atrial fibrillation - wikipedia, the free encyclopedia.pdf

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5/21/13 Atrial fibrillation - Wikipedia, the free encyclopedia

en.wikipedia.org/wiki/Atrial_fibrillation

Atrial fibrillation

Classification and external resources

Schematic diagram of normal sinus rhythm for a human heart as seen on

ECG. In atrial fibrillation, however, the P waves, which represent

depolarization of the atria, are absent.

ICD-10 I48

(http://apps.who.int/classifications/icd10/browse/2010/en#/I48

ICD-9 427.31 (http://www.icd9data.com/getICD9Code.ashx?

icd9=427.31)

DiseasesDB 1065 (http://www.diseasesdatabase.com/ddb1065.htm)

MedlinePlus 000184

(http://www.nlm.nih.gov/medlineplus/ency/article/000184.htm)

eMedicine med/184 (http://www.emedicine.com/med/topic184.htm)

emerg/46 (http://www.emedicine.com/emerg/topic46.htm#)

MeSH D001281 (http://www.nlm.nih.gov/cgi/mesh/2013/MB_cgi?

field=uid&term=D001281)

Atrial fibrillationFrom Wikipedia, the free encyclopedia

Atrial fibrillation (AF orA-fib) is

the most common cardiac arrhythmia

(irregular heart beat). It may cause

no symptoms, but it is often

associated with palpitations, fainting,chest pain, or congestive heart

failure. However, in some people

atrial fibrillation is caused by

otherwise idiopathic or benign

conditions.

AF increases the risk of stroke. The

degree of increase can be substantial,

depending on the presence of

additional risk factors (such as highblood pressure). It may be identified

clinically when taking a pulse, and the

presence of AF can be confirmed

with an electrocardiogram (ECG or

EKG) which demonstrates the

absence of P waves together with an

irregular ventricular rate.

In AF, the normal regular electrical

impulses generated by the sinoatrialnode are overwhelmed by

disorganized electrical impulses

usually originating in the roots of the

pulmonary veins, leading to irregular

conduction of impulses to the

ventricles which generate the

heartbeat. AF may occur in episodes

lasting from minutes to days

("paroxysmal"), or be permanent in

nature. A number of medical conditions increase the risk of AF, particularly mitral stenosis (narrowing of the mitravalve of the heart).

Atrial fibrillation may be treated with medications to either slow the heart rate to a normal range ("rate control") or

revert the heart rhythm back to normal ("rhythm control"). Synchronized electrical cardioversion can be used to

convert AF to a normal heart rhythm. Surgical and catheter-based therapies may be used to prevent recurrence of

AF in certain individuals. Depending on the risk of stroke and systemic embolism, people with AF may use

anticoagulants such as warfarin, which substantially reduces the risk but may increase the risk of major bleeding,

mainly in geriatric patients. The prevalence of AF in a population increases with age, with 8% of people over 80

having AF. Chronic AF leads to a small increase in the risk of death.
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en.wikipedia.org/wiki/Atrial_fibrillation 2

Classification system

AF Category Defining Characteristics

First detected only one diagnosed episode

Paroxysmal recurrent episodes that self-terminate in less than 7 days

Persistent recurrent episodes that last more than 7 days

Permanent an ongoing long-term episode

Contents

1 Classification

2 Signs and symptoms

2.1 Rapid heart rate

2.2 Association with other conditions

3 Diagnosis

3.1 Screening

3.2 Minimal evaluation

3.3 Extended evaluation

4 Causes

5 Pathophysiology

5.1 Morphology

5.2 Electrophysiology

6 Management

6.1 Anticoagulation6.2 Rate control versus rhythm control using drugs

6.3 Rate control

6.4 Cardioversion

6.5 Ablation

6.6 Maze Procedure

6.7 Following surgery

7 Prognosis

7.1 Thromboembolism

7.2 Mitral valve

8 Epidemiology

8.1 Genetics

9 History

10 References

11 External links

Classification

The American 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.[1]
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All atrial fibrillation patients are initially in the category calledfirst 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 ofparoxysmal AF. Although patients in thi

category have episodes lasting up to 7 days, in most cases of paroxysmal AF the episodes will self-terminate in les

than 24 hours. If instead the episode lasts for more than 7 days, it is unlikely to self-terminate, [2] and it is called

ersistent AF. In this case, the episode may be still terminated by cardioversion. If cardioversion is unsuccessful o

it is not attempted, and the episode is ongoing for a long time (e.g., a year or more), the patient's AF is called

ermanent.

