View source for Atrial fibrillation

{| border="1" style="border-collapse:collapse" cellpadding="3" align="right"
| colspan="3" align="center" bgcolor="#ABCDEF" | Conduction
|-
| <small>Sinus rhythm</small> [[Image:Heart conduct sinus.gif|none|230px]]
| <small>Atrial fibrillation</small> [[Image:Heart conduct atrialfib.gif|none|230px]] 
|}
{{Infobox_Disease |
  Name           = Atrial fibrillation |
  Image          = SinusRhythmLabels.png  |
  Caption        = The P waves, which represent depolarization of the atria, are irregular or absent during atrial fibrillation. |
  DiseasesDB     = 1065 |
  ICD10          = {{ICD10|I|48||i|30}} |
  ICD9           = {{ICD9|427.31}} |
  ICDO           = |
  OMIM           = |
  MedlinePlus    = 000184 |
  eMedicineSubj  = med |
  eMedicineTopic = 184 |
  eMedicine_mult = {{eMedicine2|emerg|46}} | 
}}
{{SI}}
{{WikiDoc Cardiology Network Infobox}}
{{CMG}}

'''Associate Editor-In-Chief:''' {{CZ}}

{{Editor Join}}

'''Synonyms and related keywords''': AF, Afib, fib

==Overview==
===[[Atrial fibrillation overview|Overview]]===

==Classification==

Although several clinical classification plans and protocols have been proposed, none of them fully account for all aspects of atrial fibrillation. The [[American Heart Association]], [[American College of Cardiology]], and the [[European Society of Cardiology]] have proposed the following classification system based on simplicity and clinical relevance:<ref name="pmid16908781">{{cite journal |author=Fuster V, Rydén LE, Cannom DS, ''et al'' |title=ACC/AHA/ESC 2006 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 Cardiology 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 Heart Rhythm Society |journal=Circulation |volume=114 |issue=7 |pages=e257-354 |year=2006 |pmid=16908781 |doi=10.1161/CIRCULATIONAHA.106.177292}}</ref>

{|class="wikitable" style="margin: 1em auto 1em auto"
|-
! width="100"| '''AF Category'''
! width="350"| '''Defining Characteristics''' 
|-
| &nbsp; First detected
| &nbsp; only one diagnosed episode
|-
| &nbsp; Paroxysmal
| &nbsp; recurrent episodes that self-terminate in less than 7 days
|-
| &nbsp; Persistent
| &nbsp;  recurrent episodes that last more than 7 days 
|-
| &nbsp; Permanent
| &nbsp; an ongoing long-term episode 
|-
|}

===First detected [[atrial fibrillation]]===

Any patient with new diagnosed [[Atrial fibrillation|AF]] is in this category, as the exact onset and chronicity of the disease is often uncertain.

===Recurrent [[atrial fibrillation]]===

Two or more identified episodes of [[atrial fibrillation]] are named as '''recurrent''' form of [[atrial fibrillation]]. This is further classified into '''paroxysmal''' and '''persistent''' based on when the episode terminates without therapy. [[Atrial fibrillation]] is said to be paroxysmal when it terminates spontaneously within 7 days, most commonly within 24 hours.

The term 'Persistent' or 'chronic' is used if diagnosis of [[atrial fibrillation]] established for more than seven days. Differentiation of paroxysmal from chronic or established [[AF]] is based on the history of recurrent episodes and the duration of the current  AF episode.<ref name="pmid16908781"/><ref>{{cite journal | author=Levy S | title=Epidemiology and classification of atrial fibrillation | journal=J Cardiovasc Electrophysiol | year=1998 | pages=S78-82 | volume=9 | issue=8 Suppl }} PMID 9727680</ref><ref>{{cite journal | author=Levy S | title=Classification system of atrial fibrillation | journal=Curr Opin Cardiol | year=2000 | pages=54-7 | volume=15 | issue=1 }} PMID 10666661</ref>

===Lone [[atrial fibrillation]] (LAF)=== 

Lone [[atrial fibrillation]] is defined as [[atrial fibrillation]] in the absence of clinical or echocardiographic findings of cardiopulmonary disease including [[hypertension]].<ref name="pmid16908781"/> Patients in this group are young individuals (less than 60 years old). 

== Prevalence==
It should be noted that the prevalence of atrial fibrillation increases with increasing age, and its prevalence is increased among Caucasians, patients with hypertension and valvular heart disease<ref name="pmid11601835">{{cite journal |author=Fuster V, Rydén LE, Asinger RW, ''et al'' |title=ACC/AHA/ESC 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 Cardiology Committee for Practice Guidelines and Policy Conferences (Committee to develop guidelines for the management of patients with atrial fibrillation) developed in collaboration with the North American Society of Pacing and Electrophysiology |journal=Eur. Heart J. |volume=22 |issue=20 |pages=1852–923 |year=2001 |month=October |pmid=11601835 |doi=10.1053/euhj.2001.2983 |url=}}</ref>. The prevalence in the general population is 0.4%.<ref name="pmid14297523">{{cite journal |author=OSTRANDER LD, BRANDT RL, KJELSBERG MO, EPSTEIN FH |title=ELECTROCARDIOGRAPHIC FINDINGS AMONG THE ADULT POPULATION OF A TOTAL NATURAL COMMUNITY, TECUMSEH, MICHIGAN |journal=Circulation |volume=31 |issue= |pages=888–98 |year=1965 |month=June |pmid=14297523 |doi= |url=http://circ.ahajournals.org/cgi/pmidlookup?view=long&pmid=14297523}}</ref>

Important genetic determinants may play a role in so far as the age-adjusted risk of developing atrial fibrillation among African-Americans is less than half that in Caucasians. <ref name="pmid">{{cite journal |author=Flegel KM, Shipley MJ, Rose G |title=Risk of stroke in non-rheumatic atrial fibrillation |journal=Lancet |volume=1 |issue=8532 |pages=526–9 |year=1987 |month=March |pmid= |doi= |url=http://linkinghub.elsevier.com/retrieve/pii/S0140-6736(87)90174-7}}</ref><ref name="pmid1866765">{{cite journal |author=Wolf PA, Abbott RD, Kannel WB |title=Atrial fibrillation as an independent risk factor for stroke: the Framingham Study |journal=Stroke |volume=22 |issue=8 |pages=983–8 |year=1991 |month=August |pmid=1866765 |doi= |url=http://stroke.ahajournals.org/cgi/pmidlookup?view=long&pmid=1866765}}</ref> <ref name="pmid8037127">{{cite journal |author=Furberg CD, Psaty BM, Manolio TA, Gardin JM, Smith VE, Rautaharju PM |title=Prevalence of atrial fibrillation in elderly subjects (the Cardiovascular Health Study) |journal=Am. J. Cardiol. |volume=74 |issue=3 |pages=236–41 |year=1994 |month=August |pmid=8037127 |doi= |url=}}</ref> The presence of atrial fibrillation often reflects the presence of underlying cardiac or lung disease.  Indeed, the proportion of patients with “lone” atrial fibrillation, (that is those patients with atrial fibrillation in whom there is no cardiac or lung disease history) is low at about 12% of cases. <ref name="pmid3627174">{{cite journal |author=Kopecky SL, Gersh BJ, McGoon MD, ''et al'' |title=The natural history of lone atrial fibrillation. A population-based study over three decades |journal=N. Engl. J. Med. |volume=317 |issue=11 |pages=669–74 |year=1987 |month=September |pmid=3627174 |doi= |url=}}</ref><ref name="pmid8037127">{{cite journal |author=Furberg CD, Psaty BM, Manolio TA, Gardin JM, Smith VE, Rautaharju PM |title=Prevalence of atrial fibrillation in elderly subjects (the Cardiovascular Health Study) |journal=Am. J. Cardiol. |volume=74 |issue=3 |pages=236–41 |year=1994 |month=August |pmid=8037127 |doi= |url=}}</ref><ref name="pmid13160271">{{cite journal |author=EVANS W, SWANN P |title=Lone auricular fibrillation |journal=Br Heart J |volume=16 |issue=2 |pages=189–94 |year=1954 |month=April |pmid=13160271 |pmc=479515 |doi= |url=http://heart.bmj.com/cgi/pmidlookup?view=long&pmid=13160271}}</ref><ref name="pmid4068186">{{cite journal |author=Brand FN, Abbott RD, Kannel WB, Wolf PA |title=Characteristics and prognosis of lone atrial fibrillation. 30-year follow-up in the Framingham Study |journal=JAMA |volume=254 |issue=24 |pages=3449–53 |year=1985 |month=December |pmid=4068186 |doi= |url=}}</ref> Patients with atrial fibrillation tend to be older with a median age of 75 years.  The proportion of patients with atrial fibrillation who are between 65 and 85 years of age is 70%, and females predominate in the very elderly (60% of atrial fibrillation patients over the age of 75 are women).<ref name="pmid7864703">{{cite journal |author=Feinberg WM, Blackshear JL, Laupacis A, Kronmal R, Hart RG |title=Prevalence, age distribution, and gender of patients with atrial fibrillation. Analysis and implications |journal=Arch. Intern. Med. |volume=155 |issue=5 |pages=469–73 |year=1995 |month=March |pmid=7864703 |doi= |url=http://archinte.ama-assn.org/cgi/pmidlookup?view=long&pmid=7864703}}</ref>  Despite the fact that there are more very elderly women with atrial fibrillation, when age is adjusted for, the prevalence of atrial fibrillation is higher in men.<ref name="pmid8037127">{{cite journal |author=Furberg CD, Psaty BM, Manolio TA, Gardin JM, Smith VE, Rautaharju PM |title=Prevalence of atrial fibrillation in elderly subjects (the Cardiovascular Health Study) |journal=Am. J. Cardiol. |volume=74 |issue=3 |pages=236–41 |year=1994 |month=August |pmid=8037127 |doi= |url=}}</ref><ref name="pmid6869222">{{cite journal |author=Kannel WB, Abbott RD, Savage DD, McNamara PM |title=Coronary heart disease and atrial fibrillation: the Framingham Study |journal=Am. Heart J. |volume=106 |issue=2 |pages=389–96 |year=1983 |month=August |pmid=6869222 |doi= |url=}}</ref>  The rate of rise per year in the risk of atrial fibrillation is slightly higher in the very elderly (1.5% per year for women and 2.0% per year for men over the age of 80 years).  These rates are nearly 15 to 20 times higher than in those under the age of 40.<ref name="pmid9337224">{{cite journal |author=Psaty BM, Manolio TA, Kuller LH, ''et al'' |title=Incidence of and risk factors for atrial fibrillation in older adults |journal=Circulation |volume=96 |issue=7 |pages=2455–61 |year=1997 |month=October |pmid=9337224 |doi= |url=http://circ.ahajournals.org/cgi/pmidlookup?view=long&pmid=9337224}}</ref><ref name="pmid3632164">{{cite journal |author=Wolf PA, Abbott RD, Kannel WB |title=Atrial fibrillation: a major contributor to stroke in the elderly. The Framingham Study |journal=Arch. Intern. Med. |volume=147 |issue=9 |pages=1561–4 |year=1987 |month=September |pmid=3632164 |doi= |url=http://archinte.ama-assn.org/cgi/pmidlookup?view=long&pmid=3632164}}</ref><ref name="pmid7733127">{{cite journal |author=Krahn AD, Manfreda J, Tate RB, Mathewson FA, Cuddy TE |title=The natural history of atrial fibrillation: incidence, risk factors, and prognosis in the Manitoba Follow-Up Study |journal=Am. J. Med. |volume=98 |issue=5 |pages=476–84 |year=1995 |month=May |pmid=7733127 |doi=10.1016/S0002-9343(99)80348-9 |url=}}</ref>


