Overview of Atrial Fibrillation: "The Electrocardiogram in Atrial Fibrillation", Section On 'Common Findings'

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Overview of atrial fibrillation

Author: Kapil Kumar, MD
Section Editor: Peter J Zimetbaum, MD
Deputy Editor: Gordon M Saperia, MD
All topics are updated as new evidence becomes available and our peer review process is complete.
Literature rev iew current through: Mar 2020. | This topic last updated: Feb 11, 2020.
INTRODUCTION
Atrial fibrillation (AF) is the most common cardiac arrhythmia that has the following
electrocardiographic characteristics (see "The electrocardiogram in atrial fibrillation", section on
'Common findings'):
● The RR intervals follow no repetitive pattern. They have been labeled as "irregularly
irregular."
● While electrical activity suggestive of P waves is seen in some leads, there are no distinct P
waves. Thus, even when an atrial cycle length (the interval between two atrial activations or
the P-P interval) can be defined, it is not regular and often less than 200 milliseconds
(translating to an atrial rate greater than 300 beats per minute).
AF can have adverse consequences related to a reduction in cardiac output and to atrial and
atrial appendage thrombus formation [1-4]. In addition, affected patients may be at increased
risk for mortality. (See 'Long-term outcome' below.)
AF is more prevalent in men and with increasing age (figure 1) [5]. (See "Epidemiology of and
risk factors for atrial fibrillation", section on 'Epidemiology'.)
This topic will provide a broad overview of AF, including the management of the patient. The
reader will be referred to more detailed discussions when appropriate.
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RISK FACTORS AND DISEASE ASSOCIATIONS
Hypertensive heart disease and coronary heart disease (CHD) are the most common underlying
disorders in patients with atrial fibrillation (AF) in developed countries. Rheumatic heart disease,
although now uncommon in developed countries, is associated with a much higher incidence of
AF. (See "Epidemiology of and risk factors for atrial fibrillation", section on 'Chronic disease
associations'.)
PATHOGENESIS
Irrespective of the underlying risk factor(s), changes in the electrophysiology of the atrial
myocardium are likely important. The pathophysiology of atrial fibrillation (AF) is discussed in
detail elsewhere. (See "Epidemiology of and risk factors for atrial fibrillation", section on
'Pathogenesis' and "Mechanisms of atrial fibrillation", section on 'Basic atrial electrophysiology'.)
NONVALVULAR VERSUS VALVULAR HEART DISEASE
Patients with atrial fibrillation may or may not have valvular heart disease. This issue is of
particular importance in choosing antithrombotic therapy; it is discussed in detail elsewhere.
(See "Atrial fibrillation: Anticoagulant therapy to prevent thromboembolism", section on 'Patients
with valvular heart disease'.)
CLASSIFICATION
General classification — Historically, the terms "acute" and "chronic" atrial fibrillation (AF) were
used to describe the temporal nature of a patient’s AF. These two terms have been replaced with
the following classification schema provided in the 2014 American Heart Association/American
College of Cardiology/Heart Rhythm Society guidelines on AF management [6-11]:
● Paroxysmal (ie, self-terminating or intermittent) AF – Paroxysmal AF is defined as AF that

terminates spontaneously or with intervention within seven days of onset. Episodes may
recur with variable frequency. (See "Paroxysmal atrial fibrillation".)
● Persistent AF – Persistent AF is defined as AF that fails to self-terminate within seven days.

Episodes often require pharmacologic or electrical cardioversion to restore sinus rhythm.
While a patient who has had persistent AF can have later episodes of paroxysmal AF, AF is
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generally considered a progressive disease.
● Long-standing persistent AF – AF that has lasted for more than 12 months.
● Permanent AF – "Permanent AF" is a term used to identify individuals with persistent atrial
fibrillation where a joint decision by the patient and clinician has been made to no longer
pursue a rhythm control strategy.
While AF typically progresses from paroxysmal to persistent states, patients can present with
both types throughout their lives. Additionally, this classification applies to recurrent episodes of
AF that last more than 30 seconds and that are unrelated to a reversible cause. If the AF is
secondary to cardiac surgery, pericarditis, myocardial infarction (MI), hyperthyroidism, pulmonary
embolism, pulmonary disease, or other reversible causes, therapy is directed toward the
underlying disease as well as the AF. (See "Epidemiology of and risk factors for atrial
fibrillation".)
Lone atrial fibrillation — The term "lone AF" is less often used than in the past. We and others
do not think that the use of the term improves the understanding of the mechanism of AF or the
care of the patient [12].
Lone AF has generally referred to patients with paroxysmal, persistent, or permanent AF who
have no structural heart disease. It has primarily been applied to patients ≤60 years of age and
identifies a group of individuals at lowest risk of complications associated with AF, including
embolization. By definition, such patients have a CHA2DS2-VASc score of "0". (See "Atrial
fibrillation: Risk of embolization", section on 'Epidemiology'.)
Subclinical atrial fibrillation — Subclinical AF (SCAF) is defined as episodes of AF detected by

intracardiac, implantable, or wearable monitors and confirmed by intracardiac electrogram or
review of the recorded rhythm on the ECG [13]. SCAF usually occurs in individuals without
characteristic symptoms of AF and without a prior diagnosis. Most of these individuals will have
paroxysmal AF. A scientific statement from the American Heart Association on subclinical and
device-detected AF was published in 2019 [13]. (See "Paroxysmal atrial fibrillation", section on
'Signs and symptoms of AF'.)
The prevalence of SCAF depends on the population studied as well as the duration, sensitivity,
and specificity of screening techniques. The following studies investigated the prevalence of
subclinical AF in different populations, using different monitoring techniques:
● In the STROKESTOP observational study of 7173 individuals 75 to 76 years of age in

