(AF or A-fib) is the most common cardiac
arrhythmia (heart rhythm disorder). It may cause no
symptoms, but it is often associated with palpitations,
pain, or congestive
heart failure. In some cases, however, AF is caused
or benign conditions.
may be identified clinically when taking a pulse,
and its presence can be confirmed with an electrocardiogram
(ECG or EKG) that demonstrates the absence of P
waves and an irregular ventricular rate.
AF, the normal regular electrical impulses generated by
node are overwhelmed by disorganized electrical impulses
usually originating in the roots of the pulmonary
veins, leading to irregular conduction of ventricles
impulses that generate the heartbeat. AF may occur in episodes
lasting from minutes to days ("paroxysmal") or may be permanent
in nature. A number of medical conditions increase the risk
of AF, in particular mitral
stenosis (narrowing of the mitral
valve of the heart).
risk of stroke is increased fivefold in individuals with
The degree of increased risk may be substantial, depending
on the presence of additional risk factors (such as high
blood pressure). AF may be treated with medications
to either slow the heart rate to a normal range ("rate control")
or revert the heart rhythm to normal ("rhythm control").
Synchronized electrical cardioversion
can be used to convert AF to a normal heart rhythm. Surgical
and catheter-based ablation may be used to prevent recurrence
of AF in some individuals. Depending on the risk of stroke
and systemic embolism, people with AF may use anticoagulants
such as warfarin,
which substantially reduces these risks but may increase
the risk of major bleeding, mainly in geriatric patients.
The prevalence of AF in a population increases with age;
8% of people over 80 have AF. Chronic AF leads to a small
increase in the risk of death.
only one diagnosed episode
recurrent episodes that self-terminate in less than
recurrent episodes that last more than 7 days
an ongoing long-term episode
College of Cardiology (ACC), American
Heart Association (AHA), and the European
Society of Cardiology (ESC) recommend in their guidelines
the following classification system based on simplicity
and clinical relevance.
patients with AF are initially in the category called first
detected AF. These patients may or may not have had
previous undetected episodes. If a first detected episode
self-terminates in less than 7 days and then another
episode begins later on, the case has moved into the category
of paroxysmal AF. Although patients in this category
have episodes lasting up to 7 days, in most cases of
paroxysmal AF the episodes will self-terminate in less than
24 hours. If instead the episode lasts for more than
7 days, it is unlikely to self-terminate,
and it is called persistent AF. In this case, the
episode may be still terminated by cardioversion. If cardioversion
is unsuccessful or not attempted and the episode is ongoing
for a long time (e.g., a year or more), the patient's AF
is called permanent.
that last less than 30 seconds are not considered in
this classification system. Also, this system does not apply
to cases where the AF is a secondary condition that occurs
in the setting of a primary condition that may be the cause
of the AF.
this classification system, it is not always clear what
an AF case should be called. For example, a case may fit
into the paroxysmal AF category some of the time, while
other times it may have the characteristics of persistent
AF. One may be able to decide which category is more appropriate
by determining which one occurs most often in the case under
addition to the above four AF categories, which are mainly
defined by episode timing and termination, the ACC/AHA/ESC
guidelines describe additional AF categories in terms of
other characteristics of the patient.
atrial fibrillation (LAF) – absence of clinical
findings of other cardiovascular
disease (including hypertension),
related pulmonary disease, or cardiac abnormalities
such as enlargement of the left atrium, and age under
AF – absence of rheumatic
mitral valve disease, a prosthetic
heart valve, or mitral
AF – occurs in the setting of a primary condition
that may be the cause of the AF, such as acute
myocardial infarction, cardiac
or other acute pulmonary disease
is usually accompanied by symptoms related to a rapid heart
rate. Rapid and irregular heart rates may be perceived as
intolerance and occasionally may produce angina
(if the rate is faster and puts the heart under strain)
symptoms of shortness
of breath or edema.
