out the long-term serious adverse effects of amiodarone,
but there are concerns about safety in patients with
severe heart failure.19,20
The choice of medication depends on the patient’s car-
diac history. For example, flecainide and propafenone are
preferred in patients with minimal or no heart disease
and preserved left ventricular systolic function, whereas
amiodarone and dofetilide are preferred in patients with
heart failure.4 Patients with paroxysmal atrial fibrilla-
tion may use the “pill-in-the-pocket” approach with
flecainide or propafenone, which involves taking a pill
when an episode begins. This method is often effec-
tive in converting the rhythm to normal, and obviates
the need to take antiarrhythmic medications long term.
Table 4 lists the most commonly used antiarrhythmic
medications, potential adverse effects, and costs.
Decreasing the ventricular response rate, known as rate
control, improves diastolic filling and coronary perfu-
sion, decreases myocardial energy demand, and prevents
tachycardia-mediated cardiomyopathy. Current guide-
lines recommend aiming for a ventricular response of
less than 80 beats per minute at rest and less than 110
beats per minute during exercise.4 However, a recent
randomized controlled trial showed that lenient rate
control, defined as a ventricular rate of less than 110
beats per minute at rest, was not inferior to strict rate
control in preventing cardiac death, heart failure, stroke,
and life-threatening arrhythmias.21
Beta blockers (e.g., metoprolol, esmolol [Brevibloc],
propranolol [Inderal]) and nondihydropyridine calcium
channel blockers (e.g., diltiazem, verapamil) are often
used for rate control. Beta blockers are generally first-
Digoxin is no longer considered a first-line agent for
atrial fibrillation, because studies have shown that it has
little effect during exercise.4 However, it may be used
in conjunction with beta blockers or calcium channel
blockers. Digoxin slows the ventricular rate mostly via
enhancing vagal tone.
In patients with atrial fibrillation, the estimated risk of
stroke without anticoagulation therapy is 5 percent per
year.22 Paroxysmal and chronic atrial fibrillation, treated
by rate or rhythm control, require long-term anticoag-
ulation therapy unless the risks of anticoagulation use
exceed the benefits.4,16
Warfarin, aspirin, and clopidogrel (Plavix) are the
most commonly used oral agents for anticoagulation.
Several trials and a Cochrane review have demonstrated
Figure 3. Transesophageal echocardiographic image of
thrombi (arrows) in the left atrial appendage. (LA = left
atrium; LV = left ventricle; RA = right atrium.)
January 1, 2011 ◆ Volume 83, Number 1
American Family Physician 65
that warfarin is more effective than aspirin but confers a
higher risk of bleeding; that warfarin is superior to aspi-
rin plus clopidogrel, with the same risk of bleeding23-25;
and that adding full-dose aspirin to warfarin should be
avoided because of an increased risk of bleeding.26
Pooled data from five randomized controlled trials
demonstrated that warfarin use reduces the risk of stroke
by about 68 percent,22 whereas data from three random-
ized controlled trials showed that aspirin reduces the
risk of stroke by about 21 percent.27
Table 4. Antiarrhythmic Medications for the Treatment of Atrial Fibrillation
Medication Suggested dosage
Cost of generic
600 to 1,200 mg per day
for one to two weeks,
then taper to lowest
200 mg per day for
400 to 800 mg per day in
$29? ($136) for
Potential adverse effects include abnormal cardiac
conduction, anaphylaxis, heart failure, pulmonary
toxicity, ocular toxicity, thyroid abnormalities,
hypersensitivity reaction, liver failure, lupus,
thrombocytopenia, Stevens-Johnson syndrome
$63 ($198) Potential adverse effects include torsades de pointes,
drug-induced lupus, hepatotoxicity, hypoglycemia,
Potential adverse effects include prolonged QT interval
and various proarrhythmias
Use is restricted to trained prescribers and facilities
In-hospital electrocardiographic monitoring required for
at least three days
Potential adverse effects include various proarrythmias,
torsades de pointes
Not recommended for use in patients with chronic atrial
500 mcg orally every
12 hours at initiation
of therapy, titrate
downward based on QT
100 to 150 mg taken at
onset of atrial fibrillation
May also be taken twice
per day for prevention
of atrial fibrillation
A one-time 1 mg
may repeat once
after 10 minutes if no
$336 ($452) for 1 mg
per 10 mL vial?