Episodes 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.

Using this classification system, it's not always clear what an AF case should be called. For example, a case may fi

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 i

the case under consideration.

In addition to the above four AF categories, which are mainly defined by episode timing and termination, theACC/AHA/ESC guidelines describe additional AF categories in terms of other characteristics of the patient. [1]

Lone atrial fibrillation (LAF) absence of clinical or echocardiographic findings of other cardiovascular

disease (including hypertension), related pulmonary disease, or cardiac abnormalities such as enlargement o

the left atrium, and age under 60 years

Nonvalvular AF absence of rheumatic mitral valve disease, a prosthetic heart valve, or mitral valve repai

Secondary AF occurs in the setting of a primary condition which may be the cause of the AF, such as

acute myocardial infarction, cardiac surgery, pericarditis, myocarditis, hyperthyroidism, pulmonary embolism

pneumonia, or other acute pulmonary disease

Signs and symptoms

Atrial fibrillation is usually accompanied by symptoms related to a rapid heart rate. Rapid and irregular heart rates

may be perceived as palpitations, exercise intolerance, and occasionally produce angina (if the rate is faster and

puts the heart under strain) and congestive 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 or ECG, as it may be asymptomatic in

many cases.[1]

As most cases of atrial fibrillation 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, heart failure and rheumatic fever, may indicate whether someone with AF is at a

higher risk of complications.[1]

Rapid heart rate
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A 12 lead ECG showing atrialfibrillation at approximately 150 beats

per minute

Presentation is similar to other forms of rapid heart rate (tachycardia), and in some cases may actually be

asymptomatic. The patient may complain of palpitations or chest discomfort. The rapid heart rate may result in the

heart being unable to provide adequate blood flow and oxygen delivery to the rest of the body. Therefore, commo

symptoms may include shortness of breath which often worsens with exertion (dyspnea on exertion), shortness of

breath when lying flat (orthopnea), 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).

The 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 confir

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 rales or crackles, which are

suggestive of pulmonary edema. Heart exam will reveal an irregular but rapid rhythm.

Association with other conditions

Central 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 wit

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 regulation.[3]

Left atrial enlargement

Mitral stenosis

iagnosis

The evaluation of atrial fibrillation involves diagnosis, determination of the

etiology of the arrhythmia, and classification of the arrhythmia. The

minimal evaluation of atrial fibrillation is a history and physical

examination, ECG, transthoracic echocardiogram, and case specific

bloodwork. Depending upon given resources, afflicted individuals may

benefit from an in-depth evaluation which may include correlation of the

heart rate response to exercise, exercise stress testing, chest X-ray,

trans-esophageal echocardiography, and other studies.

If 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.

Provoking causes should be sought out. A common cause of any tachycardia is dehydration, as well as other form

of hypovolemia. Acute coronary syndrome should be ruled out. Intercurrent illness such as pneumonia may be

present.
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Screening

Screening for atrial fibrillation is not generally 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. [4]

This estimated sensitivity of the routine primary care visit is 64%. This low result probably reflects the pulse not

being checked routinely or carefully.

[4]

When ECGs are used for screening, the SAFE trial found that electronic software, primary care physicians and the

combination of the two had the following sensitivities and specificities:[5]

Interpreted by software: sensitivity = 83%, specificity = 99%

Interpreted by a primary care physician: sensitivity = 80%, specificity = 92%

Interpreted by a primary care physician with software: sensitivity = 92%, specificity = 91%

Minimal evaluation

The minimal evaluation of atrial fibrillation should generally 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 warra

it, further studies may then be performed.

History and physical examination

The 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 rhythm.