Sometimes the arrhythmia will be identified only with the
onset of a stroke or a transient
ischemic attack (TIA). It is not uncommon for a patient
to first become aware of AF from a routine physical examination
as it may be asymptomatic in many cases.
most cases of AF are secondary to other medical problems,
the presence of chest
pain or angina,
symptoms of hyperthyroidism
(an overactive thyroid
gland) such as weight
loss and diarrhea,
and symptoms suggestive of lung
disease would indicate an underlying cause. A history
of stroke or TIA, as well as hypertension
(high blood pressure), diabetes,
failure and rheumatic
fever, may indicate whether someone with AF is at a
higher risk of complications.
A higher risk of embolus
can be assessed using the CHADS2
is similar to other forms of rapid
heart rate and in some cases may be asymptomatic.
The patient may complain of palpitations
or chest discomfort.
The rapid uncoordinated heart rate may result in the heart
being unable to provide adequate blood flow and oxygen delivery
to the rest of the body. Therefore, common symptoms may
breath when lying flat, and sudden onset of shortness
of breath during the night (paroxysmal
nocturnal dyspnea), and may progress to swelling of
the lower extremities (peripheral
edema). Owing to inadequate blood flow, patients may
also complain of light-headedness,
may feel like they are about to faint (presyncope),
or may actually lose consciousness (syncope).
patient may be in significant respiratory
distress. Because of inadequate oxygen delivery, the
patient may appear blue (cyanosis).
By definition, the heart rate will be greater than 100 beats
per minute. Blood pressure will be variable, and often difficult
to measure as the beat-by-beat variability causes problems
for most digital (oscillometric) non-invasive
blood pressure monitors. It is most worrying if consistently
lower than usual (hypotension).
Respiratory rate will be increased in the presence of respiratory
distress. Pulse oximetry may confirm the presence of hypoxia
related to any precipitating factors such as pneumonia.
Examination of the jugular
veins may reveal elevated pressure
(jugular venous distention). Lung exam may reveal crackles,
which are suggestive of pulmonary
edema. Heart exam will reveal an irregular but rapid
with other conditions
sleep apnea (CSA) – A study found that the prevalence
of atrial fibrillation among patients with idiopathic
central sleep apnea was significantly higher than the
prevalence among patients with obstructive
sleep apnea or no sleep
apnea (27%, 1.7%, and 3.3%, respectively). There
was a total of 180 subjects with 60 people in each of
the 3 groups. Possible explanations for the association
between CSA and AF are a causal relationship between
the two conditions, or an abnormality of central cardiorespiratory
12 lead ECG showing atrial fibrillation at approximately
150 beats per minute
evaluation of atrial fibrillation involves diagnosis, determination
of the etiology
of the arrhythmia, and classification of the arrhythmia.
The evaluation of atrial fibrillation typically entails
a history and physical examination, ECG, transthoracic echocardiogram,
blood count, and serum thyroid
stimulating hormone level.
Depending upon given resources, afflicted individuals may
benefit from an in-depth evaluation that may include correlation
of the heart rate response to exercise, exercise stress
testing, chest X-ray, trans-esophageal echocardiography,
and other studies.
a patient presents with a sudden onset of severe symptoms
other forms of tachyarrhythmia
must be ruled-out, as some may be immediately life threatening,
such as ventricular
tachycardia. While most patients will be placed on continuous
cardiorespiratory monitoring, an electrocardiogram
is essential for diagnosis.
causes should be sought out. A common cause of any tachycardia
as well as other forms of hypovolemia.
coronary syndrome should be ruled out. Intercurrent
illness such as pneumonia
may be present.
for atrial fibrillation is not performed, although a study
of routine pulse checks or ECGs during routine office visits
found that the annual rate of detection of AF in elderly
patients improved from 1.04% to 1.63%; selection of patients
for prophylactic anticoagulation would improve stroke risk
in that age category.