Sweden, previously unknown AF was detected using intermittent electrocardiographic
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recordings over three weeks in 3 percent [14].
● The ASSERT study monitored (using a dual chamber pacemaker or implantable

cardioverter defibrillator) 2580 patients (65 years or older) with hypertension and no history
of AF for the development of AF (defined as episodes of atrial rate >190 beats per minute for
more than six minutes) [15]. The following findings were noted:
• At three months, subclinical AF was detected in about 10 percent of patients. The

median number of episodes was two, and the median time to detection of the first
episode was 36 days.
• At 2.5 years, SCAF was detected in about 35 percent of individuals. Clinical AF

developed in about 16 percent of patients with SCAF.
• This study also evaluated the relationship between the presence of SCAF and stroke.
This issue is discussed elsewhere. (See "Cryptogenic stroke", section on 'Occult atrial
fibrillation'.)
● In the ASSERT-II study of 256 patients (mean age of 74 years; mean CHA2DS2-VASc score
of 4.1) with an implanted subcutaneous electrocardiographic monitor who were followed for
about 16 months, one or more episodes of SCAF lasting ≥5 minutes occurred in 34 percent
[16]. This was a high-risk population, as 48 percent (of the 256 patients) had prior stroke,
transient ischemic attack, or systemic embolism.
● Two studies have evaluated the prevalence of AF specifically in individuals with cryptogenic
transient ischemic attack or stroke:
• In a study of 56 patients who were evaluated with an outpatient mobile cardiac monitor
for a mean of 21 days, AF was detected in 23 percent [17].
• In a study of 149 patients who were evaluated with either a 24-hour Holter monitor or, if
that study was normal, an event-loop recording device for seven days, AF was detected
in 11 percent [18].
Additional information is as follows:
● Multiple studies have generally found that a higher CHA2DS2-VASc score (table 1) is
predictive [13]. The individual studies were inconsistent regarding the predictive ability of the
individual components of the score.
● SCAF often progresses to clinical AF [19].
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● SCAF is often found in patients with heart failure [13]. (See "The management of atrial
fibrillation in patients with heart failure" and "The management of atrial fibrillation in patients
with heart failure", section on 'Prevalence'.)
● SCAF is associated with an increased risk of stroke. (See "Cryptogenic stroke", section on
'Occult atrial fibrillation'.)
Finally, it is not known whether the approach to anticoagulation in patients with SCAF should be
identical to that in patients with symptoms. This issue is discussed separately. (See "Atrial
fibrillation: Anticoagulant therapy to prevent thromboembolism", section on 'Short duration atrial
fibrillation'.)
PREVENTION
Risk factors for the development of new or recurrent AF have been identified (see "Epidemiology
of and risk factors for atrial fibrillation"). However, for many of these, preventive strategies that
significantly reduce the risk have not been identified. The following are some preventive
strategies:
● There is weak evidence that dietary modifications, such as extra virgin olive oil or n-3
polyunsaturated fatty acids (n-3 PUFA) in fish oil, lower the risk of the development of AF
[20,21].
● The PREDIMED primary prevention trial found that a Mediterranean diet enriched with either
extra virgin olive oil or mixed nuts reduces the incidence of stroke, myocardial infarction, and
cardiovascular mortality [22]. (See "Overview of the prevention of cardiovascular disease
events in those with established disease (secondary prevention) or at high risk", section on
'Diet'.) In a post-hoc analysis of PREDIMED, the group that received the Mediterranean diet
supplemented with extra virgin olive oil had a lower risk of development of AF compared to
the control group (hazard ratio 0.62; 95% CI 0.45-0.85) [23].
● Physical activity and weight loss can significantly reduce AF burden [24,25].
● Alcohol is a modifiable risk factor for AF, and abstinence (or a significant reduction in weekly
consumption) in those who consume an excessive amount appears to decrease the risk of
recurrent AF or the time in AF. The issue was evaluated in a study of 140 symptomatic
patients with paroxysmal or persistent AF who were in sinus rhythm at baseline and who
consumed 10 or more standard drinks per week (about 120 grams of pure alcohol).
Individuals were randomly assigned to alcohol abstention or usual alcohol consumption
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and followed for six months [26]. All patients underwent comprehensive rhythm monitoring.
Individuals in the abstinence group reduced their alcohol intake from 16.8 to 2.1 standard
drinks per week, while those in the usual consumption group reduced their consumption
from 16.4 to 13.2 per week. After a two-week blanking period, AF recurred in 53 and 73
percent of the two groups, respectively, during follow-up. In addition, recurrence of AF was
delayed in the abstinence group, and the AF burden was significantly lower.
EVALUATION
The history, physical examination, and specific laboratory and cardiologic testing are all part of
the evaluation of the patient with atrial fibrillation (AF).
History and physical examination — Not all patients with AF are symptomatic. Among those that
are, symptoms associated with AF are variable and the history should focus on obtaining the
following information:
● A description of the symptoms: onset or date of discovery, the frequency and duration,
severity, and qualitative characteristics.
Typical symptoms include palpitations, tachycardia, fatigue, weakness, dizziness,

lightheadedness, reduced exercise capacity, increased urination, or mild dyspnea. More
severe symptoms include dyspnea at rest, angina, presyncope, or infrequently, syncope. In
addition, some patients present with an embolic event or the insidious onset of heart failure
(as manifested by pulmonary edema, peripheral edema, weight gain, and ascites).
A semi-quantitative method to classify symptoms has been developed, but the clinical utility
of such a system has not been demonstrated [27].
● Precipitating causes: exercise, emotion, or alcohol.
● The presence of the following disease associations: cardiovascular or cerebrovascular

disease, diabetes, hypertension, chronic obstructive pulmonary disease, obstructive sleep
apnea, or potentially reversible causes (eg, hyperthyroidism, excessive alcohol ingestion).
(See "Epidemiology of and risk factors for atrial fibrillation".)
● A complete examination of the cardiovascular system should be performed in all individuals

with newly diagnosed AF and in those with a change in symptom status. Abnormal findings
may inform healthcare providers about either contributing factors for (eg, murmur of mitral
stenosis) or the impact of (eg, evidence of heart failure) AF. (See "Examination of the
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precordial pulsation" and "Auscultation of cardiac murmurs in adults" and "Examination of