Routine bloodwork

While 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 count.[1]

In acute-onset AF associated with chest pain, cardiac troponins or other markers of damage to the heart muscle

may be ordered. Coagulation studies (INR/aPTT) are usually performed, as anticoagulant medication may be

commenced.[1]

Electrocardiogram

Atrial 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. [1] At ver

fast heart rates atrial fibrillation may look more regular which may make it more difficult to separate from SVT or

ventricular tachycardia.[6]
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ECG of atrial fibrillation (top) and normal sinus rhythm (bottom). The

purple arrow indicates a P wave, which is lost in atrial fibrillation.

QRS 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 for ventricular tachycardia,

although in cases where there is disease of the conduction system, wide complexes may be present in A-Fib with

rapid ventricular response.

If paroxysmal AF is suspected but an ECG

during an office visit only shows a regular

rhythm, AF episodes may be detected and

documented with the use of ambulatoryHolter 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 monitor.[1]

Echocardiography

A non-invasive transthoracic echocardiogram (TTE) is generally 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

valvular 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 pericardial disease.[1]

Significant 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 tha

the individual's symptoms.

Extended evaluation

An extended evaluation is generally not necessary in most individuals with atrial fibrillation, and is only performed i

abnormalities are noted in the limited evaluation, if a reversible cause of the atrial fibrillation is suggested, or if furth

evaluation may change the treatment course.

Chest X-ray

A chest X-ray is generally only performed if a pulmonary cause of atrial fibrillation is suggested, or if other cardiacconditions are suspected (particularly congestive heart failure.) This may reveal an underlying problem in the lungs

or the blood vessels in the chest.[1] In particular, if an underlying pneumonia is suggested, then treatment of the

pneumonia may cause the atrial fibrillation to terminate on its own.

Transesophageal echocardiogram

A 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.[1]
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The 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.[7] TEE has a high sensitivity for locating thrombi in this area[

and can also detect sluggish bloodflow in this area that is suggestive of thrombus formation. [9]

If no thrombus is seen on TEE, the incidence of stroke, (immediately after cardioversion is performed), is very

low.[citation needed]

Ambulatory Holter monitoring

A Holter 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 if rapid heart rates (or unusually

slow heart rates) during atrial fibrillation are the cause of the symptoms.

Exercise stress testing

Some individuals with atrial fibrillation do well with normal activity but develop shortness of breath with exertion. Imay be unclear if 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 due to 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.

Causes

AF is linked to several cardiac causes, but may occur in otherwise normal hearts. Known associations include:

Hypertension (High blood pressure)

Primary heart diseases including coronary artery disease, mitral stenosis (e.g., due to rheumatic heart diseas

or mitral valve prolapse), mitral regurgitation, hypertrophic cardiomyopathy (HCM), pericarditis, congenital

heart disease, previous heart surgery

Lung diseases (such as pneumonia, lung cancer, pulmonary embolism, sarcoidosis)

Excessive alcohol consumption ("binge drinking" or "holiday heart syndrome"). Even otherwise healthy

middle-aged women who consumed more than 2 drinks daily were 60% more likely to develop AF. [10]

Hyperthyroidism

Dual-chamber pacemakers in the presence of normal atrioventricular conduction.[11]

A family history of AF may increase the risk of AF. A study of more than 2,200 AF patients found that 30percent had parents with AF.[12] Various genetic mutations may be responsible.[13][14]