of the routine primary care visit is 64%. This low result
probably reflects the pulse not being checked routinely
ECGs are used for screening, the SAFE trial found that electronic
care physicians and the combination of the two had the
following sensitivities and specificities:
by software: sensitivity
= 83%, specificity
by a primary care physician: sensitivity = 80%, specificity
by a primary care physician with software: sensitivity
= 92%, specificity = 91%
general, the minimal evaluation of atrial fibrillation should
be performed in all individuals with AF. The goal of this
evaluation is to determine the general treatment regimen
for the individual. If results of the general evaluation
warrant it, further studies may then be performed.
and physical examination
history of the individual's atrial fibrillation episodes
is probably the most important part of the evaluation. Distinctions
should be made between those who are entirely asymptomatic
when they are in AF (in which case the AF is found as an
incidental finding on an ECG or physical examination) and
those who have gross and obvious symptoms due to AF and
can pinpoint whenever they go into AF or revert to sinus
many cases of AF have no definite cause, it may be the result
of various other problems (see below). Hence, renal
function and electrolytes
are routinely determined, as well as thyroid-stimulating
hormone (commonly suppressed in hyperthyroidism
and of relevance if amiodarone
is administered for treatment) and a blood
acute-onset AF associated with chest
troponins or other markers of damage to the heart muscle
may be ordered. Coagulation
are usually performed, as anticoagulant
medication may be commenced.
of atrial fibrillation (top) and normal sinus rhythm
(bottom). The purple arrow indicates a P wave, which
is lost in atrial fibrillation.
fibrillation is diagnosed on an electrocardiogram (ECG),
an investigation performed routinely whenever an irregular
heart beat is suspected. Characteristic findings are the
absence of P waves, with disorganized electrical activity
in their place, and irregular R-R intervals due to irregular
conduction of impulses to the ventricles.
At very fast heart rates atrial fibrillation may look more
regular, which may make it more difficult to separate from
SVT or ventricular tachycardia.
complexes should be narrow, signifying that they are
initiated by normal conduction of atrial electrical activity
through the intraventricular
conduction system. Wide QRS complexes are worrisome
tachycardia, although in cases where there is disease
of the conduction system, wide complexes may be present
in A-Fib with rapid ventricular response.
paroxysmal AF is suspected but an ECG during an office visit
shows only a regular rhythm, AF episodes may be detected
and documented with the use of ambulatory Holter
monitoring (e.g., for a day). If the episodes are too
infrequent to be detected by Holter monitoring with reasonable
probability, then the patient can be monitored for longer
periods (e.g., a month) with an ambulatory event
general, a non-invasive transthoracic echocardiogram
(TTE) is performed in newly diagnosed AF, as well as if
there is a major change in the patient's clinical state.
This ultrasound-based scan of the heart may help identify
heart disease (which may greatly increase the risk of
stroke), left and right atrial size (which indicates likelihood
that AF may become permanent), left ventricular size and
function, peak right ventricular pressure (pulmonary
hypertension), presence of left atrial thrombus (low
sensivity), presence of left ventricular hypertrophy and
enlargement of both the left and right atria is associated
with long-standing atrial fibrillation and, if noted at
the initial presentation of atrial fibrillation, suggests
that the atrial fibrillation is likely to be of a longer
duration than the individual's symptoms.
general, an extended evaluation is not necessary in most
individuals with atrial fibrillation, and is performed only
if abnormalities are noted in the limited evaluation, if
a reversible cause of the atrial fibrillation is suggested,
or if further evaluation may change the treatment course.
general, a chest
X-ray is performed only if a pulmonary cause of atrial
fibrillation is suggested, or if other cardiac conditions
are suspected (in particular congestive
heart failure.) This may reveal an underlying problem
in the lungs or the blood vessels in the chest.