==Epidemiology==

Atrial fibrillation is the most common arrhythmia found in clinical practice.<ref name="pmid16908781"/> It also accounts for 1/3 of hospital admissions for cardiac rhythm disturbances<ref name="pmid16908781"/>, and the rate of admissions for AF has risen in recent years.<ref name="Friberg-2003">{{cite journal | author=Friberg J, Buch P, Scharling H, Gadsbphioll N, Jensen GB. | title=Rising rates of hospital admissions for atrial fibrillation | journal=Epidemiology | year=2003 | volume=14 | issue=6 | pages=666–72 | pmid=14569181 | doi=10.1097/01.ede.0000091649.26364.c0}}</ref> Approximately 2.2&nbsp;million individuals in the United States and 4.5&nbsp;million in the European Union have AF.<ref name="pmid16908781"/><ref>{{cite journal |author=Go AS, Hylek EM, Phillips KA, ''et al'' |title=Prevalence of diagnosed atrial fibrillation in adults: national implications for rhythm management and stroke prevention: the AnTicoagulation and Risk Factors in Atrial Fibrillation (ATRIA) Study |journal=JAMA |volume=285 |issue=18 |pages=2370–5 |year=2001 |pmid=11343485|doi=10.1001/jama.285.18.2370}}</ref>

The incidence of atrial fibrillation increases with age. The prevalence in individuals over the age of 80 is about 8%.<ref>{{cite journal |author=Furberg CD, Psaty BM, Manolio TA, Gardin JM, Smith VE, Rautaharju PM |title=Prevalence of atrial fibrillation in elderly subjects (the Cardiovascular Health Study) |journal=Am. J. Cardiol. |volume=74 |issue=3 |pages=236–41 |year=1994 |pmid=8037127|doi=10.1016/0002-9149(94)90363-8}}</ref> In developed countries, the number of patients with atrial fibrillation is likely to increase during the next 50&nbsp;years, due to the growing proportion of elderly individuals.<ref>{{cite journal | author=Go AS, Hylek EM, Phillips KA, Chang Y, Henault LE, Selby JV, Singer DE | title=Prevalence of diagnosed atrial fibrillation in adults: national implications for rhythm management and stroke prevention: the AnTicoagulation and Risk Factors in Atrial Fibrillation (ATRIA) Study | journal=JAMA | year=2001 | pages=2370–5 | volume=285 | issue=18  | doi=10.1001/jama.285.18.2370 | pmid=11343485}} PMID 11343485</ref>

==Pathophysiology== 

==Etiology of atrial fibrillation==

[[Atrial fibrillation|AF]] can be associated with underlying cardiac diseases, but it may also occur in otherwise normal hearts.

===Common Causes===
*[[Hypertension]]
*[[Heart failure]]
*[[Coronary artery bypass surgery]]

===Complete Differential Diagnosis of Underlying Etiologies for Atrial Fibrillation===
{|style="width:70%; height:100px" border="1"
|style="height:100px"; style="width:25%" border="1" bgcolor="LightSteelBlue" | '''Cardiovascular'''
|style="height:100px"; style="width:65%" border="1" bgcolor="Beige" | [[Acute myocardial infarction]] • [[Congenital heart disease]] especially [[atrial septal defect]] in adults • [[Coronary artery disease]] • [[Heart failure]] (especially diastolic dysfunction and diastolic heart failure) • [[Hypertrophic cardiomyopathy]] (HCM) • [[Hypertension]] • [[Mitral regurgitation]]
[[Mitral stenosis]] (e.g. due to [[Rheumatic heart disease]] or [[Mitral valve prolapse]]) • [[Myocarditis]] • [[Pericarditis]] • Previous [[heart surgery]] • Dual-chamber [[pacemaker]]s in the presence of normal atrioventricular conduction.<ref>{{cite journal |author=Sweeney MO, Bank AJ, Nsah E, ''et al'' |title=Minimizing ventricular pacing to reduce atrial fibrillation in sinus-node disease |journal=N. Engl. J. Med. |volume=357 |issue=10 |pages=1000-8 |year=2007 |pmid=17804844 |doi=10.1056/NEJMoa071880}}</ref> • Restrictive cardiomyopathies (such as [[amyloidosis]], [[hemochromatosis]], and [[endomyocardial fibrosis]]), [[cardiac tumors]], and [[constrictive pericarditis]]
|-
|-bgcolor="LightSteelBlue"
| '''Congenital'''
|bgcolor="Beige"| 
|-
|-
|-bgcolor="LightSteelBlue"
| '''Dermatologic'''
|bgcolor="Beige"| No underlying causes
|-
|-
|-bgcolor="LightSteelBlue"
| '''Drugs'''
|bgcolor="Beige"| [[Digoxin]] in patients with vagally mediated AF
|-
|-bgcolor="LightSteelBlue"
| '''Ear Nose Throat'''
|bgcolor="Beige"| No underlying causes
|- 
|-bgcolor="LightSteelBlue"
| '''Endocrine'''
|bgcolor="Beige"| [[Hyperthyroidism]] • [[Hypothyroidism]] • [[Pheochromocytoma]]
|-
|-bgcolor="LightSteelBlue"
| '''Gastroenterologic'''
|bgcolor="Beige"| [[Vomiting]]
|-
|-bgcolor="LightSteelBlue"
| '''Genetic'''
|bgcolor="Beige"| A family history of AF increases risk by 30%.<ref name="pmid15199036">{{cite journal |author=Fox CS, Parise H, D'Agostino RB, ''et al'' |title=Parental atrial fibrillation as a risk factor for atrial fibrillation in offspring |journal=JAMA |volume=291 |issue=23 |pages=2851-5 |year=2004 |pmid=15199036 |doi=10.1001/jama.291.23.2851}}</ref> Various genetic mutations may be responsible.<ref name="pmid16790707">{{cite journal |author=Saffitz JE |title=Connexins, conduction, and atrial fibrillation |journal=N. Engl. J. Med. |volume=354 |issue=25 |pages=2712-4 |year=2006 |pmid=16790707 |doi=10.1056/NEJMe068088}}</ref>
|-
|-bgcolor="LightSteelBlue"
| '''Hematologic'''
|bgcolor="Beige"| No underlying causes
|-
|-bgcolor="LightSteelBlue"
| '''Infectious Disease'''
|bgcolor="Beige"| No underlying causes
|-
|-bgcolor="LightSteelBlue"
| '''Musculoskeletal / Ortho'''
|bgcolor="Beige"| No underlying causes
|-
|-bgcolor="LightSteelBlue"
| '''Neurologic'''
|bgcolor="Beige"| [[Multiple sclerosis]]
|-
|-bgcolor="LightSteelBlue"
| '''Nutritional / Metabolic'''
|bgcolor="Beige"| No underlying causes
|-
|-bgcolor="LightSteelBlue"
| '''Oncologic'''
|bgcolor="Beige"| No underlying causes
|-
|-bgcolor="LightSteelBlue"
| '''Opthalmologic'''
|bgcolor="Beige"| No underlying causes
|-
|-bgcolor="LightSteelBlue"
| '''Overdose / Toxicity'''
|bgcolor="Beige"| Excessive [[alcoholic beverage|alcohol]] consumption ("[[binge drinking]]" or "[[holiday heart syndrome]]") • [[Carbon monoxide poisoning]] • [[Caffeine]] • Stimulants
|-
|-bgcolor="LightSteelBlue"
| '''Post-Op Complication'''
|bgcolor="Beige"|[[Surgery]],particularly [[coronary artery bypass surgery]]  •  During [[pulmonary artery line placement]] and right heart catheterization trauma to the [[right atrium]] can result in atrial fibrillation
|-
|-bgcolor="LightSteelBlue"
| '''Pulmonary'''
|bgcolor="Beige"| [[Hypoxia]] of any cause • [[Lung cancer]] • [[Pneumonia]] • [[Pulmonary embolism]] • [[Sarcoidosis]] • [[Sleep apnea|sleep apnea syndrome]]
|-
|-bgcolor="LightSteelBlue"
| '''Renal / Electrolyte'''
|bgcolor="Beige"| [[Hypokalemia]]
|-
|-bgcolor="LightSteelBlue"
| '''Rheum / Immune / Allergy'''
|bgcolor="Beige"| No underlying causes
|-
|-bgcolor="LightSteelBlue"
| '''Trauma'''
|bgcolor="Beige"| [[Electrocution]] • [[Cardiac contusion]]
|-
|-bgcolor="LightSteelBlue"
| '''Miscellaneous'''
|bgcolor="Beige"| [[Hypothermia]] • [[Fever]]
|-
|}

==The autonomic nervous system may trigger [[AF]] in susceptible patients through heightened vagal or adrenergic tone==



===Morphology===
The primary pathologic change seen in atrial fibrillation is the progressive fibrosis of the atria.  This fibrosis is primarily due to atrial dilatation, however genetic causes and inflammation may have a cause in some individuals.

Dilatation 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]] AC'' gene is also associated with fibrosis of the atria that can lead to atrial fibrillation.

Once dilatation of the atria has occurred, this begins a chain of events that leads to the activation of the [[renin-angiotensin system|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.