Pathophysiology

Morphology
http://en.wikipedia.org/wiki/Atrial_fibrillation#cite_note-OMIM-14http://en.wikipedia.org/wiki/Atrial_fibrillation#cite_note-pmid16790707-13http://en.wikipedia.org/wiki/Atrial_fibrillation#cite_note-pmid15199036-12http://en.wikipedia.org/wiki/Atrial_fibrillation#cite_note-11http://en.wikipedia.org/wiki/Pacemakerhttp://en.wikipedia.org/wiki/Hyperthyroidismhttp://en.wikipedia.org/wiki/Atrial_fibrillation#cite_note-10http://en.wikipedia.org/wiki/Holiday_heart_syndromehttp://en.wikipedia.org/wiki/Binge_drinkinghttp://en.wikipedia.org/wiki/Alcoholic_beveragehttp://en.wikipedia.org/wiki/Sarcoidosishttp://en.wikipedia.org/wiki/Pulmonary_embolismhttp://en.wikipedia.org/wiki/Lung_cancerhttp://en.wikipedia.org/wiki/Pneumoniahttp://en.wikipedia.org/wiki/Heart_surgeryhttp://en.wikipedia.org/wiki/Congenital_heart_diseasehttp://en.wikipedia.org/wiki/Pericarditishttp://en.wikipedia.org/wiki/Hypertrophic_cardiomyopathyhttp://en.wikipedia.org/wiki/Mitral_regurgitationhttp://en.wikipedia.org/wiki/Mitral_valve_prolapsehttp://en.wikipedia.org/wiki/Rheumatic_heart_diseasehttp://en.wikipedia.org/wiki/Mitral_stenosishttp://en.wikipedia.org/wiki/Coronary_artery_diseasehttp://en.wikipedia.org/wiki/Hypertensionhttp://en.wikipedia.org/wiki/Cardiac_stress_testhttp://en.wikipedia.org/wiki/Holter_monitorhttp://en.wikipedia.org/wiki/Wikipedia:Citation_neededhttp://en.wikipedia.org/wiki/Atrial_fibrillation#cite_note-Fatkin1994-9http://en.wikipedia.org/wiki/Atrial_fibrillation#cite_note-Acar1991-8http://en.wikipedia.org/wiki/Atrial_fibrillation#cite_note-pmid8572814-7http://en.wikipedia.org/wiki/Atrial_Flutterhttp://en.wikipedia.org/wiki/Left_atriumhttp://en.wikipedia.org/wiki/Left_atrial_appendage


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Conduction

Sinus rhythm Atrial fibrillation

The primary pathologic change seen in atrial fibrillation is the progressive fibrosis of the atria. This fibrosis is

primarily due to atrial dilation, however genetic causes and inflammation may have a cause in some individuals. On

study found that atrial dilation can occur as a consequence of AF, [15] although another study found that AF by itse

does not cause it.[16]

Dilation 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 mitral stenosis, mitral 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 ACgene is also associated with fibrosis of the

atria that can lead to atrial fibrillation.

Once 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, whic

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.

Fibrosis is not limited to the muscle mass of the atria, and may occur in the sinus node (SA node) andatrioventricular 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,[1][17][18] suggesting that dysfunction of

the SA node is progressive with prolonged episodes of atrial fibrillation.

Electrophysiology

The normal electrical 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.

There 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.
http://en.wikipedia.org/wiki/Pulmonary_veinshttp://en.wikipedia.org/wiki/Myocardiumhttp://en.wikipedia.org/wiki/Sinoatrial_nodehttp://en.wikipedia.org/wiki/Electrical_conduction_system_of_the_hearthttp://en.wikipedia.org/wiki/Atrial_fibrillation#cite_note-pmid11469431-18http://en.wikipedia.org/wiki/Atrial_fibrillation#cite_note-pmid8941126-17http://en.wikipedia.org/wiki/Atrial_fibrillation#cite_note-pmid16908781-1http://en.wikipedia.org/wiki/Sick_sinus_syndromehttp://en.wikipedia.org/wiki/Atrioventricular_nodehttp://en.wikipedia.org/wiki/Sinus_nodehttp://en.wikipedia.org/wiki/Renin-angiotensin_systemhttp://en.wikipedia.org/wiki/Laminhttp://en.wikipedia.org/wiki/Atrial_fibrillation#cite_note-Osranek2005-16http://en.wikipedia.org/wiki/Atrial_fibrillation#cite_note-Sanfilippo1990-15http://en.wikipedia.org/wiki/File:Heart_conduct_atrialfib.gifhttp://en.wikipedia.org/wiki/File:Heart_conduct_sinus.gif


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Because 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, [19] which was experimentally proven by

Allessie et al.

AF can be distinguished from atrial flutter (AFL), which appears as an organized electrical circuit usually in the righ

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

500 bpm.