In particular, if an underlying pneumonia is suggested,
then treatment of the pneumonia may cause the atrial fibrillation
to terminate on its own.
normal echocardiography (transthoracic or TTE) has a low
sensitivity for identifying thrombi
(blood clots) in the heart. If this is suspected (e.g.,
when planning urgent electrical cardioversion) a transesophageal
echocardiogram (TEE or TOE where British spelling is
used) is preferred.
TEE has much better visualization of the left
atrial appendage than transthoracic echocardiography.
This structure, located in the left
atrium, is the place where thrombus is formed in more
than 90% of cases in non-valvular (or non-rheumatic) atrial
fibrillation or flutter.
TEE has a high sensitivity for locating thrombi in this
and can also detect sluggish bloodflow in this area that
is suggestive of thrombus formation.
no thrombus is seen on TEE, the incidence of stroke, (immediately
after cardioversion is performed), is very low.[citation
monitor is a wearable ambulatory heart monitor that
continuously monitors the heart rate and heart rhythm for
a short duration, typically 24 hours. In individuals with
symptoms of significant shortness of breath with exertion
or palpitations on a regular basis, a holter monitor may
be of benefit to determine whether rapid heart rates (or
unusually slow heart rates) during atrial fibrillation are
the cause of the symptoms.
individuals with atrial fibrillation do well with normal
activity but develop shortness of breath with exertion.
It may be unclear whether the shortness of breath is due
to a blunted heart rate response to exertion caused by excessive
AV node-blocking agents, a very rapid heart rate during
exertion, or other underlying conditions such as chronic
lung disease or coronary ischemia. An exercise
stress test will evaluate the individual's heart rate
response to exertion and determine if the AV node blocking
agents are contributing to the symptoms.
is linked to several cardiac causes, but may occur in otherwise-normal
hearts. Known associations include:
(High blood pressure)
heart diseases including coronary
artery disease, mitral
stenosis (e.g., due to rheumatic
heart disease or mitral
valve prolapse), mitral
cardiomyopathy (HCM), pericarditis,
heart disease, previous heart
diseases (such as pneumonia,
drinking" or "holiday
heart syndrome"). Even otherwise-healthy middle-age
women having consumed more than 2 drinks daily were
60% more likely to develop AF.
in the presence of normal atrioventricular conduction.
family history of AF may increase the risk of AF. A
study of more than 2,200 AF patients found that 30 percent
had parents with AF.
Various genetic mutations may be responsible.
types of genetic disorder are associated with atrial fibrillation:
primary pathologic change seen in atrial fibrillation is
the progressive fibrosis of the atria. This fibrosis is
due primarily to atrial dilation, however genetic causes
and inflammation may have a cause in some individuals. One
study found that atrial dilation can occur as a consequence
although another study found that AF by itself does not
of the atria can be due to almost any structural abnormality
of the heart that can cause a rise in the intra-cardiac
pressures. This includes valvular heart disease (such as
regurgitation, and tricuspid
regurgitation), hypertension, and congestive heart failure.
Any inflammatory state that affects the heart can cause
fibrosis of the atria. This is typically due to sarcoidosis
but may also be due to autoimmune disorders that create
autoantibodies against myosin heavy chains. Mutation of
the lamin AC
gene is also associated with fibrosis of the atria that
can lead to atrial fibrillation.
dilation of the atria has occurred, this begins a chain
of events that leads to the activation of the renin
aldosterone angiotensin system (RAAS) and subsequent
increase in matrix metaloproteinases and disintegrin, which
leads to atrial remodeling and fibrosis, with loss of atrial
muscle mass. This process is not immediate, and experimental
studies have revealed patchy atrial fibrosis may precede
the occurrence of atrial fibrillation and may progress with
prolonged durations of atrial fibrillation.
is not limited to the muscle mass of the atria, and may
occur in the sinus
node (SA node) and atrioventricular
node (AV node), correlating with sick
sinus syndrome. Prolonged episodes of atrial fibrillation
have been shown to correlate with prolongation of the sinus
node recovery time,
suggesting that dysfunction of the SA node is progressive
with prolonged episodes of atrial fibrillation.
conduction system of the heart allows the impulse that
is generated by the sinoatrial
node (SA node) of the heart to be propagated to and
stimulate the myocardium
(muscle of the heart). When the myocardium is stimulated,
it contracts. It is the ordered stimulation of the myocardium
that allows efficient contraction of the heart, thereby
allowing blood to be pumped to the body.
are multiple theories about the etiology of atrial fibrillation.