the jugular venous pulse" and "Examination of the arterial pulse".)
Electrocardiogram — The electrocardiogram (ECG) is used to verify the presence of AF and is

necessary to make the diagnosis. AF has the following electrocardiographic characteristics (see
"The electrocardiogram in atrial fibrillation", section on 'Common findings'):
● The RR intervals follow no repetitive pattern. They have been labeled as “irregularly
irregular.”
● While electrical activity suggestive of P waves may be seen in some leads, there are no
distinct P waves. Thus, even when an atrial cycle length (the interval between two atrial
activations or the P-P interval) can be defined, it is not regular and often less than 200
milliseconds (translating to an atrial rate greater than 300 beats per minute).
There are a number of potential pitfalls in the electrocardiographic diagnosis of AF. Errors in the
diagnosis of AF are especially common with computerized ECG interpretation and in patients
who are continuously or intermittently paced. Hence, it is important that the automated ECG
interpretation provided by the machine is confirmed by a skilled reader. (See "The
electrocardiogram in atrial fibrillation", section on 'Difficulties in diagnosis'.)
A baseline ECG, preferably in sinus rhythm, should also be evaluated for the following
information:
● Markers of nonelectrical cardiac disease, such as left ventricular hypertrophy (possible

hypertension) or Q waves (possible coronary artery disease).
● Markers of electrical heart disease, including the presence of ventricular pre-excitation or

infranodal conduction disease (bundle branch block).
● The QT interval (to identify the potential risk of antiarrhythmic therapy)
● Evidence of severe bradycardia or sinus node dysfunction
Echocardiogram — The transthoracic echocardiogram (TTE) is performed to evaluate the size

of the right and left atria and the size and function of the right and left ventricles; to detect
possible valvular heart disease, left ventricular hypertrophy, and pericardial disease; and to
assess peak right ventricular pressure.
The TTE may also identify left atrial thrombus, although the sensitivity is low. Transesophageal
echocardiography is much more sensitive for identifying thrombi in the left atrium or left atrial
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appendage and can be used to determine the need for anticoagulation prior to any attempt at
pharmacologic or electrical cardioversion. (See "Role of echocardiography in atrial fibrillation"
and 'Prevention of systemic embolization' below.)
Additional cardiac testing — Exercise testing is reasonable for patients with signs or
symptoms of ischemic heart disease. It is also useful to help guide pharmacotherapy for AF, as
some antiarrhythmic medications are contraindicated in patients with coronary artery disease. In
addition, stress testing may be helpful in gauging adequacy of heart rate control in AF during
exercise. Insufficient heart rate control in AF is a major factor for exercise intolerance in AF. (See
"Antiarrhythmic drugs to maintain sinus rhythm in patients with atrial fibrillation:
Recommendations", section on 'Selecting an antiarrhythmic drug'.)
Ambulatory cardiac monitoring with event recorders, adhesive extended time event monitors, or
insertable cardiac monitors (ICM; also sometimes referred to as implantable cardiac monitor or
implantable loop recorder) can be used to identify the arrhythmia if it is intermittent and not
captured on routine electrocardiography. Ambulatory ECG monitoring can also be utilized to
correlate symptoms to the arrhythmia along with assessment of the AF burden. Twenty-four- to
48-hour Holter monitoring mainly aids in the evaluation of overall ventricular response rates in
individuals where a rate control strategy has been chosen and there is concern for inadequate
heart rate control or bradycardia. (See "Ambulatory ECG monitoring".)
Baseline laboratory testing — Clinical or subclinical hyperthyroidism is present in less than 5