Although 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 the atrioventricular (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.[20]

Management

Main article: Management of atrial fibrillation

The main goals of treatment are to prevent circulatory instability and stroke. Rate or rhythm control are used to

achieve the former, while anticoagulation is used to decrease the risk of the latter. [21] If cardiovascularly unstable

due to uncontrolled tachycardia, immediate cardioversion is indicated.[1]

Anticoagulation

Anticoagulation can be achieved through a number of means including the use of heparin, warfarin, dabigatran and

rivaroxaban . Which method is used depends on a number issues including: cost, risk of stroke, risk of falls,

compliance, and speed of desired onset of anticoagulation.[22] Some other anticoagulants were discussed in a 201

state-of-the-art paper but were not generally approved at that time for stroke prevention in AF: apixaban, and

edoxaban.[23]

Rate control versus rhythm control using drugs

AF can cause disabling and bothersome symptoms. Palpitations, chest discomfort, anxiety, and decreased exercis

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.

There are two ways to approach these symptoms using drugs: rate control and rhythm control.Rate controllowe

the heart rate closer to normal, usually 60 to 100 bpm, without trying to convert to a regular rhythm.Rhythm

controlrestores normal heart rhythm in a process called cardioversion and maintains the normal rhythm with drug

Studies suggest that rhythm control is most important in the acute setting AF, while rate control is more important i
http://en.wikipedia.org/wiki/Tachycardia_induced_cardiomyopathyhttp://en.wikipedia.org/wiki/Heart_failurehttp://en.wikipedia.org/wiki/Palpitationshttp://en.wikipedia.org/wiki/Atrial_fibrillation#cite_note-DeCaterina2012-23http://en.wikipedia.org/wiki/Edoxabanhttp://en.wikipedia.org/wiki/Apixabanhttp://en.wikipedia.org/wiki/Atrial_fibrillation#cite_note-Singer2004-22http://en.wikipedia.org/wiki/Rivaroxabanhttp://en.wikipedia.org/wiki/Dabigatranhttp://en.wikipedia.org/wiki/Warfarinhttp://en.wikipedia.org/wiki/Heparinhttp://en.wikipedia.org/wiki/Anticoagulationhttp://en.wikipedia.org/wiki/Atrial_fibrillation#cite_note-pmid16908781-1http://en.wikipedia.org/wiki/Tachycardiahttp://en.wikipedia.org/wiki/Atrial_fibrillation#cite_note-21http://en.wikipedia.org/wiki/Anticoagulationhttp://en.wikipedia.org/wiki/Strokehttp://en.wikipedia.org/wiki/Shock_(circulatory)http://en.wikipedia.org/wiki/Management_of_atrial_fibrillationhttp://en.wikipedia.org/wiki/Atrial_fibrillation#cite_note-Klabunde2005-20http://en.wikipedia.org/wiki/Cardiac_outputhttp://en.wikipedia.org/wiki/Ventricular_tachycardiahttp://en.wikipedia.org/wiki/Atrioventricular_nodehttp://en.wikipedia.org/wiki/Electrocardiogramhttp://en.wikipedia.org/wiki/Atrial_flutterhttp://en.wikipedia.org/wiki/Atrial_fibrillation#cite_note-AHA2001-19http://en.wikipedia.org/wiki/Wavelet


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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

ears (end of study).[24]

There is no difference in risk of stroke in patients who have converted to a normal rhythm with anti-arrhythmic

treatment compared to those who have only rate control.[24] 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.[25]

A 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.[26] However, the diagnosis and progression of atrial fibrillation and other

cardiovascular disease requires further investigation.

In patients with a fast ventricular response, intravenous magnesium significantly increases the chances of successfu

rate and rhythm control in the urgent setting without major side-effects.[27] A patient with fluctuating vital signs,

mental status changes, preexcitation, or chest pain often will go to immediate treatment with synchronized DC

cardioversion.[1] Otherwise the decision of rate control versus rhythm control using drugs is made. This is based o

a number of criteria that includes whether or not symptoms persist with rate control.