Fibrosis 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,<ref name="pmid16908781"/> <ref name="pmid8941126">{{cite journal |author=Elvan A, Wylie K, Zipes D |title=Pacing-induced chronic atrial fibrillation impairs sinus node function in dogs. Electrophysiological remodeling |journal=Circulation |volume=94 |issue=11 |pages=2953–60 |year=1996 |url=http://www.circ.ahajournals.org/cgi/content/abstract/94/11/2953 |pmid=8941126 }}</ref><ref name="pmid11469431">{{cite journal |author=Manios EG, Kanoupakis EM, Mavrakis HE, Kallergis EM, Dermitzaki DN, Vardas PE |title=Sinus pacemaker function after cardioversion of chronic atrial fibrillation: is sinus node remodeling related with recurrence? |journal=Journal of Cardiovascular Electrophysiology |volume=12 |issue=7 |pages=800–6 |year=2001 |pmid=11469431 |doi=10.1046/j.1540-8167.2001.00800.x }}</ref> suggesting that dysfunction of the SA node is progressive with prolonged episodes of atrial fibrillation.

==Signs and symptoms==

In general, clinical manifestations are;
# [[Palpitations]]
# [[Chest pain]]
# [[Dyspnea]]
# [[Fatigue]]
# [[Lightheadedness]]
# Syncope: [[Syncope]] is an uncommon but serious complication that is usually associated with [[sinus node]] dysfunction or hemodynamic obstruction, such as valvular [[aortic stenosis]], [[HCM]], [[cerebrovascular disease]], or an accessory AV pathway.

[[Atrial fibrillation]] is usually accompanied by symptoms related to the rapid heart rate. Rapid and irregular heart rates may be perceived as [[palpitations]], [[exercise intolerance]], and occasionally produce [[Angina pectoris|angina]] (if the rate is faster and puts the heart under strain) and [[heart failure|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]], [[stroke]] symptoms resolving within 24 hours). It is not uncommon to identify [[atrial fibrillation]] on a routine physical examination or [[electrocardiogram]] (ECG/EKG), as it may be asymptomatic in many cases.<ref name="pmid16908781"/>

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 previous history of [[stroke]] or [[Transient ischemic attack|TIA]], as well as [[hypertension]] (high blood pressure), [[diabetes mellitus|diabetes]], [[heart failure]] and [[rheumatic fever]], may indicate whether someone with [[atrial fibrillation]] is at a higher risk of complications.<ref name="pmid16908781"/>

==Diagnosis of [[atrial fibrillation]]==

The evaluation of atrial fibrillation involves diagnosis, determination of the etiology of the arrhythmia, and classification of the arrhythmia. A minimal evaluation performed should be performed in all individuals with atrial fibrillation. This includes a history and physical examination, surface electrocardiogram, transthoracic echocardiogram, and routine blood work. Certain individuals may benefit from an extended evaluation which may include an evaluation of the heart rate response to exercise, exercise stress testing, a chest x-ray, trans-esophageal echocardiography, and other studies.

#[[Screening and routine primary care visit for atrial fibrillation]]
#[[History and physical examination for atrial fibrillation]]
#[[Electrocardiogram for diagnosis of atrial fibrillation]]
#[[Chest x-ray for diagnosis of atrial fibrillation]]
#[[Echocardiography for diagnosis of atrial fibrillation]]
#[[Recorders (Holter monitors) for diagnosis of atrial fibrillation]]
#[[Exercise stress tests (Tilt-Table Test) for diagnosis of atrial fibrillation]]
#[[Electrophysiologic Testing or Electrophysiologic Studies for diagnosis of atrial fibrillation]]

==Screening and routine primary care visit==
[[Screening (medicine)|Screening]] for atrial fibrillation is not generally performed, although a study of routine pulse checks or [[electrocardiograms]] during routine office visits, found that the annual rate of detection of atrial fibrillation in elderly patients improved from 1.04% to 1.63%; selection of patients for prophylactic anticoagulation would improve stroke risk in that age category.<ref name="pmid17673732">{{cite journal |author=Fitzmaurice DA, Hobbs FD, Jowett S, ''et al'' |title=Screening versus routine practice in detection of atrial fibrillation in patients aged 65 or over: cluster randomized controlled trial |journal= |volume= |issue= |pages= |year=2007 |pmid=17673732 |doi=10.1136/bmj.39280.660567.55}}</ref>

Estimated [[sensitivity (tests)|sensitivity]] of the routine primary care visit is 64%. This low result probably reflects the pulse not being checked routinely or carefully.<ref name="pmid17673732">{{cite journal |author=Fitzmaurice DA, Hobbs FD, Jowett S, ''et al'' |title=Screening versus routine practice in detection of atrial fibrillation in patients aged 65 or over: cluster randomized controlled trial |journal= |volume= |issue= |pages= |year=2007 |pmid=17673732 |doi=10.1136/bmj.39280.660567.55}}</ref>

==History and physical examination for atrial fibrillation==
The history of the individual's atrial fibrillation episodes is likely the most important part of the evaluation. Distinctions should be made to those who are entirely asymptomatic when they are in atrial fibrillation (in which case the atrial fibrillation is found as an incidental finding on an electrocardiogram or physical examination) and those who have gross and obvious symptoms due to atrial fibrillation and can pinpoint whenever they go into atrial fibrillation and revert to sinus rhythm.

Detailed history and physical examination are essential to define;
* The presence and nature of symptoms associated with AF
* The clinical type of AF (first episode, paroxysmal, persistent, or permanent)
* The onset of the first symptomatic attack or date of discovery of AF
* The frequency, duration, precipitating factors, and modes of termination of AF
* The response to any pharmacological agents that have been administered
* The presence of any underlying heart disease or other reversible conditions (e.g., hyperthyroidism or alcohol consumption)

===Routine blood work===
While many cases of [[AF]] have no definite cause, it may be the result of various other problems (Blood tests of thyroid function are required, especially for a first episode of [[AF]], when the ventricular rate is difficult to control, or when [[AF]] recurs unexpectedly after [[cardioversion]]) 

Hence, [[renal function]] and [[electrolyte]]s are routinely determined, as well as [[thyroid-stimulating hormone]] (commonly suppressed in [[hyperthyroidism]] and of relevance if [[amiodarone]] is administered for treatment) and a [[complete blood count|blood count]].<ref name="pmid16908781"/>

In acute-onset [[AF]] associated with [[chest pain]], [[troponin|cardiac troponins]] or other markers of damage to the heart muscle may be ordered. [[Coagulation]] studies ([[International normalized ratio|INR]]/aPTT) are usually performed, as [[anticoagulant]] medication may be commenced.<ref name="pmid16908781"/>

==Electrocardiogram==
{{main|Electrocardiogram}}
[[Image:Afib ecg.jpg|thumb|400px|right|[[electrocardiogram|ECG]] of atrial fibrillation (top) and sinus rhythm (bottom). The purple arrow indicates a P wave, which is lost in atrial fibrillation.]]

Atrial fibrillation is diagnosed on an [[electrocardiogram]], an investigation performed routinely whenever irregular heart beat is suspected. Characteristic findings are the absence of P waves, with unorganized electrical activity in their place, and irregularity of R-R interval due to irregular conduction of impulses to the ventricles.<ref name="pmid16908781"/>

EKG is helpful to identify;
* Rhythm (verify AF)
* LV hypertrophy
* P-wave duration and morphology or fibrillatory waves
* Preexcitation
* Bundle-branch block
* Prior MI
* Other atrial arrhythmias
* To measure and follow the RR, QRS, and QT intervals in conjunction with antiarrhythmic drug therapy

===Summary of Electrocardiographic findings===
#Absent P waves
#Irregularly irregular ventricular response rate. Regular RR intervals are possible in the presence of AV block or interference due to ventricular or junctional [[tachycardia]].
#An atrial rate that ranges from 400 to 700 BPM.
#sometimes V1 may look as though there is atrial flutter. This may be because the electrode overlies a portion of the RA with rhythmic activity.  
#Some authors believe that fine f waves (<.5 mm) are associated with coronary artery disease and that coarse F waves are associated with LA enlargement and [[rheumatic heart disease]].
#the ventricular rate is usually between 100 and 180 BPM.
#if the atrial rate is greater than 200 BPM, then consider WPW or an accessory pathway.
#In the presence of AV junctional disease, the ventricular rate may be below 70 bpm.
#a rapid, irregular, sustained, wide-QRS-complex [[tachycardia]] strongly suggests AF with conduction over an accessory pathway or AF with underlying bundle-branch block.
# Complete AV block is indicated by a slow ventricular rhythm with a regular RR interval.
#In patients with electronic pacemakers, diagnosis of AF may require temporary inhibition of the pacemaker to expose atrial fibrillatory activity.
#Differential diagnosis includes tremor due to artifact. The oscillations in this case are largest in the limb leads.

When electrocardiograms are used for screening? The SAFE trial found that electronic software, [[primary care physician]]s and the combination of the two had the following sensitivities and specificities:<ref name="pmid17604299">{{cite journal |author=Mant J, Fitzmaurice DA, Hobbs FD, ''et al'' |title=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 |journal= |volume= |issue= |pages= |year=2007 |pmid=17604299 |doi=10.1136/bmj.39227.551713.AE}}</ref>:
* Interpreted by software: [[sensitivity (tests)|sensitivity]] = 83%, [[specificity (tests)|specificity]] = 99%
* Interpreted by a primary care physician: sensitivity = 80%, specificity = 92%
* Interpreted by a primary care physician with software: sensitivity = 92%, specificity = 91%

If paroxysmal AF is suspected but the [[electrocardiogram]] shows a regular rhythm, episodes may be documented with the use of [[Holter monitor]]ing (continuous ECG recording for 24 hours). If the symptoms are very infrequent, longer periods of continuous monitoring may be required.<ref name="pmid16908781"/>

==Chest X-ray==
{{main|Chest X-ray}}
A [[chest X-ray]] is generally only performed if a pulmonary cause of atrial fibrillation is suggested. This may reveal an underlying problem in the lungs or the blood vessels in the chest. <ref name="pmid16908781"/> In particular, if an underlying pneumonia is suggested, then treatment of the pneumonia may cause the atrial fibrillation to terminate on its own.

As a summary a chest radiograph is required to evaluate;
* The lung parenchyma, when clinical findings suggest an abnormality
* The pulmonary vasculature, when clinical findings suggest an abnormality

==Echocardiography==
{{main|Echocardiogram}}

Performing an echocardiogram is essential to identify;
* Valvular heart disease
* Left and right atrial size
* LV size and function
* Peak RV pressure (pulmonary hypertension)
* LV hypertrophy
* LA thrombus (low sensitivity)
* Pericardial disease

===Transthoracic echocardiography (TTE)===
A transthoracic [[echocardiogram]] 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 increase the risk of [[stroke]] manifold), 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 ventricular hypertrophy and pericardial disease.<ref name="pmid16908781"/>

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 of a longer duration than the individual's symptoms.