percent of patients with AF [28]. A thyroid-stimulating hormone (TSH) and free T4 levels should
be obtained in all patients with a first episode of AF, or in those who develop an increase in AF
frequency. (See "Epidemiology of and risk factors for atrial fibrillation", section on
'Hyperthyroidism'.)
Other important baseline tests include a complete blood count, a serum creatinine, and a test
for diabetes mellitus [29].
TREATMENT ISSUES
Healthcare providers are presented with two broad types of patients with atrial fibrillation (AF):
those with newly diagnosed AF and those who have been previously diagnosed and managed.
Care of the former includes decisions regarding the need for anticoagulation and the choice
between rate or rhythm control strategies. For patients with established diagnosis, periodic
assessment of the adequacy of treatment is necessary.
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Hospitalization — Some patients with AF may require care at an acute care facility or an inpatient
unit of a hospital. Common indications for care at one or both of these facilities include:
● Management of heart failure, hypotension, or difficulty with rate control.
● Initiation of antiarrhythmic drug therapy.
● Treatment of an associated medical problem, which is often the reason for the arrhythmia.
Examples include the treatment of hypertension, infection, thyroid storm, exacerbation of
chronic obstructive pulmonary disease, pulmonary embolism, persistent myocardial
ischemia, or acute pericarditis.
Other indications for hospitalization are discussed separately. (See "New onset atrial fibrillation",
section on 'Indications for hospitalization'.)
New onset atrial fibrillation — Most patients with new onset (ie, first detected or diagnosed) AF
present with symptoms related to the arrhythmia. (See 'History and physical examination' above.)
Except for embolization, the symptoms associated with new onset AF are primarily due to a rapid
ventricular response. Thus, many patients have dramatic improvement in their sense of well-
being when the ventricular rate is slowed. (See "New onset atrial fibrillation", section on 'Rate
control'.)
There are two broad management issues that must be addressed early in patients with new
onset AF: the prevention of systemic embolization and the choice between a rhythm or rate
control strategy, both of which may improve symptoms. These issues will be addressed briefly
here. More detailed discussions are found elsewhere. (See "Rhythm control versus rate control
in atrial fibrillation" and "Atrial fibrillation: Anticoagulant therapy to prevent thromboembolism".)
Prevention of systemic embolization — Every patient with AF should be evaluated for the
need of antithrombotic therapy to prevent systemic embolization even for the first AF episode.
This is accomplished by use of the CHA2DS2-VASc score (table 1). Patients who require
antithrombotic therapy include those in whom cardioversion (whether electrically or
pharmacologically) to sinus rhythm is being considered (regardless of the CHA2DS2-VASc score
or method of cardioversion [electrical or pharmacologic]) and those who meet criteria for long-
term anticoagulation. All patients whose risk of embolization exceeds the risk of bleeding are
candidates for long-term antithrombotic therapy. These issues are discussed in detail
elsewhere. (See "Prevention of embolization prior to and after restoration of sinus rhythm in atrial
fibrillation" and "Atrial fibrillation: Anticoagulant therapy to prevent thromboembolism".)
Rate versus rhythm control — Most patients who present with AF will require slowing of the
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ventricular rate to improve symptoms. (See "Control of ventricular rate in atrial fibrillation:
Pharmacologic therapy".)
Once ventricular rate control is achieved, a decision regarding the long-term management
(rhythm versus rate control) of AF should be made. A rhythm control strategy uses either
antiarrhythmic drug therapy, percutaneous catheter ablation, and/or a surgical procedure.
Electrical cardioversion may be necessary to restore sinus rhythm. Antiarrhythmic medications
are generally started before cardioversion and continued to maintain sinus rhythm (in the event
of AF recurrence). (See "Surgical ablation to prevent recurrent atrial fibrillation", section on 'Maze
procedure' and "Atrial fibrillation: Catheter ablation", section on 'Efficacy'.)
A rate control strategy generally uses drugs that slow conduction across the atrioventricular (AV)
node, such as beta blockers, non-dihydropyridine calcium channel blockers, or digoxin. (See
"Rhythm control versus rate control in atrial fibrillation", section on 'Definitions'.)
Data suggest that rhythm and rate control strategies are associated with similar rates of
mortality and serious morbidity, such as embolic risk. However, there are several reasons why
pursuing a rhythm-control strategy would be preferred, including symptom improvement,
younger patient age, and irreversible structural and electrical remodeling that can occur with
longstanding persistent AF. (See "Rhythm control versus rate control in atrial fibrillation", section
on 'Comparative studies'.)
The decision to adopt a rhythm or rate control strategy is often dictated by the (1) presence of
symptoms associated with atrial fibrillation and/or (2) development of left ventricular systolic
dysfunction thought secondary to the arrhythmia. Some patients with new onset AF who report
being asymptomatic may have some subtle symptoms such as fatigue, especially when
palpitations are not a prominent component of the presentation. These more subtle symptoms
are sometimes only realized after restoration of sinus rhythm, which is why many physicians will
at least offer a rhythm control approach to new onset AF patients. (See "Rhythm control versus
rate control in atrial fibrillation", section on 'Preference for rate control' and "Rhythm control
versus rate control in atrial fibrillation", section on 'Preference for rhythm control'.)
The methods to achieve either rate or rhythm control are discussed in detail elsewhere. (See
"New onset atrial fibrillation" and "Antiarrhythmic drugs to maintain sinus rhythm in patients with
atrial fibrillation: Recommendations" and "Atrial fibrillation: Cardioversion" and "Antiarrhythmic
drugs to maintain sinus rhythm in patients with atrial fibrillation: Clinical trials" and "Control of
ventricular rate in atrial fibrillation: Nonpharmacologic therapy" and "Control of ventricular rate in
atrial fibrillation: Pharmacologic therapy" and "Surgical ablation to prevent recurrent atrial
fibrillation" and "Atrial fibrillation: Catheter ablation".)
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Paroxysmal, persistent, longstanding persistent, or permanent atrial fibrillation — Patients

with paroxysmal, persistent, longstanding persistent, or permanent AF will need periodic care as
well as occasional urgent evaluation during the natural history of their disease. (See
'Classification' above.)
We suggest routine follow-up every 12 months in stable patients and sooner if there are
changes in symptoms. Patients on high-risk antiarrhythmic therapy, such as dofetilide or sotalol,
are often seen every six months.
Routine care — From time to time, patients should be monitored for the following:
● Efficacy and safety of antithrombotic therapy (International Normalized Ratio for patients on
warfarin and creatinine clearance for patients on antiarrhythmic therapy and other newer
anticoagulants). (See "Atrial fibrillation: Anticoagulant therapy to prevent thromboembolism",
section on 'Select an anticoagulant'.)
● Functional status, including change in symptoms (history).
● Efficacy and safety of antiarrhythmic drug therapy (electrocardiogram [ECG], assessment of

renal and hepatic function, and perhaps other tests). (See "Antiarrhythmic drugs to maintain
sinus rhythm in patients with atrial fibrillation: Recommendations".)
● Efficacy of rate control (history, ECG, and perhaps extended Holter monitoring). (See
"Control of ventricular rate in atrial fibrillation: Pharmacologic therapy".)
Urgent care — Urgent care is necessary in patients who present with symptoms or signs of
symptomatic AF. (See 'History and physical examination' above.)
In addition to evaluating the efficacy of rate or rhythm control, the healthcare provider may need to
evaluate and manage changes in the symptoms and signs of coronary artery disease or heart
failure.
LONG-TERM OUTCOME
Recurrence of atrial fibrillation — Continuous monitoring studies have shown that