Rate control

Rate control is achieved with medications that work by increasing the degree of block at the level of the AV node

effectively decreasing the number of impulses that conduct into the ventricles. This can be done with:[1][28]

Beta blockers (preferably the "cardioselective" beta blockers such as metoprolol, atenolol, bisoprolol,

nebivolol)

Non-dihydropyridine calcium channel blockers (e.g., diltiazem or verapamil)

Cardiac glycosides (e.g., digoxin) have limited use, apart from in the sedentary elderly patient

In addition to these agents, amiodarone has some AV node blocking effects (particularly when administered

intravenously), and can be used in individuals when other agents are contraindicated or ineffective (particularly due

to hypotension).

Diltiazem has been shown to be more effective than either digoxin or amiodarone.[29]

Cardioversion

Cardioversion is a noninvasive conversion of an irregular heartbeat to a normal heartbeat using electrical orchemical means.[1]

Electrical cardioversion involves the restoration of normal heart rhythm through the application of a DC

electrical shock.

Chemical cardioversion is performed with drugs, such as amiodarone, dronedarone,[30] procainamide,

dofetilide, ibutilide, propafenone, or flecainide.

Vernakalant, an investigational drug which is unavailable in the U.S., has been found to safely and rapidly convert

new onset atrial fibrillation in one published study.[31]
http://en.wikipedia.org/wiki/Atrial_fibrillation#cite_note-31http://en.wikipedia.org/wiki/Vernakalanthttp://en.wikipedia.org/wiki/Flecainidehttp://en.wikipedia.org/wiki/Propafenonehttp://en.wikipedia.org/wiki/Ibutilidehttp://en.wikipedia.org/wiki/Dofetilidehttp://en.wikipedia.org/wiki/Procainamidehttp://en.wikipedia.org/wiki/Atrial_fibrillation#cite_note-30http://en.wikipedia.org/wiki/Dronedaronehttp://en.wikipedia.org/wiki/Amiodaronehttp://en.wikipedia.org/wiki/Atrial_fibrillation#cite_note-pmid16908781-1http://en.wikipedia.org/wiki/Cardioversionhttp://en.wikipedia.org/wiki/Atrial_fibrillation#cite_note-29http://en.wikipedia.org/wiki/Digoxinhttp://en.wikipedia.org/wiki/Cardiac_glycosideshttp://en.wikipedia.org/wiki/Verapamilhttp://en.wikipedia.org/wiki/Diltiazemhttp://en.wikipedia.org/wiki/Calcium_channel_blockerhttp://en.wikipedia.org/wiki/Nebivololhttp://en.wikipedia.org/wiki/Bisoprololhttp://en.wikipedia.org/wiki/Atenololhttp://en.wikipedia.org/wiki/Metoprololhttp://en.wikipedia.org/wiki/Beta_blockershttp://en.wikipedia.org/wiki/Atrial_fibrillation#cite_note-NICE2006-28http://en.wikipedia.org/wiki/Atrial_fibrillation#cite_note-pmid16908781-1http://en.wikipedia.org/wiki/Atrial_fibrillation#cite_note-pmid16908781-1http://en.wikipedia.org/wiki/Atrial_fibrillation#cite_note-27http://en.wikipedia.org/wiki/Magnesiumhttp://en.wikipedia.org/wiki/Atrial_fibrillation#cite_note-26http://en.wikipedia.org/wiki/Atrial_fibrillation#cite_note-25http://en.wikipedia.org/wiki/Atrial_fibrillation#cite_note-pmid12466506-24http://en.wikipedia.org/wiki/Atrial_fibrillation#cite_note-pmid12466506-24http://en.wiktionary.org/wiki/mortality


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After 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.[32]

Ablation

In young patients where rhythm control is desired and cannot be maintained by medication or cardioversion then

radiofrequency ablation may be attempted and is preferred over years of drug therapy.[1]

Maze Procedure

The Maze 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 lowe

chambers of the heart (ventricles), thus restoring the normal heart rhythm. [33]

Following surgery

AF often occurs after cardiac surgery and is usually self-limiting. It is strongly associated with age, pre-operativehypertension, and the number of vessels grafted. Measures should be taken to control hypertension pre-operativel

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.[34] 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.