Potential adverse effects include polymorphic ventricular
tachycardia, hypotension, headache
Caution is needed in patients with QT prolongation,
hypokalemia, hypomagnesemia, bradycardia
Continuous electrocardiographic monitoring required for
four hours after last dosage
Potential adverse effects include agranulocytosis,
aplastic anemia, coagulation disorder, arrhythmia,
hepatotoxicity, drug-induced lupus
Potential adverse effects include granulocytosis, angina,
chest pain, heart failure, atrioventricular block,
bradyarrhythmias, hypotension, palpitations, sinus
arrest, drug-induced lupus, bronchospasm
Potential adverse effects include various proarrhythmias,
torsades de pointes, hepatoxicity, kidney disease,
myelosuppression, drug-induced lupus
Potential adverse effects include torsades de pointes,
various proarrhythmias, heart failure, bradycardia, heart
Continuous electrocardiographic monitoring required for
three days after initiation of therapy
Avoid in patients with renal insufficiency
Procainamide Up to 50 mg per kg per
day in divided dosages
$37 (NA) for 500 mg
every six hours?
225 to 425 mg orally
every 12 hours
Quinidine324 to 648 mg; one to
two tablets every eight
to 12 hours
80 to 160 mg twice per
NA = not available in designated form.
*—Estimated retail price of one month’s treatment based on information obtained at http://www.drugstore.com (accessed September 8, 2010),
except where noted. Generic price listed first; brand price listed in parentheses. Prices based on lowest suggested dosage.
?—May be available at discounted prices ($10 or less for one month’s treatment) at one or more national retail chains.
?—Estimated cost to the pharmacist based on average wholesale prices in Red Book. Montvale, N.J.: Medical Economics Data; 2010. Cost to the
patient will be higher, depending on prescription filling fee.
66 American Family Physician
Volume 83, Number 1 ◆ January 1, 2011
Warfarin poses significant challenges
because of its narrow therapeutic range, the
need for frequent monitoring, multiple drug
and food interactions, and the risk of bleed-
ing. The warfarin dosage should be adjusted
to achieve a target International Normal-
ized Ratio (INR) of 2 to 3. An INR less than
1.8 doubles the risk of stroke, whereas an
INR greater than 3.5 does not further ben-
efit patients and increases the risk of bleed-
ing.4 Contraindications to warfarin therapy
include hypersensitivity to warfarin, severe
liver disease, recent trauma or surgery, and
As patients age, the risk of experiencing
a thromboembolic event increases, as does
the risk of experiencing adverse effects from
anticoagulation therapy. Balancing these
risks is key to optimizing outcomes.26,28
The stroke risk prediction tool known by the acronym
CHADS2 has been validated in several trials.29,30 CHADS2
uses the following risk factors: congestive heart failure;
hypertension, age 75 years or older, diabetes mellitus,
and stroke or transient ischemic attack. Each risk factor
counts as one point, except for the stroke and transient
ischemic attack risk factor, which counts as two points.
Risk is stratified into high (score of 4 or greater), mod-
erate (score of 2 or 3), and low (score of 0 or 1). Table 5
shows the corresponding stroke rates.16 The CHADS2
tool has limitations; it does not include coronary artery
disease and sex as risk factors, although women are at a
higher risk of thromboembolic events than men.30
The American College of Physicians, the American
Academy of Family Physicians, and the American Col-
lege of Cardiology/American Heart Association/Euro-
pean Society of Cardiology recommend that patients
with nonvalvular atrial fibrillation who are at low risk
of stroke be treated with 81 to 325 mg of aspirin per day,
whereas patients at higher risk should be treated with
warfarin (at a dosage necessary to achieve a target INR
of 2 to 3).4,16 There is general agreement that warfarin
should be recommended in patients with atrial fibrilla-
tion and a CHADS2 score of 2 or greater.