===Transesophageal echocardiography (TEE)===
A normal [[echocardiography]] (transthoracic or TTE) has a low sensitivity for identifying [[thrombus|thrombi]] (blood clots) in the heart. If this is suspected - e.g. when planning urgent electrical [[cardioversion]] - a [[Echocardiogram#Transesophageal echocardiogram|transesophageal echocardiogram]] (TEE) is preferred.<ref name="pmid16908781"/>

The TEE has much better visualization of the [[left auricular appendix|left atrial appendage]] than transthoracic echocardiography.  This structure, located in the [[left atrium]], is the place where thrombus most commonly is formed in the setting of atrial fibrillation or flutter.  TEE has a very high sensitivity for locating thrombus in this area and can also detect sluggish bloodflow in this area that is suggestive of thrombus formation.

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

==Ambulatory Holter monitoring==
{{main|Holter monitor}}
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==
{{main|Cardiac stress test}}
Some individuals with atrial fibrillation do well with normal activity but develop shortness of breath with exertion. It may be unclear if the shortness of breath is due to a blunted heart rate response to exertion due to 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 [[cardiac stress test|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. As a summary the main benefits of performing an exercise stress testing;

*If the adequacy of rate control is in question (permanent AF)
*To reproduce exercise-induced AF
*To exclude ischemia before treatment of selected patients with a type IC antiarrhythmic drug

==Electrophysiologic Testing or Electrophysiologic Studies==


==Treatment of [[atrial fibrillation]]==
#Pharmacological treatment
#Invasive treatment
#Surgical treatment

==Pharmacological treatment of atrial fibrillation==

The main goals of treatment of atrial fibrillation are to prevent temporary circulatory instability and to prevent [[stroke]]. Rate and rhythm control are principally used to achieve the former, while [[anticoagulation]] may be required to decrease the risk of the latter.<ref>{{cite journal | author=Prystowsky EN | title=Management of atrial fibrillation: therapeutic options and clinical decisions | journal=Am J Cardiol | year=2000 | pages=3D-11D | volume=85 | issue=10A }} PMID 10822035</ref> In emergencies, when circulatory collapse is imminent due to uncontrolled [[tachycardia]], immediate [[cardioversion]] may be indicated.<ref name="pmid16908781"/>

The primary factors determining atrial fibrillation treatment are duration and evidence of hemodynamic instability. [[Cardioversion]] is indicated with new onset AF (for less than 48 hours) and with hemodynamic instability. If rate and rhythm control cannot be maintained by medication or cardioversion, [[Cardiac electrophysiology|electrophysiological studies]] with pathway [[Radiofrequency ablation|ablation]] may be required.<ref name="pmid16908781"/>

=== Antithrombotic Strategies for Prevention of Ischemic Stroke and Systemic Embolism ===

Oral anticoagulation is a mainstay of atrial fibrillation management.  For both primary and secondary prevention of stroke, there is a 61% relative risks reduction in the incidence of all cause stroke (both ischemic and hemorrhagic) associated with adjusted-dose oral anticoagulation.<ref name="pmid">{{cite journal |author=Hart RG, Benavente O, McBride R, Pearce LA |title=Antithrombotic therapy to prevent stroke in patients with atrial fibrillation: a meta-analysis |journal=Ann. Intern. Med. |volume=131 |issue=7 |pages=492–501 |year=1999 |month=October |pmid= |doi= |url=http://www.annals.org/cgi/pmidlookup?view=long&pmid=10507957}}</ref>

Increasing patient age (which is associated with smaller body weight, female gender and a progressive decline in renal function) and higher INRs or greater intensity of anticoagulation are both associated with a higher risk of major bleeding. This is critical in so far as bleeding is in turn associated with non-compliance with pharmacotherapy. <ref name="pmid">{{cite journal |author= |title=Bleeding during antithrombotic therapy in patients with atrial fibrillation. The Stroke Prevention in Atrial Fibrillation Investigators |journal=Arch. Intern. Med. |volume=156 |issue=4 |pages=409–16 |year=1996 |month=February |pmid= |doi= |url=http://archinte.ama-assn.org/cgi/pmidlookup?view=long&pmid=8607726}}</ref><ref name="pmid10522891">{{cite journal |author=Gorter JW |title=Major bleeding during anticoagulation after cerebral ischemia: patterns and risk factors. Stroke Prevention In Reversible Ischemia Trial (SPIRIT). European Atrial Fibrillation Trial (EAFT) study groups |journal=Neurology |volume=53 |issue=6 |pages=1319–27 |year=1999 |month=October |pmid=10522891 |doi= |url=http://www.neurology.org/cgi/pmidlookup?view=long&pmid=10522891}}</ref><ref name="pmid8172435">{{cite journal |author=Hylek EM, Singer DE |title=Risk factors for intracranial hemorrhage in outpatients taking warfarin |journal=Ann. Intern. Med. |volume=120 |issue=11 |pages=897–902 |year=1994 |month=June |pmid=8172435 |doi= |url=http://www.annals.org/cgi/pmidlookup?view=long&pmid=8172435}}</ref> <ref name="pmid">{{cite journal |author=Fihn SD, Callahan CM, Martin DC, McDonell MB, Henikoff JG, White RH |title=The risk for and severity of bleeding complications in elderly patients treated with warfarin. The National Consortium of Anticoagulation Clinics |journal=Ann. Intern. Med. |volume=124 |issue=11 |pages=970–9 |year=1996 |month=June |pmid= |doi= |url=http://www.annals.org/cgi/pmidlookup?view=long&pmid=8624064}}</ref><ref name="pmid10577332">{{cite journal |author=Hart RG, Halperin JL |title=Atrial fibrillation and thromboembolism: a decade of progress in stroke prevention |journal=Ann. Intern. Med. |volume=131 |issue=9 |pages=688–95 |year=1999 |month=November |pmid=10577332 |doi= |url=http://www.annals.org/cgi/pmidlookup?view=long&pmid=10577332}}</ref>  Given that many patients with atrial fibrillation are elderly, there is often a narrow therapeutic window in achieving the optimal INR.  The optimal INR should obviously maximize efficacy in reducing the risk of stroke and simultaneously minimize the risk of bleeding.  In the setting of atrial fibrillation, an INR of 2 to 3 appears to be optimal.  INRs lower than this, such as those in the range of 1.6 to 2.5, are associated with efficacy that is only 80% of that in the target range.<ref name="pmid8678931">{{cite journal |author=Hylek EM, Skates SJ, Sheehan MA, Singer DE |title=An analysis of the lowest effective intensity of prophylactic anticoagulation for patients with nonrheumatic atrial fibrillation |journal=N. Engl. J. Med. |volume=335 |issue=8 |pages=540–6 |year=1996 |month=August |pmid=8678931 |doi= |url=http://content.nejm.org/cgi/pmidlookup?view=short&pmid=8678931&promo=ONFLNS19}}</ref><ref name="pmid8782752">{{cite journal |author= |title=Adjusted-dose warfarin versus low-intensity, fixed-dose warfarin plus aspirin for high-risk patients with atrial fibrillation: Stroke Prevention in Atrial Fibrillation III randomised clinical trial |journal=Lancet |volume=348 |issue=9028 |pages=633–8 |year=1996 |month=September |pmid=8782752 |doi= |url=}}</ref> <ref name="pmid7776995">{{cite journal |author= |title=Optimal oral anticoagulant therapy in patients with nonrheumatic atrial fibrillation and recent cerebral ischemia. The European Atrial Fibrillation Trial Study Group |journal=N. Engl. J. Med. |volume=333 |issue=1 |pages=5–10 |year=1995 |month=July |pmid=7776995 |doi= |url=http://content.nejm.org/cgi/pmidlookup?view=short&pmid=7776995&promo=ONFLNS19}}</ref><ref name="pmid9490603">{{cite journal |author=Hart RG |title=Intensity of anticoagulation to prevent stroke in patients with atrial fibrillation |journal=Ann. Intern. Med. |volume=128 |issue=5 |pages=408 |year=1998 |month=March |pmid=9490603 |doi= |url=http://www.annals.org/cgi/pmidlookup?view=long&pmid=9490603}}</ref>

====Interruption of anticoagulation with coumadin====

No mechanical valve, high risk of bleeding with procedure:  Coumadin can be discontinued for one week without heparin bridging.

Presence of mechanical valve, patients with AF who are at high risk of stroke, or patients in whom Coumadin must be interrupted for over a week:  These patients should be administered either [[unfractionated heparin]] or [[low molecular weight heparin]].

====Investigational antithrombin agents====

Newer agents that inhibit [[factor Xa]] are under investigation for the management of atrial fibrillation. These agents include [[apixabin]] and [[rivaroxaban]].

====Antiplatelet therapy for atrial fibrillation====

=====Aspirin Monotherapy=====
Aspirin monotherapy is associated with only a modest  and inconsistent reduction in the risk of stroke associated with atrial fibrillation. <ref name="pmid9490603">{{cite journal |author=Hart RG |title=Intensity of anticoagulation to prevent stroke in patients with atrial fibrillation |journal=Ann. Intern. Med. |volume=128 |issue=5 |pages=408 |year=1998 |month=March |pmid=9490603 |doi= |url=http://www.annals.org/cgi/pmidlookup?view=long&pmid=9490603}}</ref>  <ref name="pmid9490603">{{cite journal |author=Hart RG |title=Intensity of anticoagulation to prevent stroke in patients with atrial fibrillation |journal=Ann. Intern. Med. |volume=128 |issue=5 |pages=408 |year=1998 |month=March |pmid=9490603 |doi= |url=http://www.annals.org/cgi/pmidlookup?view=long&pmid=9490603}}</ref>

<ref name="pmid9183235">{{cite journal |author= |title=The efficacy of aspirin in patients with atrial fibrillation. Analysis of pooled data from 3 randomized trials. The Atrial Fibrillation Investigators |journal=Arch. Intern. Med. |volume=157 |issue=11 |pages=1237–40 |year=1997 |month=June |pmid=9183235 |doi= |url=http://archinte.ama-assn.org/cgi/pmidlookup?view=long&pmid=9183235}}</ref>  Studies suggest that the efficacy of aspirin may be greater in patients with [[hypertension]] or [[ diabetes]].  Aspirin may also be more efficacious in reducing the risk of non cardioembolic stroke as opposed to the more disabling cardioembolic form of stroke. <ref name="pmid8423907">{{cite journal |author=Miller VT, Rothrock JF, Pearce LA, Feinberg WM, Hart RG, Anderson DC |title=Ischemic stroke in patients with atrial fibrillation: effect of aspirin according to stroke mechanism. Stroke Prevention in Atrial Fibrillation Investigators |journal=Neurology |volume=43 |issue=1 |pages=32–6 |year=1993 |month=January |pmid=8423907 |doi= |url=}}</ref><ref name="pmid10629345">{{cite journal |author=Hart RG, Pearce LA, Miller VT, ''et al'' |title=Cardioembolic vs. noncardioembolic strokes in atrial fibrillation: frequency and effect of antithrombotic agents in the stroke prevention in atrial fibrillation studies |journal=Cerebrovasc. Dis. |volume=10 |issue=1 |pages=39–43 |year=2000 |pmid=10629345 |doi= |url=http://content.karger.com/produktedb/produkte.asp?typ=fulltext&file=ced10039}}</ref>