An important theory is that, in atrial fibrillation, the
regular impulses produced by the sinus node for a normal
heartbeat are overwhelmed by rapid electrical discharges
produced in the atria and adjacent parts of the pulmonary
veins. Sources of these disturbances are either automatic
foci, often localized at one of the pulmonary veins, or
a small number of localized sources in the form of either
reentrant electrical spiral waves (rotors) or repetitive
focal beats; these localized sources may be found in the
left atrium near the pulmonary veins or in a variety of
other locations through both the left or right atrium.
recovery of the atria from excitation is heterogeneous,
the electrical waves generated by the AF sources undergo
repetitive, spatially distributed breakup and fragmentation
in a process known as "fibrillatory conduction". Another
theory is the multiple wavelet
theory first formulated by Moe,
which was experimentally proven by Allessie et al.
can be distinguished from atrial
flutter (AFL), which appears as an organized electrical
circuit usually in the right atrium. AFL produces characteristic
saw-toothed F-waves of constant amplitude and frequency
on an ECG
whereas AF does not. In AFL, the discharges circulate rapidly
at a rate of 300 beats per minute (bpm) around the
atrium. In AF, there is no regularity of this kind, except
at the sources where the local activation rate can exceed
the electrical impulses of AF occur at a high rate, most
of them do not result in a heart beat. A heart beat results
when an electrical impulse from the atria passes through
(AV) node to the ventricles and causes them to contract.
During AF, if all of the impulses from the atria passed
through the AV node, there would be severe ventricular
tachycardia, resulting in severe reduction of cardiac
output. This dangerous situation is prevented by the
AV node since its limited conduction velocity reduces the
rate at which impulses reach the ventricles during AF.
main goals of treatment are to prevent circulatory
instability and stroke.
Rate or rhythm control are used to achieve the former, whereas
is used to decrease the risk of the latter.
If cardiovascularly unstable due to uncontrolled tachycardia,
immediate cardioversion is indicated.
can be achieved through a number of means including the
use of heparin,
Aspirin is somewhat
effective in reducing the risk of stroke in AF patients,
but is inferior to warfarin and is typically reserved for
AF patients at lower risk for stroke.
The method used depends on a number of issues, including:
cost, risk of stroke, risk of falls, compliance, and speed
of desired onset of anticoagulation.
Some other anticoagulants were discussed in a 2012 state-of-the-art
paper but were not generally approved at that time for stroke
prevention in AF: apixaban,
new oral anticoagulants (rivaroxaban, dabigatran, apixaban)
compared to warfarin in those with non-valvular atrial fibrillation
are of no benefit for preventing non-hemorrhagic stroke
and systemic embolic events. They do have a lower risk of
versus rhythm control
can cause disabling and bothersome symptoms. Palpitations,
chest discomfort, anxiety, and decreased exercise tolerance
are related to rapid heart rate and inefficient cardiac
output caused by AF. Furthermore, AF with a persistent rapid
rate can cause a form of heart
failure called tachycardia
induced cardiomyopathy. This can significantly increase
mortality and morbidity, which can be prevented by early
and adequate treatment of the AF.
are two ways to approach these symptoms using drugs: rate
control and rhythm control. Rate control lowers the
heart rate closer to normal, usually 60 to 100 bpm,
without trying to convert to a regular rhythm. Rhythm
control restores normal heart rhythm in a process called
cardioversion and maintains the normal rhythm with drugs.