Prognosis

Thromboembolism

See also: CHADS score

In atrial fibrillation, the lack of an organized atrial contraction can result in some stagnant blood in the left atrium

(LA) or left atrial appendage (LAA). This lack of movement of blood can lead to thrombus formation (blood

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 flowingthrough 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, while emboli follow the blood circulation to

specific points in the body. Emboli in the brain may result in an ischemic stroke or a transient ischemic attack (TIA

More than 90% of cases of thrombi associated with non-valvular atrial fibrillation evolve in the left atrial

appendage.[7] 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 th

left ventricle, if there is good ventricular function.[35]
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If the LA is enlarged, there is an increased risk of thrombi that originate in the LA. Moderate to severe,

non-rheumatic, mitral regurgitation (MR) reduces this risk of stroke.[36] This risk reduction may be due to a

beneficial stirring effect of the MR blood flow into the LA.[37]

Mitral valve

Atrial 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 annulus.[38]

With a normal sinus 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.[38]

Epidemiology

Atrial fibrillation is the most common arrhythmia found in clinical practice.[1] It also accounts for 1/3 of hospital

admissions for cardiac rhythm disturbances,[1] and the rate of admissions for AF has risen in recent years.[39]

Strokes from AF account for 6-24% of all ischemic strokes.[40] Between 311% of those with AF have

structurally normal hearts.[15] Approximately 2.2 million individuals in the United States and 4.5 million in the

European Union have AF.[1][41]

The incidence of atrial fibrillation increases with age. The prevalence in individuals over the age of 80 is about

8%.[42] 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.[43]

Genetics

Four type of genetic disorder are associated with atrial fibrillation:[44]

familial AF as a monogenic disease

familial AF presenting in the setting of another inherited cardiac disease (hypertrophic cardiomyopathy,

dilated cardiomyopathy, familial amyloidosis)

inherited arrhythmic syndromes (congenital long QT syndrome, short QT syndrome, Brugada syndrome)

non-familial AF associated with genetic backgrounds (polymorphism in the ACE gene) that may predisposeto atrial fibrillation

History

Because the diagnosis of atrial fibrillation requires measurement of the electrical activity of the heart, atrial fibrillatio

was not truly described until 1874, when Edm Flix Alfred Vulpian observed the irregular atrial electrical behavio

that he termed "fremissement fibrillaire"in dog hearts.[45] In the mid-eighteenth century, Jean-Baptiste de Sna

made note of dilated, irritated atria in people with mitral stenosis.[46] The irregular pulse associated with AF was
http://en.wikipedia.org/wiki/Atrial_fibrillation#cite_note-46http://en.wikipedia.org/wiki/Mitral_stenosishttp://en.wikipedia.org/wiki/Jean-Baptiste_de_S%C3%A9nachttp://en.wikipedia.org/wiki/Atrial_fibrillation#cite_note-45http://en.wikipedia.org/wiki/Edm%C3%A9_F%C3%A9lix_Alfred_Vulpianhttp://en.wikipedia.org/wiki/Brugada_syndromehttp://en.wikipedia.org/wiki/Short_QT_syndromehttp://en.wikipedia.org/wiki/Long_QT_syndromehttp://en.wikipedia.org/w/index.php?title=Familial_amyloidosis&action=edit&redlink=1http://en.wikipedia.org/wiki/Dilated_cardiomyopathyhttp://en.wikipedia.org/wiki/Hypertrophic_cardiomyopathyhttp://en.wikipedia.org/wiki/Atrial_fibrillation#cite_note-Shimizu2013-44http://en.wikipedia.org/wiki/Atrial_fibrillation#cite_note-43http://en.wikipedia.org/wiki/Atrial_fibrillation#cite_note-42http://en.wikipedia.org/wiki/Atrial_fibrillation#cite_note-41http://en.wikipedia.org/wiki/Atrial_fibrillation#cite_note-pmid16908781-1http://en.wikipedia.org/wiki/Atrial_fibrillation#cite_note-Sanfilippo1990-15http://en.wikipedia.org/wiki/Atrial_fibrillation#cite_note-Narumiya2003-40http://en.wikipedia.org/wiki/Stroke#Ischemichttp://en.wikipedia.org/wiki/Atrial_fibrillation#cite_note-Friberg-2003-39http://en.wikipedia.org/wiki/Atrial_fibrillation#cite_note-pmid16908781-1http://en.wikipedia.org/wiki/Atrial_fibrillation#cite_note-pmid16908781-1http://en.wikipedia.org/wiki/Atrial_fibrillation#cite_note-Pai2003-38http://en.wikipedia.org/wiki/Sphincterhttp://en.wikipedia.org/wiki/Left_atriumhttp://en.wikipedia.org/wiki/Systole_(medicine)http://en.wikipedia.org/wiki/Diastolehttp://en.wikipedia.org/wiki/Cardiac_cyclehttp://en.wikipedia.org/wiki/Normal_sinus_rhythmhttp://en.wikipedia.org/wiki/Atrial_fibrillation#cite_note-Pai2003-38http://en.wikipedia.org/wiki/Mitral_valve#Anatomyhttp://en.wikipedia.org/wiki/Mitral_valvehttp://en.wikipedia.org/wiki/Atrial_fibrillation#cite_note-Cheng1999-37http://en.wikipedia.org/wiki/Atrial_fibrillation#cite_note-Nakagami1998-36http://en.wikipedia.org/wiki/Mitral_regurgitationhttp://en.wikipedia.org/wiki/Rheumatic_fever