=====Dual Antiplatelet therapy=====

Among patients who are not deemed candidates for [[Coumadin]] therapy (estimated to be approximately 40-50% of patients), dual antiplatelet therapy with both [[aspirin]] and [[clopidogrel]] (at a maintenance dose of 75 mg/day) was superior to [[aspirin]] monotherapy in the [[ACTIVE A trial]].  The primary endpoint of the trial was the composite of stroke, myocardial infarction, non–central nervous system systemic embolism, or death from vascular causes.  After a median of 3.6 years of follow-up in 7,554 randomized patients, the addition of [[clopidogrel]] to [[aspirin]] alone yielded a reduction in events from 7.6% to 6.8% (relative risk reduction with clopidogrel, 0.89; 95% confidence interval [CI], 0.81 to 0.98; P=0.01).  The addition of [[clopidogrel]] to [[aspirin]] alone reduced the risk of stroke by 28% (from 3.3% to 2.4%, p<0.001) and reduced the risk of MI by 22% (from 0.9% per year to 0.7% per year, p=0.08). The risk of major bleeding among patients treated with aspirin and clopidogrel was 2.0% per year whereas it was 1.3% per year among patients treated with aspirin alone (relative risk, 1.57; 95% CI, 1.29 to 1.92; P<0.001). If 1000 patients were treated for 3 years, the combination of aspirin plus clopidogrel would prevent 28 strokes (17 disabling or fatal), and 6 myocardial infarctions, at a cost of 20 major bleeds compared to aspirin alone.

 

====Oral Anticoagulation (Coumadin) versus Dual Antiplatelet Therapy (ASA/Clopidogrel)====
In the ACTIVE W trial, dual antiplatelet therapy with [[aspirin]](75-100 mg per day) and [[clopidogrel]] (75 mg per day) was found to be statistically inferior to [[coumadin]] therapy (target INR 2.0 to 3.0) in the management of patients with [[atrial fibrillation]] who had one or more risk factors for [[stroke]]<ref> The ACTIVE Writing Group on behalf of the ACTIVE Investigators. Lancet 2006;367:1903-12.</ref>. The primary endpoint of ACTIVE W was the first occurrence of [[stroke]], non-CNS systemic embolus, [[myocardial infarction]], or vascular death. The annual risk in the [[coumadin]] group was 3.93% per year, and in the [[Aspirin]]/[[Clopidogrel]] group it was 5.60% per year yielding a relative risk of 1.44 (1.18-1.76; p=0.0003). The efficacy was not as great among patients who were coumadin naive, although the p-value for the interaction was negative. There was no excess bleeding among patients treated with [[coumadin]], and in  fact there was an excess of minor bleeds among patients treated with [[ASA]] and [[clopidogrel]] (13.6% / yr vs 11.5% year, p=0.0009). 

When examining the data from atrial fibrillation trials, it is critical to evaluate the results in patients who were previously treated with [[coumadin]] separate from those patients who were naive to coumadin. Patients previously treated with coumadin are likely to be those patients who best tolerate coumadin and have passed their "bleeding stress test" and have a lower rate of bleeding on coumadin. Those patients who bleed while on [[coumadin]] have already been culled out from the population. When the data in ACTIVE W were evaluated including only those patients previously treated with [[coumadin]](again a population to be anticipated to be at low risk of bleeding), the risk of major bleeding was indeed statistically significantly lower among patients previously treated with coumadin (p=0.03) than patients not previously treated.

The majority of the reduction in events was due to a reduction in [[stroke]] and non-CNS emolization associated with [[coumadin therapy. The pathophysiology of stroke among patients with atrial fibrillation is thought to be embolization from clot in the [[left atrium]]. The data from ACTIVE W suggest that platelet activation and its treatment may not play a pivotal role in the treatment of mural thrombus and embolization in atrial fibrillation.  Coumadin was more effective in the reduction of non-disabling stroke rather than disabling stroke. There were more fatal hemorrhagic strokes (which may more often be fatal), and this may explain in part why coumadin was not associated with a reduction in mortality in the study.

While clopidogrel plus aspirin has been found to reduce the risk of recurrent [[myocardial infarction]] among patients with presumed plaque rupture and [[acute coronary syndromes]], it is notable in ACTIVE W that the risk of [[myocardial infarction]] tended to be higher among patients treated with [[aspirin]] plus [[clopidogrel]] versus [[coumadin]] (0.86% vs 0.55%,p=0.09)<ref> The ACTIVE Writing Group on behalf of the ACTIVE Investigators. Lancet 2006;367:1903-12.</ref>.

=== Conversion to sinus rhythm and thromboembolism ===


===Electrical & mechanical dissociation===
Despite the restoration of sinus rhythm on the ECG following cardioversion (either spontaneous, pharmacologic or electrical or after radiofrequency catheter ablation of [[atrial flutter]]), in some patients there is a persistent lack of atrial contractility.  This state is known as electrical mechanical dissociation and may be sue to mechanical stunning in the atrium and the atrial appendage. <ref name="pmid8294679">{{cite journal |author=Fatkin D, Kuchar DL, Thorburn CW, Feneley MP |title=Transesophageal echocardiography before and during direct current cardioversion of atrial fibrillation: evidence for "atrial stunning" as a mechanism of thromboembolic complications |journal=J. Am. Coll. Cardiol. |volume=23 |issue=2 |pages=307–16 |year=1994 |month=February |pmid=8294679 |doi= |url=}}</ref> <ref name="pmid10569673">{{cite journal |author=Antonielli E, Pizzuti A, Bassignana A, ''et al'' |title=Transesophageal echocardiographic evidence of more pronounced left atrial stunning after chemical (propafenone) rather than electrical attempts at cardioversion from atrial fibrillation |journal=Am. J. Cardiol. |volume=84 |issue=9 |pages=1092–6, A9–10 |year=1999 |month=November |pmid=10569673 |doi= |url=http://linkinghub.elsevier.com/retrieve/pii/S0002914999005081}}</ref><ref name="pmid8752189">{{cite journal |author=Falcone RA, Morady F, Armstrong WF |title=Transesophageal echocardiographic evaluation of left atrial appendage function and spontaneous contrast formation after chemical or electrical cardioversion of atrial fibrillation |journal=Am. J. Cardiol. |volume=78 |issue=4 |pages=435–9 |year=1996 |month=August |pmid=8752189 |doi= |url=http://linkinghub.elsevier.com/retrieve/pii/S0002-9149(96)00333-5}}</ref><ref name="pmid8752189">{{cite journal |author=Falcone RA, Morady F, Armstrong WF |title=Transesophageal echocardiographic evaluation of left atrial appendage function and spontaneous contrast formation after chemical or electrical cardioversion of atrial fibrillation |journal=Am. J. Cardiol. |volume=78 |issue=4 |pages=435–9 |year=1996 |month=August |pmid=8752189 |doi= |url=http://linkinghub.elsevier.com/retrieve/pii/S0002-9149(96)00333-5}}</ref><ref name="pmid9604945">{{cite journal |author=Bellotti P, Spirito P, Lupi G, Vecchio C |title=Left atrial appendage function assessed by transesophageal echocardiography before and on the day after elective cardioversion for nonvalvular atrial fibrillation |journal=Am. J. Cardiol. |volume=81 |issue=10 |pages=1199–202 |year=1998 |month=May |pmid=9604945 |doi= |url=http://linkinghub.elsevier.com/retrieve/pii/S0002-9149(98)00089-7}}</ref><ref name="pmid9605054">{{cite journal |author=Harjai K, Mobarek S, Abi-Samra F, ''et al'' |title=Mechanical dysfunction of the left atrium and the left atrial appendage following cardioversion of atrial fibrillation and its relation to total electrical energy used for cardioversion |journal=Am. J. Cardiol. |volume=81 |issue=9 |pages=1125–9 |year=1998 |month=May |pmid=9605054 |doi= |url=http://linkinghub.elsevier.com/retrieve/pii/S0002914998001416}}</ref><ref name="pmid9708477">{{cite journal |author=Sparks PB, Jayaprakash S, Vohra JK, ''et al'' |title=Left atrial "stunning" following radiofrequency catheter ablation of chronic atrial flutter |journal=J. Am. Coll. Cardiol. |volume=32 |issue=2 |pages=468–75 |year=1998 |month=August |pmid=9708477 |doi= |url=http://linkinghub.elsevier.com/retrieve/pii/S0735-1097(98)00253-8}}</ref> The lack of atrial contraction can be diagnosed on echocardiography by the appearance of spontaneous echo contrast. <ref name="pmid8294679">{{cite journal |author=Fatkin D, Kuchar DL, Thorburn CW, Feneley MP |title=Transesophageal echocardiography before and during direct current cardioversion of atrial fibrillation: evidence for "atrial stunning" as a mechanism of thromboembolic complications |journal=J. Am. Coll. Cardiol. |volume=23 |issue=2 |pages=307–16 |year=1994 |month=February |pmid=8294679 |doi= |url=}}</ref> In general, the longer the patient was in atrial fibrillation, the longer the time it takes for the recoery of atrial mechanical function. The period of recovery can be quite variable, and it can take several weeks in total. Recovery of mechanical function can be delayed for several weeks, depending in part on the duration of [[AF]] before restoration of [[sinus rhythm]]<ref name="pmid7733009">{{cite journal |author=Mitusch R, Garbe M, Schmücker G, Schwabe K, Stierle U, Sheikhzadeh A |title=Relation of left atrial appendage function to the duration and reversibility of nonvalvular atrial fibrillation |journal=Am. J. Cardiol. |volume=75 |issue=14 |pages=944–7 |year=1995 |month=May |pmid=7733009 |doi= |url=http://linkinghub.elsevier.com/retrieve/pii/S000291499980695X}}</ref><ref name="pmid7887393">{{cite journal |author=Manning WJ, Silverman DI, Katz SE, ''et al'' |title=Temporal dependence of the return of atrial mechanical function on the mode of cardioversion of atrial fibrillation to sinus rhythm |journal=Am. J. Cardiol. |volume=75 |issue=8 |pages=624–6 |year=1995 |month=March |pmid=7887393 |doi= |url=http://linkinghub.elsevier.com/retrieve/pii/S0002914999806328}}</ref><ref name="pmid7611109">{{cite journal |author=Grimm RA, Leung DY, Black IW, Stewart WJ, Thomas JD, Klein AL |title=Left atrial appendage "stunning" after spontaneous conversion of atrial fibrillation demonstrated by transesophageal Doppler echocardiography |journal=Am. Heart J. |volume=130 |issue=1 |pages=174–6 |year=1995 |month=July |pmid=7611109 |doi= |url=http://linkinghub.elsevier.com/retrieve/pii/0002-8703(95)90253-8}}</ref>  This kind of electrical mechanical dissociation may explain in part the observation that some patients develop thromboembolic events following cardioversion despite the fact that they had no visible [[left atrial]] clot on [[TEE]]. <ref name="pmid8205657">{{cite journal |author=Black IW, Fatkin D, Sagar KB, ''et al'' |title=Exclusion of atrial thrombus by transesophageal echocardiography does not preclude embolism after cardioversion of atrial fibrillation. A multicenter study |journal=Circulation |volume=89 |issue=6 |pages=2509–13 |year=1994 |month=June |pmid=8205657 |doi= |url=http://circ.ahajournals.org/cgi/pmidlookup?view=long&pmid=8205657}}</ref> It has been hypothesized that the low shear state and turbulent nature of left atrial hemodynamics during this period leads to the development of clot which then embolizes once there is restoration of sufficient mechanical force.<ref name="pmid9874066">{{cite journal |author=Berger M, Schweitzer P |title=Timing of thromboembolic events after electrical cardioversion of atrial fibrillation or flutter: a retrospective analysis |journal=Am. J. Cardiol. |volume=82 |issue=12 |pages=1545–7, A8 |year=1998 |month=December |pmid=9874066 |doi= |url=http://linkinghub.elsevier.com/retrieve/pii/S000291499800705X}}</ref> It is in part due to the presence of atrial mechanical dissociation and the risk of clot formation and embolization that oral anticoagulation is recommended for 3 to 4 weeks following successful electrical cardioversion in patients in whom the duration of Afib is unknown or in whom the duration of atrial fibrillation has been documented to be longer than 48 hours.  Among patients in whom the duration of atrial fibrillation is less than 48 hours, the necessity for anticoagulation is not as clear, although it should be noted that stroke has been observed in these patients as well.   No matter what the duration of atrial fibrillation, if a patient becomes hemodynamically unstable, this is an indication for immediate cardioversion.   