approximately 90 percent of patients have recurrent episodes of atrial fibrillation (AF) [30].
However, up to 90 percent of episodes are not recognized by the patient [31], and asymptomatic
episodes lasting more than 48 hours are not uncommon, occurring in 17 percent of patients in a
report using continuous monitoring [30]. The latter study also showed that 40 percent of patients
had episodes of AF-like symptoms in the absence of AF [30]. (See "Paroxysmal atrial
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fibrillation".)
Embolization — Systemic embolization, and particularly stroke, is the most frequent major
complication of AF. This issue is discussed separately. (See "Atrial fibrillation: Risk of
embolization" and "Atrial fibrillation: Anticoagulant therapy to prevent thromboembolism".)
Silent cerebral ischemia — Silent cerebral ischemia (SCI) occurs in a patient who has
specific lesions on imaging studies in the absence of clinical complaints or findings. These
lesions have a radiographic appearance consistent with cerebral infarction.
In a systematic review and meta-analysis of 17 studies, the overall prevalence of SCI lesions on
magnetic resonance imaging and computed tomography among patients with AF was 40 and
22 percent, respectively [32]. In this review, AF was associated with more than a twofold
increased risk of SCI in patients with no history of symptomatic stroke (odds ratio, 2.62, 95% CI
1.81-3.80) in 11 studies. However, most studies pooled in this meta-analysis were cross-
sectional, making uncertain the causal link between AF and silent cerebral infarction.
The potential relationship of SCI to cognitive performance in patients with AF was studied in a
registry that included 90 patients with paroxysmal and 90 patients with persistent AF, as well as
90 matched controls [33]. Patients received clinical assessment, which included a medical
history, physical examination with standardized neurologic examination, brain magnetic
resonance imaging, and the Repeatable Battery for the Assessment of Neuropsychological
Status (RBANS) test for cognitive impairment [34]. At least one SCI was present in 89, 92, and 46
percent of the three groups, respectively (p<0.01 for both groups compared to controls), and the
number of SCI lesions per person was significantly higher in the persistent group than the
paroxysmal group (with both groups higher than controls). Cognitive impairment was
significantly greater in persistent and paroxysmal AF patients compared to controls.
Further evidence in support of the relationship between AF and development of dementia, as

well as the impact of anticoagulation, comes from two population cohort studies. Age- and sex-
matched individuals from the United Kingdom Clinical Practice Research Datalink (2008 to
2016) with and without a diagnosis of AF were selected and followed for development of new
dementia [35]. Over 193,082 person-years, the AF group had a higher rate of
dementia. Furthermore, after excluding patients with a history of transient ischemic attack/stroke,
only those AF patients not on anticoagulants had a significantly higher rate of dementia than
non-AF patients (adjusted HR 1.42, 95% CI 1.18–1.72 without anticoagulation and HR 1.09, 95%
CI 0.87–1.36 with anticoagulation). Anticoagulation protected against the development of
dementia, presumably by a reduction of SCI. Similarly, 2685 dementia-free participants from the
Swedish National Study on Aging and Care were followed for nine years [36]. AF was associated
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with a significantly faster annual Mini-Mental State Examination decline and an increased HR of
all-cause dementia (HR 1.40, 95% CI 1.11-1.77) and vascular and mixed dementia (HR 1.88,
95% CI 1.09-3.23), but not Alzheimer disease (HR 1.33, 95% CI 0.92-1.94). In addition, the use
of anticoagulants, but not antiplatelet medications, was associated with a 60 percent decrease
in the risk of cognitive decline (HR 0.40, 95% CI 0.18-0.92).
It is unclear if episodes of AF are acute triggers of stroke or if AF is simply a marker of left atrial
dysfunction that predisposes an increased risk for stroke [37]. This was highlighted in an
analysis of the ASSERT trial that showed very few individuals with subclinical AF who developed
a stroke had AF in the month prior to their embolic event [38]. Another concern is that patients
with paroxysmal AF felt to be at high risk for stroke also have a high risk for atherosclerosis, and
as indicated above, there may be other non-cardiac reasons for stroke in these patients,
especially aortic plaques.
Mortality — AF is an independent risk factor for mortality across a wide age range and in both
men and women. However, we and others believe the evidence is insufficient to label AF as
causal [39]. The following studies illustrate the range of risk:
● In a secondary analysis of the randomized controlled AFFIRM trial of rhythm versus rate
control in AF, the presence of sinus rhythm was associated with a significant reduction in
mortality (hazard ratio 0.53) [40]. A similar benefit from being in sinus rhythm (relative risk
0.44) was noted in the DIAMOND trial that compared dofetilide to placebo in patients with
reduced left ventricular function [41].
● In a retrospective observational study of 272,186 patients with incidental AF at the time of

hospitalization and 544,344 matched AF-free controls, the adjusted relative risk of death for
women and men <65 years was 2.15 and 1.76 (respectively); 65 to 74 years was 1.72 and
1.36; and 75 to 85 years was 1.44 and 1.24 [42]. All values were statistically significant.
● In a report from the Framingham Heart Study 621 subjects between the ages of 55 and 94
who developed AF were compared to those who did not [43]. AF almost doubled the risk of
death in both men and women (figure 2). After adjustment for the pre-existing cardiovascular
diseases with which AF was associated, AF was still associated with a significantly
increased risk of death (odds ratio 1.9 for women and 1.5 for men). Both heart failure (HF)
and stroke contributed to the excess mortality.
● In a 20-year follow-up of over 15,000 men and women between the ages of 45 and 64 in
which 47 women and 53 men had AF on a single electrocardiogram (ECG) at baseline, the
presence of AF was associated with a marked increase in the risk of a cardiovascular event
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(death or hospitalization) (89 versus 27 percent in women and 66 versus 45 percent in men)
and was a significant independent predictor of all-cause mortality (relative risk 2.2 in women
and 1.5 in men) [44].
In a post-hoc analysis of the Women’s Health Study of 34,772 women with a median age of 53
who were free of AF, about 3 percent developed AF at a median follow-up of 15.4 years [45]. New
onset AF was associated with a significantly increased adjusted risk of all-cause,
cardiovascular, and non-cardiovascular mortality (hazard ratios [HR] 2.14, 95% CI 1.64-2.77;
4.18, 95% CI 2.69-6.51; and 1.66, 95% CI 1.19-2.30, respectively). Adjustment for nonfatal
cardiovascular events, such as myocardial infarction, stroke, or heart failure, lowered these risks
but incident AF remained significantly associated with all types of mortality (HR 1.7, 2.57, and
1.42, respectively).
The coexistence of cardiovascular disease and chronic AF worsens the patient's prognosis,
doubling the cardiovascular mortality [46]:
● In patients with a recent myocardial infarction (MI), the development of AF increases