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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 tensio

of the individual pulse waves are continuously changing".[47] Correlation of delirium cordis with the loss of atrial

contraction as reflected in the loss ofa waves in the jugular venous pulse was made by Sir James MacKenzie in

1904.[48] Willem Einthoven published the first ECG showing AF in 1906.[49] The connection between the anatom

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.[50][51][52]

References

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Guidelines for the Management of Patients with Atrial Fibrillation: a report of the American College of

Cardiology/American Heart Association Task Force on Practice Guidelines and the European Society of Cardiolog

Committee for Practice Guidelines (Writing Committee to Revise the 2001 Guidelines for the Management of

Patients With Atrial Fibrillation): developed in collaboration with the European Heart Rhythm Association and the

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(http://dx.doi.org/10.1161%2FCIRCULATIONAHA.106.177292). PMID 16908781

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2. ^ Levy S (2000). "Classification system of atrial fibrillation". Curr Opin Cardiol15 (1): 547.

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PMID 10666661 (//www.ncbi.nlm.nih.gov/pubmed/10666661).

3. ^ Leung, RS; Huber MA, Rogge T, Maimon N, Chiu KL, Bradley TD (2005-12-01). "Association between atrial

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4. ^ ab Fitzmaurice DA, Hobbs FD, Jowett S et al. (2007). "Screening versus routine practice in detection of atrial

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5. ^ Mant J, Fitzmaurice DA, Hobbs FD et al. (2007). "Accuracy of diagnosing atrial fibrillation on electrocardiogram

by primary care practitioners and interpretative diagnostic software: analysis of data from screening for atrial

fibrillation in the elderly (SAFE) trial" (http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1952490).BMJ335 (7616

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6. ^ Zipes, Ziad F. Issa, John M. Miller, Douglas P. (2009). Clinical arrhythmology and electrophysiology : a

companion to Braunwald's heart disease (http://books.google.ca/books?id=a8s8nd2JAiwC&pg=PA221).

Philadelphia: Saunders. p. 221. ISBN 978-1-4160-5998-1.

7. ^ ab Blackshear JL, Odell JA (February 1996). "Appendage obliteration to reduce stroke in cardiac surgical patien

with atrial fibrillation".Ann. Thorac. Surg.61 (2): 7559. doi:10.1016/0003-4975(95)00887-X

(http://dx.doi.org/10.1016%2F0003-4975%2895%2900887-X). PMID 8572814


8. ^ Acar J, Cormier B, Grimberg D et al. (1991). "Diagnosis of left atrial thrombi in mitral stenosis usefulness of

ultrasound techniques compared with other methods"

(http://eurheartj.oxfordjournals.org/cgi/content/abstract/12/suppl_B/70).European Heart Journal. 12 (Supplemen

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