== Management Strategies ==

=== New diagnosed or First Episode of Atrial Fibrillation ===
In patients who have self-limited episodes of paroxysmal AF, antiarrhythmic drugs to prevent recurrence are usually unnecessary, unless AF is associated with severe symptoms related to hypotension, myocardial ischemia, or HF. Whether these individuals require longterm or even short-term anticoagulation is not clear, and the decision must be individualized for each patient based on the intrinsic risk of thromboembolism.

=== Persistent Atrial Fibrillation ===


=== Recurrent Paroxysmal Atrial Fibrillation=== 


=== Vagally mediated [[Atrial fibrillation]]===
[[Disopyramide]] or [[flecainide]]

=== Adrenergically induced Atrial Fibrillation===
Beta blockers (sotalol)

=== Congestive Heart Failure ===
amiodarone or dofetilide to maintain sinus rhythm. 

=== Ischemic heart disease ===



=== Hypertension without LVH ===
 

===Left ventricular hypertrophy===

==ACC / AHA Guidelines- Recommendation for Pacing to Prevent Atrial Fibrillation (DO NOT EDIT) <ref name="Epstein"> Epstein AE, DiMarco JP, Ellenbogen KA, Estes NAM III, Freedman RA, Gettes LS, Gillinov AM, Gregoratos G, Hammill SC, Hayes DL, Hlatky MA, Newby LK, Page RL, Schoenfeld MH, Silka MJ, Stevenson LW, Sweeney MO. ACC/AHA/HRS 2008 guidelines for device-based therapy of cardiac rhythm abnormalities: executive summary: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Writing Committee to Revise the ACC/AHA/NASPE 2002 Guideline Update for Implantation of Cardiac Pacemakers and Antiarrhythmia Devices). Circulation. 2008; 117: 2820–2840. PMID 18483207 </ref>==
{{cquote|  
===Class III===
1. Permanent [[pacemaker|pacing]] is not indicated for the prevention of AF in patients without any other indication for [[pacemaker]] implantation. ''(Level of Evidence: B)''}}

==Sources==
* The ACC/AHA/HRS 2008 Guidelines for Device-Based Therapy of Cardiac Rhythm Abnormalities <ref name="Epstein"> Epstein AE, DiMarco JP, Ellenbogen KA, Estes NAM III, Freedman RA, Gettes LS, Gillinov AM, Gregoratos G, Hammill SC, Hayes DL, Hlatky MA, Newby LK, Page RL, Schoenfeld MH, Silka MJ, Stevenson LW, Sweeney MO. ACC/AHA/HRS 2008 guidelines for device-based therapy of cardiac rhythm abnormalities: executive summary: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Writing Committee to Revise the ACC/AHA/NASPE 2002 Guideline Update for Implantation of Cardiac Pacemakers and Antiarrhythmia Devices). Circulation. 2008; 117: 2820–2840. PMID 18483207 </ref>

== Recurrent Persistent AF == 


== Permanent AF == 

===Anticoagulation===
Patients with atrial fibrillation, even lone atrial fibrillation without other evidence of heart disease, are at increased risk of stroke during long term follow up.<ref name="pmid4068186">{{cite journal |author=Brand FN, Abbott RD, Kannel WB, Wolf PA |title=Characteristics and prognosis of lone atrial fibrillation. 30-year follow-up in the Framingham Study |journal=JAMA |volume=254 |issue=24 |pages=3449-53 |year=1985 |pmid=4068186 |doi=}}</ref>  A [[systematic review]] of risk factors for [[stroke]] in patients with nonvalvular atrial fibrillation concluded that a prior history of stroke or TIA is the most powerful risk factor for future stroke, followed by advancing age, hypertension, diabetes.<ref name="pmid17679673">{{cite journal |author= |title=Independent predictors of stroke in patients with atrial fibrillation: a systematic review |journal=Neurology |volume=69 |issue=6 |pages=546-54 |year=2007 |pmid=17679673 |doi=10.1212/01.wnl.0000267275.68538.8d}}</ref> The risk of stroke increases whether the lone atrial fibrillation was an isolated episode, recurrent, or chronic.<ref name="pmid3627174">{{cite journal |author=Kopecky SL, Gersh BJ, McGoon MD, ''et al'' |title=The natural history of lone atrial fibrillation. A population-based study over three decades |journal=N. Engl. J. Med. |volume=317 |issue=11 |pages=669-74 |year=1987 |pmid=3627174 |doi=}}</ref> The risk of systemic embolization (atrial clots migrating to other organs) depends strongly on whether there is an underlying structural problem with the heart (e.g. [[mitral stenosis]]) and on the presence of other risk factors, such as diabetes and high blood pressure. Finally, patients under 65 are much less likely to develop embolization compared with patients over 75. In young patients with few risk factors and no structural heart defect, the benefits of anticoagulation may be outweighed by the risks of [[hemorrhage]] (bleeding). Those at a low risk may benefit from mild (and low-risk) anticoagulation with [[aspirin]] (or [[clopidogrel]] in those who are allergic to aspirin). In contrast, those with a high risk of stroke derive most benefit from [[anticoagulant]] treatment with [[warfarin]] or similar drugs.

In the United Kingdom, the [[National Institute for Health and Clinical Excellence|NICE]] guidelines recommend using a [[clinical prediction rule]] for this purpose.<ref name="nice">{{cite web |author=National Institute for Health and Clinical Excellence|url=http://guidance.nice.org.uk/CG36 |title=Clinical Guideline 36 - Atrial fibrillation | date=June 2006 | accessdate=2007-08-15 |format= |work=}}</ref> The ''[[CHADS Score|CHADS/CHADS2]]'' score is the best validated clinical prediction rule for determining risk of stroke (and therefore who should be anticoagulated); it assigns points (totaling 0-6) depending on the presence or absence of co-morbidities such hypertension and diabetes. In a comparison of seven [[clinical prediction rule|prediction rule]]s, the best rules were the [[CHADS Score|CHADS2]] which performed similarly to the SPAF<ref name="pmid10356104">{{cite journal |author=Hart RG, Pearce LA, McBride R, Rothbart RM, Asinger RW |title=Factors associated with ischemic stroke during aspirin therapy in atrial fibrillation: analysis of 2012 participants in the SPAF I-III clinical trials. The Stroke Prevention in Atrial Fibrillation (SPAF) Investigators |journal=Stroke |volume=30 |issue=6 |pages=1223–9 |year=1999 |pmid=10356104 |doi=}}</ref> and [[Framingham Heart Study|Framingham]]<ref name="pmid12941677">{{cite journal |author=Wang TJ, Massaro JM, Levy D, ''et al'' |title=A risk score for predicting stroke or death in individuals with new-onset atrial fibrillation in the community: the Framingham Heart Study |journal=JAMA |volume=290 |issue=8 |pages=1049–56 |year=2003 |pmid=12941677 |doi=10.1001/jama.290.8.1049}}</ref> [[clinical prediction rule|prediction rule]]s. <ref name="pmid17673721">{{cite journal |author=Baruch L, Gage BF, Horrow J, ''et al'' |title=Can patients at elevated risk of stroke treated with anticoagulants be further risk stratified? |journal=Stroke |volume=38 |issue=9 |pages=2459–63 |year=2007 |pmid=17673721 |doi=10.1161/STROKEAHA.106.477133}}</ref>

To compensate for the increased risk of stroke, anticoagulants may be required.  However, in the case of warfarin, if a patient has a yearly risk of stroke that is less than 2%, then the risks associated with taking warfarin outweigh the risk of getting a stroke. <ref>{{cite journal | author=van Walraven C, Hart RG, Singer DE, ''et al.'' | title=Oral anticoagulants vs aspirin in nonvalvular atrial fibrillation: an individual patient meta-analysis | journal=JAMA | year=2002 | volume=288 | issue=19 | pages=2441&ndash;48 | url=http://jama.ama-assn.org/cgi/content/abstract/288/19/2441|id=PMID 12435257}}</ref><ref>{{cite journal | author=Gage BF, Cardinalli AB, Owens D. | title=Cost-effectiveness of preference-based antithrombotic therapy for patients with nonvalvular atrial fibrillation | journal=Stroke | year=1998 | volume=29 | pages=1083&ndash;91 | url=http://stroke.ahajournals.org/cgi/content/abstract/29/6/1083|id=PMID 9626276 }}</ref>

====Acute anticoagulation====
If anticoagulation is required urgently (e.g. for cardioversion), [[heparin]] or similar drugs achieve the required level of protection much quicker than warfarin, which may take several days to reach adequate levels.