mortality [47,48]. This effect is primarily due to associated risk factors, such as HF and
cardiogenic shock, not AF itself [48,49].
● The effect of AF in the setting of HF is less clear, since published studies have yielded
conflicting results and any effect of AF to increase mortality may have diminished with better
treatment of HF. (See "The management of atrial fibrillation in patients with heart failure",
section on 'Prevalence'.)
In addition, in an observational study of over 20,000 individuals in two cohorts, incident AF was
associated with an increased risk of sudden cardiac death (hazard ratio 2.47, 95% CI 1.95-3.13)
as well as non-sudden cardiac death (hazard ratio 2.98, 95% CI 2.52-3.53) [50]. This study
reconfirms that AF is associated with increased all-cause mortality (with death often attributable
to events related to coronary artery disease and stroke) and it advances our knowledge in that it
demonstrates that there is a proportional increase in sudden death as well.
None of these nonrandomized observations prove that AF directly causes an increase in

mortality, since they cannot distinguish this possibility from AF being a marker of a confounding
factor or factors that affect survival.
The specific causes of death, as well as their frequency and predictors, were evaluated using
follow-up data from the RE-LY trial comparing dabigatran to warfarin [51]. (See "Atrial fibrillation:
Anticoagulant therapy to prevent thromboembolism", section on 'Select an anticoagulant'.)
Among 18,113 randomized patients with a median follow-up of two years, the annual mortality
14 of 28 4/24/2020, 11:02 PM
rate was 3.84 percent. Cardiac deaths (sudden cardiac death and progressive heart failure)
accounted for 37.4 percent of these; stroke and hemorrhagic death accounted for 9.9 percent.
Predictors of poor outcome — In the RE-LY trial (see 'Mortality' above), the strongest
independent clinical predictors of cardiac death were heart failure, intraventricular conduction
delay on an electrocardiogram, and prior myocardial infarction [51].
In a post-hoc analysis of the RACE II trial, the risk of cardiovascular morbidity and mortality was
highest in those with the greatest symptom burden as assessed with the Toronto AF Severity
Scale [52]. This finding was driven by the increased rate of heart failure hospitalizations.
Beta-trace protein (BTP), which is found in myocardial cells, is a proposed marker for renal
damage. (See "Chronic kidney disease and coronary heart disease", section on 'Cystatin C and
other markers of kidney function'.) In a study of 1279 anticoagulated AF patients, elevated BTP
was associated with mortality (hazard ratio 2.08, 95% CI 1.49-2.90), even after adjusting for
CHA2DS2-VASc factors (table 1) and renal function [53]. The significance of this association will
need to be validated in larger, independent cohorts. The findings are intriguing and potentially
point to a risk factor that has yet to be recognized by the CHA2DS2-VASc score. (See "Atrial
fibrillation: Risk of embolization", section on 'Options for estimating risk in the individual patient'.)
Myocardial infarction — MI is a risk factor for AF. (See "Epidemiology of and risk factors for atrial
fibrillation", section on 'Coronary disease'.)
Although there have been observations of MI after AF, including proven cases of MI due to
thromboembolism, the association between AF and MI has not been formally evaluated [54,55].
This relationship was evaluated using data from the prospective cohort (the REGARDS cohort)
study of nearly 24,000 United States citizens without coronary heart disease [56]. After
adjustment for multiple risk factors, AF at baseline was associated with an increased risk of
incident MI (hazard ratio [HR] 1.70, 95% CI 1.26-2.30). In subgroup analysis, the risk was
significantly higher in women and blacks (HR 2.16 and 2.53) but not men or whites.
Mechanisms to explain the relationship are speculative.
SCREENING/DETECTION
Despite the known increase in morbidity, such as stroke, and mortality in patients with atrial
fibrillation (AF), the issues of how or whether to screen for AF have not been well studied.
However, no studies have demonstrated better outcomes with a screening strategy [57]. We and
others do not recommend screening asymptomatic patients for AF [58,59].
15 of 28 4/24/2020, 11:02 PM
Patients with an irregular pulse at the time of a physical examination should have an
electrocardiogram (ECG) performed to determine its cause. The approach to patients with
palpitations is presented separately. (See "Evaluation of palpitations in adults", section on
'Ambulatory cardiac rhythm monitoring'.)
A 2018 United States Preventive Services Task Force (USPSTF) review of randomized trials and
observational studies (17 studies and 135,300 patients age 65 years and older) found that
systematic screening with electrocardiogram (ECG) identified more cases of AF than no
screening (absolute increase from 0.6 to 2.8 percent over 12 months) [57]. Systematic screening
with ECG did not detect more cases than a systematic approach using pulse palpation (two
trials and 17,803 patients).
A number of potential tools (including wearable devices) to screen for AF have been developed
and evaluated. Using these tools, many individuals with asymptomatic, paroxysmal AF are
identified. The following are two examples:
● The mSToPS trial randomly assigned 2659 individuals with risk factors for AF to immediate
continuous active monitoring with a wearable, self-applied patch for two weeks or to delayed
monitoring at four months [60]. Immediate active monitoring found a higher rate of a new
diagnosis of AF at four months compared with delayed monitoring (3.9 versus 0.9 percent;
absolute difference 3 percent, 95% CI 1.8-4.1 percent). Although a higher incidence of AF
was found with this monitoring tool, treatment based on this information has not been
studied.
● The Apple Heart Study evaluated a novel technology for the detection of AF [61]. Over
400,000 individuals without a history of AF who owned both an Apple Watch and iPhone
were recruited to participate. The watch is capable of detecting irregular heart rhythms using
an optical sensor that uses pulse wave data. Participants downloaded an iPhone
application that identifies episodes (recorded by the watch) suggestive of AF and prompted
them to initiate a telemedicine visit. If possibility of AF was confirmed, participants were sent
an ECG patch to wear for seven days. In the study, 419,297 participants were recruited, 2161
received irregular pulse notification, 658 had an ECG patch sent to them, and 450 returned
the patch containing data that could be analyzed. (See "Ambulatory ECG monitoring",
section on 'Patch monitor'.)
AF was present in 34 percent of patients who returned the patch. Among those who were notified
of an irregular pulse on the watch, 84 percent were concordant with AF; that is, the positive
predictive value for AF was 0.84.
16 of 28 4/24/2020, 11:02 PM
This study provides evidence that the technology used could be adapted for the detection,
screening, evaluation and treatment of AF. Further research is in process. However, as
mentioned in the opening paragraph of this section, there are no good data that intervention
based on screening with this or other similar device improves clinical outcomes. For patients
who have downloaded the application used in the trial and are concerned that they might have
findings suggestive of AF, it is reasonable to use traditional methods (such as ambulatory
monitoring) to detect AF. (See "Evaluation of palpitations in adults", section on 'Ambulatory
cardiac rhythm monitoring'.)
The role of evaluating patients with cryptogenic stroke for AF is discussed separately. (See
"Cryptogenic stroke", section on 'Occult atrial fibrillation'.)
SOCIETY GUIDELINE LINKS
Links to society and government-sponsored guidelines from selected countries and regions
around the world are provided separately. (See "Society guideline links: Atrial fibrillation" and
"Society guideline links: Arrhythmias in adults".)
INFORMATION FOR PATIENTS
UpToDate offers two types of patient education materials, “The Basics” and “Beyond the Basics.”
The Basics patient education pieces are written in plain language, at the 5 th to 6th grade reading
level, and they answer the four or five key questions a patient might have about a given condition.
These articles are best for patients who want a general overview and who prefer short, easy-to-
read materials. Beyond the Basics patient education pieces are longer, more sophisticated, and
more detailed. These articles are written at the 10 th to 12th grade reading level and are best for
patients who want in-depth information and are comfortable with some medical jargon.
Here are the patient education articles that are relevant to this topic. We encourage you to print or
e-mail these topics to your patients. (You can also locate patient education articles on a variety of
subjects by searching on “patient info” and the keyword(s) of interest.)
● Basics topics (see "Patient education: Atrial fibrillation (The Basics)" and "Patient education:
Medicines for atrial fibrillation (The Basics)" and "Patient education: Coping with high drug
prices (The Basics)" and "Patient education: Heart failure and atrial fibrillation (The Basics)")
● Beyond the Basics topics (see "Patient education: Atrial fibrillation (Beyond the Basics)" and
17 of 28 4/24/2020, 11:02 PM
"Patient education: Coping with high drug prices (Beyond the Basics)")
SUMMARY
The following are essential points addressed in this topic:
● Atrial fibrillation (AF) is the most common cardiac arrhythmia that can have adverse
consequences related to a reduction in cardiac output (symptoms) and to atrial and atrial
appendage thrombus formation (stroke and peripheral embolization). In addition, affected
patients may be at increased risk for mortality. (See 'Long-term outcome' above.)
● Hypertensive heart disease and coronary heart disease are the most common underlying
disorders in developed countries associated with atrial fibrillation. (See 'Risk factors and
disease associations' above.)
● Patients are classified as having new onset, paroxysmal, persistent, longstanding