Decisions about the use of warfarin versus aspirin can
be challenging in older patients and in those at risk of
bleeding. The Outpatient Bleeding Risk Index is a vali-
dated tool used to predict the risk of bleeding in patients
taking warfarin.31,32 The Outpatient Bleeding Risk Index
includes four risk factors, each counting as one point: (1)
age older than 65 years; (2) history of stroke; (3) history
of gastrointestinal bleeding; and (4) one or more of the
following: recent myocardial infarction, severe anemia
(hematocrit level less than 30 percent), diabetes, or renal
impairment (serum creatinine level greater than 1.5 mg
per dL [132.6 µmol per L]).32 A score of 0 is considered low
risk, a score of 1 or 2 is intermediate risk, and a score of
3 or 4 is high risk.31 One study evaluating the Outpatient
Bleeding Risk Index found that the risk of major bleed-
ing after one year in low-, intermediate-, and high-risk
patients was 3, 12, and 48 percent, respectively.33 Point-
of-care guides from the American Academy of Family
Physicians are useful tools to assess the risk of stroke and
bleeding using CHADS2, the American College of Chest
Physicians risk assessment, and the Outpatient Bleed-
ing Risk Index. These guides are available at http://www.
aafp.org/afp/2005/0615/p2348.html and http://www.
The anticoagulation agent dabigatran (Pradaxa), a
direct thrombin inhibitor, was recently approved by the
U.S. Food and Drug Administration for the prevention
of stroke and systemic embolism with atrial fibrillation.
In a randomized trial, 150 mg of dabigatran twice per
day was shown to be superior to warfarin in decreas-
ing the incidence of ischemic and hemorrhagic strokes.
Patients assigned to dabigatran had a higher incidence of
myocardial infarction than those assigned to warfarin,
but the difference was not statistically significant.34,35
There are two surgical therapies for atrial fibrillation:
disruption of abnormal conduction pathways in the
atria, and obliteration of the left atrial appendage.
The maze procedure disrupts the initiation and
Table 5. Risk of Stroke Stratified by CHADS2 Score
Adjusted stroke rate*
(95% confidence interval)Risk level
1.9 (1.2 to 3.0)
2.8 (2.0 to 3.8)
4.0 (3.1 to 5.1)
5.9 (4.6 to 7.3)
8.5 (6.3 to 11.1)
12.5 (8.2 to 17.5)
18.2 (10.5 to 27.4)
Aspirin; 81 to 325 mg
target INR of 2 to 3
Warfarin; target INR
of 2 to 3
NOTE: CHADS2 = congestive heart failure; hypertension; age 75 years or older; diabetes
mellitus; stroke or transient ischemic attack. To assess risk, add one point for each
risk factor, except the stroke and transient ischemic attack risk factor, which counts
as two points.
INR = International Normalized Ratio.
*—Expected stroke rate per 100 person-years.
Adapted with permission from Snow V, Weiss KB, LeFevre M, et al. Management
of newly detected atrial fibrillation: a clinical practice guideline from the American
Academy of Family Physicians and the American College of Physicians. Ann Intern
January 1, 2011 ◆ Volume 83, Number 1
American Family Physician 67
conduction of electrical activity of the arrhythmogenic
foci. Incisions are made in both atria to isolate and inter-
rupt the multiple reentry circuits while maintaining the
physiologic activation of the atria.36,37
The rationale for left atrial appendage obliteration is
that more than 90 percent of thrombi form in the left
atrial appendage (Figure 3). If successful, obliteration
decreases the patient’s risk of stroke and potentially
avoids the need for long-term anticoagulation therapy.
Preliminary data on percutaneous left atrial appendage
obliteration show promise, but little long-term follow-up
data are available.38,39 Direct left atrial appendage oblit-
eration is an option in patients who will undergo valvu-
lar surgery, particularly involving the mitral valve.
The discovery of specific foci that trigger atrial fibrilla-
tion (e.g., at or near the pulmonary veins, at the cristae
terminalis, at the coronary sinus ostium) has stimulated
research and development of ablation approaches. In
2009, a systematic review of six trials showed that cath-
eter ablation is effective for up to 12 months as second-
line therapy in patients with minimal cardiac disease
(mean age of 55 years).40 A later study found that ablation
was significantly more effective than medical treatment
for preventing recurrences in patients with intermittent
atrial fibrillation.41 Currently, ablation therapy is a good
option in patients with paroxysmal atrial fibrillation and
normal left atrial size.
Cardiology referral is warranted in the following situa-
tions: (1) when patients have complex cardiac disease;
(2) when they remain symptomatic on pharmacologic
rate control or cannot tolerate pharmacologic rate con-
trol; (3) when they are potential candidates for ablation
or other surgical treatment; or (4) when they require a
pacemaker or defibrillator.