In the initial stages after an embolic stroke, anticoagulation may be risky, as the damaged area of the brain is relatively prone to bleeding (hemorrhagic transformation).<ref name="pmid17204681">{{cite journal  |author=Paciaroni M, Agnelli G, Micheli S, Caso V |title=Efficacy and safety of anticoagulant treatment in acute cardioembolic stroke: a meta-analysis of randomized controlled trials |journal=Stroke |volume=38  |issue=2 |pages=423-30 | year=2007 |pmid=17204681 |doi=10.1161/01.STR.0000254600.92975.1f }} [http://www.acpjc.org/Content/147/1/issue/ACPJC-2007-147-1-017.htm ACP JC synopsis ]</ref> As a result, a [[clinical practice guideline]] by [[National Institute for Health and Clinical Excellence]] recommends that anticoagulation should begin two weeks after stroke if no hemorrhage occurred.<ref name=nice/>

====Chronic anticoagulation====

Among patients with "non-valvular" atrial fibrillation, anticoagulation with warfarin can reduce stroke by 60% while antiplatelet agents can reduce stroke by 20%. <ref name="pmid17577005">{{cite journal |author=Hart RG, Pearce LA, Aguilar MI |title=Meta-analysis: antithrombotic therapy to prevent stroke in patients who have nonvalvular atrial fibrillation |journal=Ann Intern Med |volume=146 |issue=12 |pages=857–67 |year=2007 |pmid=17577005 |doi=}}</ref><ref name="pmid17636831">{{cite journal |author=Aguilar M, Hart R, Pearce L |title=Oral anticoagulants versus antiplatelet therapy for preventing stroke in patients with non-valvular atrial fibrillation and no history of stroke or transient ischemic attacks |journal= Cochrane Database Syst Rev |volume=3 |issue= |pages=CD006186 |year=2007 |pmid=17636831 |doi=10.1002/14651858.CD006186.pub2}}</ref>. There is evidence that [[aspirin]] and [[clopidogrel]] are effective when used together, but the combination is still inferior to [[warfarin]].<ref name="pmid16765759">{{cite journal |author=Connolly S, Pogue J, Hart R, ''et al'' |title=Clopidogrel plus aspirin versus oral anticoagulation for atrial fibrillation in the Atrial fibrillation Clopidogrel Trial with Irbesartan for prevention of Vascular Events (ACTIVE W): a randomised controlled trial |journal=Lancet |volume=367 |issue=9526 |pages=1903–12 |year=2006 |pmid=16765759 |doi=10.1016/S0140-6736(06)68845-4}}</ref>

Warfarin treatment requires frequent monitoring with a blood test called the [[Prothrombin time|international normalized ratio]] (INR); this determines whether the correct dose is being used. In atrial fibrillation, the usual target INR is between 2.0 and 3.0 (higher targets are used in patients with mechanical [[artificial heart valve]]s, many of whom may also have atrial fibrillation). A high INR may indicate increased bleeding risk, while a low INR would indicate that there is insufficient protection from stroke.

An attempt was made to find a better method of implementing warfarin therapy without the inconvenience of regular monitoring and risk of intracranial hemorrhage. A combination of aspirin and fixed-dose warfarin (initial INR 1.2-1.5) was tried. Unfortunately, in a study of AF patients with additional risk factors for thromboembolism, the combination of aspirin and the lower dose of warfarin  was significantly inferior to the standard adjusted-dose warfarin  (INR 2.0-3.0), yet still had a similar risk of intracranial hemorrhage.<ref>{{cite journal | title=Adjusted-dose warfarin versus low-intensity, fixed-dose warfarin plus aspirin for high-risk patients with atrial fibrillation: Stroke Prevention in Atrial Fibrillation III randomised clinical trial | journal=Lancet | volume=348 | issue=9028 | pages=633–638 | year=1996 |url=http://www.thelancet.com/journals/lancet/article/PIIS0140673696034873/abstract | pmid=8782752 | doi=10.1016/S0140-6736(96)03487-3}}</ref>

===Elderly patients===
The very elderly (patients aged 75 years or more) may benefit from anticoagulation provided that their anticoaguation does not increase hemorrhagic complications, which is a difficult goal. Patients aged 80 years or more may be especially susceptible to bleeding complications, with a rate of 13 bleeds per 100 person-years.<ref name="pmid17515465">{{cite journal |author=Hylek EM, Evans-Molina C, Shea C, Henault LE, Regan S |title=Major hemorrhage and tolerability of warfarin in the first year of therapy among elderly patients with atrial fibrillation |journal=Circulation |volume=115 |issue=21 |pages=2689-96 |year=2007 |pmid=17515465 |doi=10.1161/CIRCULATIONAHA.106.653048}}</ref> A rate of 13 bleeds per 100 person years would seem to preclude use of warfarin; however, a [[randomized controlled trial]] found benefit in treating patients 75 years or over with a [[number needed to treat]] of 50.<ref name="pmidpendingMant"> {{cite journal  |author=Mant J et al |title=Warfarin versus aspirin for stroke prevention in an elderly community population with atrial fibrillation (the Birmingham Atrial Fibrillation Treatment of the Aged Study, BAFTA): a randomised controlled trial |journal=Lancet |volume=370  |issue= |pages=493-503 | year=2007 |pmid= |doi=10.1016/S0140-6736(07)61233-1}}</ref> Of note, this study had very low rate of hemorrhagic complications in the warfarin group.

===Rate control versus rhythm control===
AF can cause disabling and annoying symptoms. [[Palpitations]], [[Angina pectoris|angina]], lassitude (weariness), 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.

There are two ways to approach these symptoms: rate control and rhythm control. ''Rate control'' treatments seek to reduce the heart rate to normal, usually 60 to 100 beats per minute. ''Rhythm control'' seeks to restore the normal heart rhythm, called normal sinus rhythm. Studies suggest that rhythm control is mainly a concern in newly diagnosed AF, while rate control is more important in the chronic phase.  Rate control with anticoagulation is as effective a treatment as rhythm control in long term mortality studies, the AFFIRM Trial.<ref name=pmid12466506>{{cite journal | author=Wyse DG, Waldo AL, DiMarco JP, Domanski MJ, Rosenberg Y, Schron EB, Kellen JC, Greene HL, Mickel MC, Dalquist JE, Corley SD | title=A comparison of rate control and rhythm control in patients with atrial fibrillation | journal=N Engl J Med | year=2002 | pages=1825-33 | volume=347 | issue=23 }} PMID 12466506</ref>

The AFFIRM study showed 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.<ref name=pmid12466506/>

===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 down into the ventricles. This can be done with:<ref name="pmid16908781"/>
* [[Beta blockers]] (preferably the "cardioselective" beta blockers such as [[metoprolol]], [[atenolol]], [[bisoprolol]])
* [[Cardiac glycosides]] (i.e. [[digoxin]])
* [[Calcium channel blocker]]s (i.e. [[diltiazem]] or [[verapamil]])

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).

====Cardioversion====
{{main|Cardioversion}}
Rhythm control methods include electrical and chemical [[cardioversion]]:<ref name="pmid16908781"/>
* ''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]]<ref>{{cite journal |author=Singh BN, Connolly SJ, Crijns HJ, ''et al'' |title=Dronedarone for maintenance of sinus rhythm in atrial fibrillation or flutter |journal=N. Engl. J. Med. |volume=357 |issue=10 |pages=987–99 |year=2007 |pmid=17804843 |doi=10.1056/NEJMoa054686}}</ref>, [[procainamide]], [[ibutilide]], [[propafenone]] or [[flecainide]].  

The main risk of cardioversion is systemic embolization of a [[thrombus]] (blood clot) from the previously fibrillating left atrium. Cardioversion should not be performed without adequate anticoagulation in patients with more than 48 hours of atrial fibrillation. Cardioversion may be performed in instances of AF lasting more than 48 hours if a [[transesophogeal echocardiogram]] (TEE) demonstrates no evidence of clot within the heart.<ref name="pmid16908781"/>

Whichever method of cardioversion is used, approximately 50% of patient [[relapse]] within one year, although the continued daily use of oral antiarrhythmic drugs may extend this period. The key risk factor for relapse is duration of AF, although other risk factors that have been identified include the presence of structural heart disease, and increasing age.

===Maintenance of sinus rhythm===
The mainstay of maintaining sinus rhythm is the use of antiarrhythmic agents.  Recently, other approaches have been developed that promise to decrease or eliminate the need for antiarrhythmic agents.

====Antiarrhythmic agents====
{{main|Antiarrhythmic agent}}
The [[antiarrhythmic agent|anti-arrhythmic medications]] often used in either pharmacological cardioversion or in the prevention of relapse to AF alter the flux of ions in heart tissue, making them less excitable, setting the stage for spontaneous and durable cardioversion. These medications are often used in concert with electrical cardioversion.

==Invasive treatment of atrial fibrillation==
====Radiofrequency ablation====
In patients with AF where rate control drugs are ineffective and it is not possible to restore sinus rhythm using cardioversion, non-pharmacological alternatives are available. For example, to control rate it is possible to destroy the bundle of cells connecting the upper and lower chambers of the heart - the [[atrioventricular node]] - which regulates heart rate, and to implant a [[artificial pacemaker|pacemaker]] instead. A more complex technique, which avoids the need for a pacemaker, involves ablating groups of cells near the pulmonary veins where atrial fibrillation is thought to originate, or creating more extensive lesions in an attempt to prevent atrial fibrillation from establishing itself.<ref name="pmid16908781"/>

[[Ablation]] is a newer technique and has shown some promise for cases of recurrent AF that are unresponsive to conventional treatments. [[Radiofrequency ablation]] (RFA) uses radiofrequency energy to destroy abnormal electrical pathways in heart tissue. The energy emitting probe ([[electrode]]) is placed into the heart through a [[catheter]] inserted into veins in the groin or neck.  Electrodes that can detect electrical activity from inside the heart are also inserted, and the electrophysiologist uses these to "map" an area of the heart in order to locate the abnormal electrical activity before eliminating the responsible tissue. 