Studies suggest that rhythm control is most important in
the acute setting AF, whereas rate control is more important
in the chronic phase. As far as mortality
is concerned, the AFFIRM trial showed that there is lower
mortality using rate control with anticoagulation treatment
versus rhythm control treatment and the difference increases
up to 5 years (end of study).
is no difference in risk of stroke in patients having converted
to a normal rhythm with anti-arrhythmic treatment compared
to those with only rate control.
AF is associated with a reduced quality of life, and, while
some studies indicate that rhythm control leads to a higher
quality of life, some did not find a difference.
further study focused on rhythm control in patients with
AF with concomitant heart failure, based on the hypothesis
that AF confers a higher mortality risk in heart failure.
In this setting, rhythm control offered no advantage compared
to rate control.
However, the diagnosis and progression of atrial fibrillation
and other cardiovascular disease requires further investigation.
patients with a fast ventricular response, intravenous magnesium
significantly increases the chances of successful rate and
rhythm control in the urgent setting without major side-effects.
A patient with fluctuating vital signs, mental status changes,
preexcitation, or chest pain often will go to immediate
treatment with synchronized DC cardioversion.
Otherwise the decision of rate control versus rhythm control
using drugs is made. This is based on a number of criteria
that includes whether or not symptoms persist with rate
control is achieved with medications that work by increasing
the degree of block at the level of the AV node, in effect
decreasing the number of impulses that conduct into the
ventricles. This can be done with:
addition to these agents, amiodarone has some AV node blocking
effects (in particular when administered intravenously),
and can be used in individuals when other agents are contraindicated
or ineffective (particularly due to hypotension).
has been shown to be more effective than either digoxin
is a noninvasive conversion of an irregular heartbeat to
a normal heartbeat using electrical or chemical means.
an investigational drug that is unavailable in the U.S.,
has been found to safely and rapidly convert new onset atrial
fibrillation in one published study.
successful cardioversion the heart may be in a stunned state,
which means that there is a normal rhythm but restoration
of normal atrial contraction has not yet occurred.
young patients with little-to-no structural heart disease
where rhythm control is desired and cannot be maintained
by medication or cardioversion, then radiofrequency
ablation or cryoablation may be attempted and is preferred
over years of drug therapy.
Although radiofrequency ablation is becoming an accepted
intervention in select younger patients, there is currently
a lack of evidence that ablation reduces all-cause mortality,
stroke, or heart failure.
There are two ongoing clinical trials (CABANA [Catheter
Ablation Versus Antiarrhythmic Drug Therapy for Atrial Fibrillation]
and EAST [Early Therapy of Atrial Fibrillation for Stroke
Prevention Trial]) that should provide new information for
assessing whether AF catheter ablation is superior to more
procedure, first performed in 1987, is an effective
invasive surgical treatment that is designed to create electrical
blocks or barriers in the atria of the heart, forcing electrical
impulses that stimulate the heartbeat to travel down to
the ventricles. The idea is to force abnormal electrical
signals to move along one, uniform path to the lower chambers
of the heart (ventricles), thus restoring the normal heart
often occurs after cardiac surgery and is usually self-limiting.
It is strongly associated with age, pre-operative hypertension,
and the number of vessels grafted. Measures should be taken
to control hypertension pre-operatively to reduce the risk
of AF. Also, patients with a higher risk of AF, e.g., patients
with pre-operative hypertension, more than 3 vessels grafted,
or greater than 70 years of age, should be considered for
prophylactic treatment. Postoperative pericardial effusion
is also suspected to be the cause of atrial fibrillation.
Prophylaxis may include prophylactic post-operative rate
and rhythm management. Some authors perform posterior pericardiotomy
to reduce the incidence of postoperative AF.
When AF occurs, management should primarily be rate and
rhythm control. However, cardioversion may be employed if
the patient is haemodynamically unstable, highly symptomatic,
or persists for 6 weeks after discharge. In persistent cases
anticoagulation should be used.
prediction of whether a embolism
will occur and cause a stroke
is essential for guiding the decision to use anticoagulants.