CECILIA GUTIERREZ, MD, is a professor of clinical medicine in the Depart-
ment of Family and Preventive Medicine, and is also the associate director
of the Family Medicine Residency Program at the University of California,
San Diego, School of Medicine in La Jolla.
DANIEL G. BLANCHARD, MD, is a professor of clinical medicine and direc-
tor of the cardiology fellowship program at the University of California,
San Diego, Medical Center. He is chief of clinical cardiology at the Univer-
sity of California, San Diego, Thornton Hospital in La Jolla.
Address correspondence to Cecilia Gutierrez, MD, UCSD School of
Medicine, 950 Gilman Dr., Mail Code 0807, La Jolla, CA 92093 (e-mail:
firstname.lastname@example.org). Reprints are not available from the authors.
Author disclosure: Nothing to disclose.
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developed in collaboration with the European Heart Rhythm Association
SORT: KEY RECOMMENDATIONS FOR PRACTICE
Rate control is the recommended treatment strategy in most patients with atrial fibrillation.
Rhythm control is an option for patients in whom rate control is not achievable or who remain
symptomatic despite rate control.
Rhythm control of atrial fibrillation through electrical or pharmacologic cardioversion requires
anticoagulation therapy three weeks before and four weeks after cardioversion.
Rate control improves diastolic filling and coronary perfusion, decreases myocardial energy demand,
and prevents tachycardia-mediated cardiomyopathy. The goal is to achieve a ventricular response
of less than 80 beats per minute at rest and less than 110 beats per minute during exercise.
Warfarin (Coumadin) is more effective than aspirin in preventing thromboembolic events in
patients with atrial fibrillation, although it confers a higher risk of bleeding. Warfarin is superior to
aspirin plus clopidogrel (Plavix) and confers the same risk of bleeding. Adding full-dose aspirin to
warfarin should be avoided because of the increased risk of bleeding.
Patients with nonvalvular atrial fibrillation who are at low risk of stroke can be treated with 81 to
325 mg of aspirin per day.
C4, 17, 18
A = consistent, good-quality patient-oriented evidence; B = inconsistent or limited-quality patient-oriented evidence; C = consensus, disease-
oriented evidence, usual practice, expert opinion, or case series. For information about the SORT evidence rating system, go to http://www.aafp.
68 American Family Physician
Volume 83, Number 1 ◆ January 1, 2011
and the Heart Rhythm Society [published correction appears in Circula-
tion. 2007;116(6):e138]. Circulation. 2006;114(7):e257-e354.
5. Wu EQ, Birnbaum HG, Mareva M, et al. Economic burden and co-
morbidities of atrial fibrillation in a privately insured population. Curr
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6. Vidaillet H, et al. A population-based study of mortality among patients
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7. Go AS, Hylek EM, Phillips KA, et al. Prevalence of diagnosed atrial fibril-
lation in adults: national implications for rhythm management and
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tion and congestive heart failure and their joint influence on mortality:
the Framingham Heart Study. Circulation. 2003;107(23):2920-2925.
9. Pedersen OD, Abildstrøm SZ, Ottesen MM, et al.; TRACE Study Investi-
gators. Increased risk of sudden and non-sudden cardiovascular death
in patients with atrial fibrillation/flutter following acute myocardial
infarction. Eur Heart J. 2006;27(3):290-295.
10. Allessie M, Ausma J, Schotten U. Electrical, contractile and structural
remodeling during atrial fibrillation. Cardiovasc Res. 2002;54(2):230-246.
11. Aimé-Sempé C, et al. Myocardial cell death in fibrillating and dilated
human right atria. J Am Coll Cardiol. 1999;34(5):1577-1586.
12. Sherman DG, Kim SG, Boop BS, et al.; National Heart, Lung, and Blood
Institute AFFIRM Investigators. Occurrence and characteristics of stroke
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Management (AFFIRM) study. Arch Intern Med. 2005;165(10):1185-1191.
13. Hagens VE, Ranchor AV, Van Sonderen E, et al. Effect of rate or rhythm
control on quality of life in persistent atrial fibrillation. Results from the
Rate Control versus Electrical Cardioversion (RACE) Study. J Am Coll
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parison of rate control and rhythm control in patients with recurrent
persistent atrial fibrillation. N Engl J Med. 2002;347(23):1834-1840.
15. Carlsson J, et al. Randomized trial of rate-control versus rhythm-control
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