persistent, or permanent AF. (See 'Classification' above.)
● Essential information from the patient's history, physical examination, electrocardiogram,

and a transthoracic echocardiogram should be obtained at the time of diagnosis and
periodically during the course of the disease. Additional laboratory testing, such as thyroid
stimulating hormone assay, and ambulatory ECG monitoring may be necessary. (See
'Evaluation' above.)
● The two principal management decisions for patients are:
• Does the patient need long-term antithrombotic therapy? All patients whose risk of
embolization exceeds the risk of bleeding are candidates for such therapy. (See
'Prevention of systemic embolization' above.)
• Should the patient be managed with either a rate or a rhythm control strategy? This
should be determined based on severity of symptoms, presence of structural heart
disease, adequacy of rate control during episodes of atrial fibrillation, and the patient’s
preference for using antiarrhythmic drug therapy or undergoing ablation-based
interventions. (See 'Rate versus rhythm control' above.)
● In the absence of a reversible precipitant, AF is typically recurrent.
18 of 28 4/24/2020, 11:02 PM
ACKNOWLEDGMENT
The UpToDate editorial staff would like to thank Dr. Alan Cheng for his prior contributions as an
author to this topic review.
Use of UpToDate is subject to the Subscription and License Agreement.
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Topic 1022 Version 67.0
24 of 28 4/24/2020, 11:02 PM
GRAPHICS
Prevalence of atrial fibrillation by sex and age
L ifetime ris k for dev eloping atrial fibrillation (A F ) from the F ramingham H eart S tudy. M en
and women without A F at 4 0 y ears of age were determined to hav e a 2 6 and 2 3 perc ent
lik elihood of dev eloping inc ident A F by 8 0 y ears of age.
Reproduced with permission from: Magnani JW, Rienstra M, Lin H, et al. Atrial fibrillation: Current knowledge
and future directions in epidemiology and genomics. Circulation 2011; 124:1982. Copyright © Lippincott
Williams & Wilkins.
Graphic 82929 Version 4.0
25 of 28 4/24/2020, 11:02 PM
Clinical risk factors for stroke, transient ischemic attack, and systemic
embolism in the CHA 2 DS 2 -VASc score
(A ) The risk factor-based approach expressed as a point based scoring system, with
the acronym CHA 2 DS 2 -VA Sc
(NOTE: maximum score is 9 since age may contribute 0, 1, or 2 points)
CHA 2 DS 2 -VASc risk factor Points
Congestive heart failure +1

Signs/symptoms of heart failure or objective evidence of reduced left
ventricular ejection fraction
Hypertension +1
Resting blood pressure >140/90 mmHg on at least two occasions or
current antihypertensive treatment
Age 75 years or older +2
Diabetes mellitus +1
Fasting glucose >125 mg/dL (7 mmol/L) or treatment with oral
hypoglycemic agent and/or insulin
Previous stroke, transient ischamic attack, or thromboembolism +2
Vascular disease +1
Previous myocardial infarction, peripheral artery disease, or aortic
plaque
Age 65-74 years +1
Sex category (female) +1
(B) A djusted stroke rate according to CHA 2 DS 2 -VA Sc score
CHA 2 DS 2 -VASc score Patients Stroke and thromboembolism