The most accurate clinical
prediction rules are:
of thrombus formation
atrial fibrillation, the lack of an organized atrial contraction
can result in some stagnant blood in the left atrium (LA)
atrial appendage (LAA). This lack of movement of blood
can lead to thrombus
clotting). If the clot becomes mobile and is carried
away by the blood circulation, it is called an embolus.
An embolus proceeds through smaller and smaller arteries
until it plugs one of them and prevents blood from flowing
through the artery. This process results in end-organ damage
due to loss of nutrients, oxygen, and removal of cellular
waste products. Thrombus can form anywhere in the body,
whereas emboli follow the blood circulation to specific
points in the body. Emboli in the brain may result in an
stroke or a transient
ischemic attack (TIA).
than 90% of cases of thrombi associated with non-valvular
atrial fibrillation evolve in the left atrial appendage.
However, the LAA lies in close relation to the free wall
of the left ventricle and thus the LAA's emptying and filling,
which determines its degree of blood stagnation, may be
helped by the motion of the wall of the left ventricle,
if there is good ventricular function.
the LA is enlarged, there is an increased risk of thrombi
that originate in the LA. Moderate to severe, non-rheumatic,
regurgitation (MR) reduces this risk of stroke.
This risk reduction may be due to a beneficial stirring
effect of the MR blood flow into the LA.
fibrillation and a corresponding enlargement of the left
atrium may cause an increase in the perimeter of the mitral
valve. The somewhat circular perimeter of the mitral
valve is defined by the mitral
rhythm, the mitral annulus undergoes dynamic changes
during the cardiac
cycle. For example, at the end of diastole
the annular area is smaller than at the end of systole.
A possible reason for this dynamic size difference is that
the coordinated contraction of the left
atrium acts like a sphincter
about the mitral annulus and reduces its size. This may
be important for mitral valve competence so that it does
not leak when the left ventricle pumps blood. However, when
the left atrium fibrillates, this sphincter action is not
possible and may contribute to, or result in, mitral regurgitation
in some cases.
fibrillation is the most common arrhythmia
affecting 0.4 to 1% of the population.
It also accounts for 1/3 of hospital admissions for cardiac
and the rate of admissions for AF has risen in recent years.
Strokes from AF account for 6-24% of all ischemic
Between 3–11% of those with AF have structurally normal
Approximately 2.2 million individuals in the United
States and 4.5 million in the European Union have AF.
incidence of atrial fibrillation increases with age. In
individuals over the age of 80 it affects about 8%.
In developed countries, the number of patients with atrial
fibrillation is likely to increase during the next 50 years,
owing to the growing proportion of elderly individuals.
the diagnosis of atrial fibrillation requires measurement
of the electrical activity of the heart, atrial fibrillation
was not truly described until 1874, when Edmé
Félix Alfred Vulpian observed the irregular atrial electrical
behavior that he termed "fremissement fibrillaire"
in dog hearts.
In the mid-eighteenth century, Jean-Baptiste
de Sénac made note of dilated, irritated atria in people
The irregular pulse associated with AF was first recorded
in 1876 by Carl
Wilhelm Hermann Nothnagel and termed "delirium cordis",
stating that "[I]n this form of arrhythmia the heartbeats
follow each other in complete irregularity. At the same
time, the height and tension of the individual pulse waves
are continuously changing".
Correlation of delirium cordis with the loss of atrial contraction
as reflected in the loss of a waves in the jugular
venous pulse was made by Sir James MacKenzie in 1904.
Einthoven published the first ECG showing AF in 1906.
The connection between the anatomic and electrical manifestations
of AF and the irregular pulse of delirium cordis was made
in 1909 by Carl Julius Rothberger, Heinrich Winterberg,
and Sir Thomas Lewis.