Most AF ablations consist of isolating the electrical pathways from the [[pulmonary vein]]s (PV)<ref>[http://www.clevelandclinic.org/heartcenter/pub/atrial_fibrillation/pulmonaryvein_ablation.htm The Cleveland Clinic]</ref>, which are located on the posterior wall of the left atrium. All other veins from the body (including neck and groin) lead to the right atrium, so in order to get to the left atrium the catheters must get across the atrial septum. This is done by piercing a small hole in the septal wall. This is called a transseptal approach. Once in the left atrium, the physician may perform ''Wide Area Circumferential Ablation'' (WACA) to electrically isolate the PVs from the left atrium.<ref>[http://www.medscape.com/viewarticle/532503_2 Medscape] </ref>

Some more recent approaches to ablating AF is to target sites that are particularly disorganized in both atria as well as in the [[coronary sinus]] (CS). These sites are termed ''complex fractionated atrial electrogram'' (CFAE) sites.<ref>{{cite journal | author= Nademanee K, McKenzie J, Kosar E, Schwab M, Sunsaneewitayakul B, Vasavakul T, Khunnawat C, Ngarmukos T. | title=A new approach for catheter ablation of atrial fibrillation: mapping of the electrophysiologic substrate | journal=J Am Coll Cardiol | year=2004 | pages=2044–53 | volume=43 | issue=11 | pmid= 15172410 | doi= 10.1016/j.jacc.2003.12.054}}</ref>. It is believed by some that the CFAE sites are the cause of AF, or a combination of the PVs and CFAE sites are to blame. New techniques include the use of [[cryoablation]] (tissue freezing using a coolant which flows through the catheter), microwave ablation, where tissue is ablated by the microwave energy "cooking" the adjacent tissue, and high intensity focused ultrasound (HIFU), which destroys tissue by heating. This is an area of active research, especially with respect to the RF ablation technique and emphasis on isolating the pulmonary veins that enter into the left atrium.

Efficacy and risks of catheter ablation of atrial fibrillation are areas of active debate.  A worldwide survey of the outcomes of 8745 ablation procedures<ref>{{cite journal | author=Cappato R, Calkins H, Chen SA, Davies W, Iesaka Y, Kalman J, Kim YH, Klein G, Packer D, Skanes A. | title=Worldwide survey on the methods, efficacy, and safety of catheter ablation for human atrial fibrillation | journal=Circulation | year=2005 | volume=111 | pages=1100–1105| pmid=15723973 | doi=10.1161/01.CIR.0000157153.30978.67}}</ref> demonstrated a 52% success rate (ranging from 14.5% to 76.5% among centers), with an additional 23.9% of patients becoming asymptomatic with addition of an antiarrhythmic medication.  In 27.3% of patients, more than one procedure was required to attain these results.  There was at least one major complication in 6% of patients.  A thorough discussion of results of catheter ablation was published in 2007<ref>{{cite journal | author=Calkins H, Brugada J, Packer DL, Cappato R, Chen SA, Crijns HJ, Damiano RJ Jr, Davies DW, Haines DE, Haissaguerre M, Iesaka Y, Jackman W, Jais P, Kottkamp H, Kuck KH, Lindsay BD, Marchlinski FE, McCarthy PM, Mont JL, Morady F, Nademanee K, Natale A, Pappone C, Prystowsky E, Raviele A, Ruskin JN, Shemin RJ. | title=HRS/EHRA/ECAS expert Consensus Statement on catheter and surgical ablation of atrial fibrillation: recommendations for personnel, policy, procedures and follow-up. A report of the Heart Rhythm Society (HRS) Task Force on catheter and surgical ablation of atrial fibrillation | journal=Heart Rhythm | year=2007 | volume=4 | issue=6 | pages= 816–61 | pmid=17556213}}</ref>; it notes that results are widely variable, due in part to differences in technique, follow-up, definitions of success, use of antiarrhythmic therapy, and in experience and technical proficiency.

==Surgical treatment of atrial fibrillation==

===Maze procedure===
{{main|Maze procedure}}

James Cox, MD, and associates developed the Cox maze procedure, an open-heart surgical procedure intended to eliminate atrial fibrillation, and performed the first one in 1987. "Maze" refers to the series of incisions made in the atria, which are arranged in a maze-like pattern. The intention was to eliminate AF by using incisional scars to block abnormal electrical circuits (atrial macro reentry) that AF requires. This procedure required an extensive series of endocardial (from the inside of the heart) incisions through both atria, a median sternotomy (vertical incision through the breastbone) and cardiopulmonary bypass (heart-lung machine). A series of improvements were made, culminating in 1992 in the Cox maze III procedure, which is now considered to be the "gold standard" for effective surgical cure of AF. The Cox maze III is sometimes referred to as the "traditional maze", the "cut and sew maze", or simply the "maze".<ref>{{cite journal |author=Cox JL, Schuessler RB, Lappas DG, Boineau JP |title=An 8 1/2-year clinical experience with surgery for atrial fibrillation |journal=Ann. Surg. |volume=224 |issue=3 |pages=267-73; discussion 273-5 |year=1996 |pmid=8813255 |doi=}}</ref>

Minimaze surgery is minimally invasive cardiac surgery similarly intended to cure atrial fibrillation.  The "Minimaze" procedure refers to "mini" versions of the original maze procedure.  These procedures are less invasive than the Cox maze procedure and do not require a median sternotomy (vertical incision in the breastbone) or [[cardiopulmonary bypass]] (heart-lung machine). These procedures use microwave, radiofrequency, or acoustic energy to ablate atrial tissue near the pulmonary veins.

== Prognosis ==



==Follow up & Secondary prevention==

===Risk factors for ischemic stroke or systemic embolization in patient with non valvular [[atrial fibrillation]]===
Numbers represents relative risks<ref>Estes NAM 3rd, Halperin JL, Calkins H, Ezekowitz MD, Gitman P, Go AS, McNamara RL, Messer JV, Ritchie JL, Romeo SJW, Waldo AL, Wyse DG. ACC/AHA/Physician Consortium 2008 clinical performance measures for adults with non valvular atrial fibrillation or atrial flutter: a report of the American College of Cardiology/American Heart Association Task Force on Performance Measures and the Physician Consortium for Performance Improvement (Writing Committee to Develop Performance Measures for Atrial Fibrillation). Circulation 2008; 117:1101–1120</ref>
#Advanced age (continuous, per decade)                                            1.4
#History of [[hypertension]]                                                      1.6
#[[Heart failure]] or impaired left ventricular systolic function                 1.4
#[[Coronary artery disease]] (CAD)                                                1.5
#[[Diabetes mellitus]] (DM)                                                       1.7
#Previous [[stroke]] or [[Transient Ischemic Attack]] (TIA)                       2.5

==Clinical Trial Data==

Results from the Pulmonary Vein Antrum Isolation versus AV Node Ablation with Bi-Ventricular Pacing for Treatment of Atrial Fibrillation in Patients with Congestive Heart Failure (PABA-CHF) study suggest that pulmonary-vein (PV) isolation leads to better morphologic and functional results than atrioventricular (AV) node ablation with biventricular pacing for congestive heart failure (CHF) in patients with atrial fibrillation. 

In this prospective, multicenter study, 41 patients were randomized to PV isolation and 40 to AV node ablation with biventricular pacing. At 6 months, patients in the PV isolation group had higher mean ejection fractions (35% vs 29%, p<0.001), greater 6 minute distances walked (340 vs 297 meters, p <0.001), and better quality of life scores as determined by the Minnesota Living with Heart Failure questionnaire (60 vs 82, p<0.001, where lower scores indicate better quality of life) than those in the AV node ablation arm. 

These PABA-CHF study findings thus suggest the potential advantages of performing PV isolation over AV node ablation with biventricular pacing for this patient population. 

Noted limitations of the study include using sites with extensive experience in performing ablations, an unblinded study design, and a relatively short follow-up time. (NEJM by Mohammed N. Khan, et al.)

==[[The Living Guidelines: Diagnosis and Management of Atrial Fibrillation|Guidelines: Diagnosis and Management of Atrial Fibrillation]]==

==External links==

* [http://www.americanheart.org/presenter.jhtml?identifier=4451 American Heart Association's page on atrial fibrillation]
* [http://www.patient.co.uk/showdoc/23068682/ Atrial fibrillation] 
* [http://www.jr2.ox.ac.uk/bandolier/booth/booths/AF.html Bandolier: Evidence-based medicine resource on atrial fibrillation]
* [http://my.clevelandclinic.org/heart/webchat/atrialfibrillation011608.aspx Cleveland Clinic Webchat - Atrial Fibrillation Webchat with Dr. Jennifer Cummings]

==See also==
* [[Atrial flutter]]
* [[Ashman phenomenon]]

==[[EKG Examples of atrial fibrillation]]==

==External EKG Sources==
*[http://www.emedu.org/ecg_lib/index.htm John Vozenilek's (MD) ECG Collection]
*[http://www.ecgpedia.org ECGpedia]

==References==
{{reflist|2}}

==Further Readings==
{{refbegin|2}}
* Fuster V, Rydén LE, Cannom DS, et al (2006). "ACC/AHA/ESC 2006 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 Cardiology 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 Heart Rhythm Society". Circulation 114 (7): e257-354. doi:10.1161/CIRCULATIONAHA.106.177292. PMID 16908781.
* Estes NAM 3rd, Halperin JL, Calkins H, Ezekowitz MD, Gitman P, Go AS, McNamara RL, Messer JV, Ritchie JL, Romeo SJW, Waldo AL, Wyse DG. ACC/AHA/Physician Consortium 2008 clinical performance measures for adults with non valvular atrial fibrillation or atrial flutter: a report of the American College of Cardiology/American Heart Association Task Force on Performance Measures and the Physician Consortium for Performance Improvement (Writing Committee to Develop Performance Measures for Atrial Fibrillation). Circulation 2008; 117:1101–1120
* Braunwald's Heart Disease, Libby P, 8th ed., 2007, ISBN 978-1-41-604105-4
* Hurst's the Heart, Fuster V, 12th ed. 2008, ISBN 978-0-07-149928-6
* Willerson JT, Cardiovascular Medicine, 3rd ed., 2007, ISBN 978-1-84628-188-4 
{{refend}}

{{Electrocardiography}}
{{Circulatory system pathology}}
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[[Category:Electrophysiology]]
[[Category:Cardiology]]
[[Category:Emergency medicine]]

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[[pl:Migotanie przedsionków]]
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