(n = 73,538) event rate at one-year follow-up
(%)
0 6369 0.78
1 8203 2.01
2 12,771 3.71
3 17,371 5.92
4 13,887 9.27
5 8942 15.26
6 4244 19.74
7 1420 21.50
8 285 22.38
9 46 23.64
CHA 2 DS 2 -VASc: Congestive heart failure, Hypertension, Age (≥75) (doubled), Diabetes, Stroke (doubled), Vascular
disease, Age (65-74), Sex.
Part A from: Kirchhof P, Benussi S, Kotecha D, et al. 2016 ESC Guidelines for the management of atrial fibrillation
developed in collaboration with EACTS. Europace 2016; 18(11):1609-1678. By permission of Oxford University Press on
behalf of the European Society of Cardiology. Copyright © 2016 Oxford University Press. Available at: www.escardio.org/.
26 of 28 4/24/2020, 11:02 PM
Atrial fibrillation increases mortality in men and

women
A mong 5 2 0 9 s ubjec ts in the F ramingham H eart S tudy, the mortality

after a 1 0 - y ear follow- up was higher in both men and women, aged 5 5
to 7 4 , who had atrial fibrillation (A F ) c ompared to thos e without A F (p
<0 .0 0 1 ) A s imilar relations hip was s een in s ubjec ts between the ages
of 7 5 and 9 4 (not s hown).
Data from Benjamin EJ, Wolf PA, D'Agostino RB, et al. Circulation 1998; 98:946.
27 of 28 4/24/2020, 11:02 PM
Contributor Disclosures
Kapil Kum ar, MD Nothing to disclose Peter J Zim etbaum , MD Consultant/Advisory Boards: Abbott
Medical [lecture on lead extraction]; In carda Pharmaceuticals [Atrial fibrillation (Novel antiarrhythmic drug in
development)]; Medtronic [Atrial fibrillation (Linq)]. Gordon M Saperia, MD Nothing to disclose
Contributor disclosures are review ed for conflicts of interest by the editorial group. When found, these are
addressed by vetting through a multi-level review process, and through requirements for references to be
provided to support the content. Appropriately referenced content is required of all authors and must
conform to UpToDate standards of evidence.
Conflict of interest policy
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Overview of atrial fibrillation

RISK FACTORS AND DISEASE ASSOCIATIONS

NONVALVULAR VERSUS VALVULAR HEART DISEASE

● Paroxysmal (ie, self-terminating or intermittent) AF – Paroxysmal AF is defined as AF that

● Persistent AF – Persistent AF is defined as AF that fails to self-terminate within seven days.

generally considered a progressive disease.

● Long-standing persistent AF – AF that has lasted for more than 12 months.

Subclinical atrial fibrillation — Subclinical AF (SCAF) is defined as episodes of AF detected by

● In the STROKESTOP observational study of 7173 individuals 75 to 76 years of age in

recordings over three weeks in 3 percent [14].

● The ASSERT study monitored (using a dual chamber pacemaker or implantable

• At three months, subclinical AF was detected in about 10 percent of patients. The

• At 2.5 years, SCAF was detected in about 35 percent of individuals. Clinical AF

Additional information is as follows:

● SCAF often progresses to clinical AF [19].

Typical symptoms include palpitations, tachycardia, fatigue, weakness, dizziness,

● Precipitating causes: exercise, emotion, or alcohol.

● The presence of the following disease associations: cardiovascular or cerebrovascular

● A complete examination of the cardiovascular system should be performed in all individuals

precordial pulsation" and "Auscultation of cardiac murmurs in adults" and "Examination of

Electrocardiogram — The electrocardiogram (ECG) is used to verify the presence of AF and is

● Markers of nonelectrical cardiac disease, such as left ventricular hypertrophy (possible

● Markers of electrical heart disease, including the presence of ventricular pre-excitation or

● The QT interval (to identify the potential risk of antiarrhythmic therapy)

● Evidence of severe bradycardia or sinus node dysfunction

Echocardiogram — The transthoracic echocardiogram (TTE) is performed to evaluate the size

Baseline laboratory testing — Clinical or subclinical hyperthyroidism is present in less than 5

● Management of heart failure, hypotension, or difficulty with rate control.

● Initiation of antiarrhythmic drug therapy.

Paroxysmal, persistent, longstanding persistent, or permanent atrial fibrillation — Patients

● Functional status, including change in symptoms (history).

● Efficacy and safety of antiarrhythmic drug therapy (electrocardiogram [ECG], assessment of

Recurrence of atrial fibrillation — Continuous monitoring studies have shown that

Further evidence in support of the relationship between AF and development of dementia, as

● In a retrospective observational study of 272,186 patients with incidental AF at the time of

● In patients with a recent myocardial infarction (MI), the development of AF increases

None of these nonrandomized observations prove that AF directly causes an increase in

SOCIETY GUIDELINE LINKS

INFORMATION FOR PATIENTS

The following are essential points addressed in this topic:

● Patients are classified as having new onset, paroxysmal, persistent, longstanding

● Essential information from the patient's history, physical examination, electrocardiogram,

● The two principal management decisions for patients are:

● In the absence of a reversible precipitant, AF is typically recurrent.

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1. Pritchett EL. Management of atrial fibrillation. N Engl J Med 1992; 326:1264.

7. American College of Cardiology Foundation, American Heart Association, European

Stroke 2004; 35:1647.

33. Gaita F, Corsinovi L, Anselmino M, et al. Prevalence of silent cerebral ischemia in

and survival in the Atrial Fibrillation Follow-Up Investigation of Rhythm Management

48. Eldar M, Canetti M, Rotstein Z, et al. Significance of paroxysmal atrial fibrillation

Topic 1022 Version 67.0

Prevalence of atrial fibrillation by sex and age

Graphic 82929 Version 4.0

CHA 2 DS 2 -VASc risk factor Points

Congestive heart failure +1

Age 75 years or older +2

Previous stroke, transient ischamic attack, or thromboembolism +2

Age 65-74 years +1

Sex category (female) +1

(B) A djusted stroke rate according to CHA 2 DS 2 -VA Sc score