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• atients with uncontrolled angina6ischemia

Initial history and physical e"amination include the following=

• Documentation of clinical type of AF (paro"ysmal, persistent, or permanent)

• Assessment of type, duration, and fre<uency of symptoms

• Assessment of precipitating factors (eg, e"ertion, sleep, caffeine, alcohol use)

• Assessment of modes of termination (eg, vagal maneuvers)

• Documentation of prior use of antiarrhythmics and ratecontrolling agents

• Assessment of presence of underlying heart disease

• Documentation of any previous surgical or percutaneous AF ablation procedures

• Airway, breathing, and circulation (A?Cs)

• $ital signs (particularly heart rate, blood pressure, respiratory rate, and o"ygen

saturation)

• @valuation of head and nec#, lungs, heart, abdomen, lower e"tremities, and nervous

system

ee Clinical Presentation for more detail.

Dianosis

Findings from %lead electrocardiography (@C4) usually confirm the diagnosis of AF andinclude the following=

• !ypically irregular ventricular rate

• Absence of discrete waves, replaced by irregular, chaotic F waves, in the setting of

irregular B+ comple"es

• Aberrantly conducted beats after longshort ++ cycles (ie, Ashman phenomenon)

• >eart rate (typically %%'%' beats6min, rarely %'%7' beats6min)

• ree"citation

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• 5eft ventricular hypertrophy

• ?undlebranch bloc#

• Acute or prior myocardial infarction (EI)

!ransthoracic echocardiography (!!@) is helpful for the following applications=

• !o evaluate for valvular heart disease

• !o evaluate atrial and ventricular chamber and wall dimensions

• !o estimate ventricular function and evaluate for ventricular thrombi

• !o estimate pulmonary systolic pressure (pulmonary hypertension)

• !o evaluate for pericardial disease

!ransesophageal echocardiography (!@@) is helpful for the following applications=

• !o evaluate for left atrial thrombus (particularly in the left atrial appendage)

• !o guide cardioversion (if thrombus is seen, cardioversion should be delayed)

ee "orkup for more detail.

#anaement

!he cornerstones of AF management are rate control and anticoagulation,2&3 as well as rhythm

control for those symptomatically limited by AF. !he clinical decision to use a rhythmcontrol or

a ratecontrol strategy re<uires integrated consideration of the following=

• Degree of symptoms

• 5i#elihood of successful cardioversion

• resence of comorbidities

• Candidacy for AF ablation

!he '' American College of Cardiology (ACC)6American >eart Association (A>A)6@uropean

ociety of Cardiology (@C) guidelines on anticoagulation for patients with nonvalvular AF

include the following23 =

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• o ris# factors= Aspirin *%&- mg6day

• % moderate ris# factor= Aspirin *%&- mg6day or warfarin (international normalied ratio

2I+3 &)

• Any highris# factor or % moderateris# factor= Garfarin (I+ &)

+is# factors are as follows=

• >ighris# factors= rior stro#e or transient ischemic attac# (!IA), systemic

thromboembolism

• Eoderateris# factors= Age 7- years, hypertension, heart failure, left ventricular function

9 &-H, diabetes mellitus

• +is# factors of un#nown significance= Female se", age -7 years, coronary artery

disease, thyroto"icosis

New-onset AF:

ACC6A>A6@C '' guidelines for newonset AF include the following23 =

• An initial ratecontrol strategy is reasonableJ for asymptomatic or minimally

symptomatic older patients with hypertension and comorbid cardiovascular disease

• For younger individuals, especially those without significant comorbid cardiovascular

disease, an initial rhythmcontrol strategy may be better

Agents used for rate control in newonset AF include the following=

• Diltiaem

• Eetoprolol

• Digo"in (rarely as monotherapy)

• Amiodarone (mainly for patients who are intolerant of or unresponsive to other agents)

Anticoagulation is indicated as follows=

• atients with newly diagnosed AF and those awaiting electrical cardioversion can be

started on intravenous (I$) heparin or lowmolecularweight heparin (5EG>)



• Concomitantly, patients can be started on warfarin in an inpatient setting while awaiting a

therapeutic I+ value (&)

• Kral direct thrombin inhibitors may present an alternative to warfarin in a higherris#

population with nonvalvular AF

ewer oral anticoagulants that have been approved by the ; Food and Drug Administration(FDA) and may be considered as alternatives to warfarin include the following=

• Dabigatran (direct thrombin inhibitor)

• +ivaro"aban (highly selective direct factor 1a inhibitor)

• Api"aban (factor 1a inhibitor)

Long-term management of AF:

Kptimal longterm strategies for AF management should be based on a thoroughly integrated

consideration of patientspecific factors and li#elihood of success. election of an appropriateantithrombotic regimen should be balanced between the ris# of stro#e and the ris# of bleeding.

Factors that increase the ris# of bleeding with warfarin therapy include the following=

• >istory of bleeding (the strongest predictive ris# factor)

• Age older than 7- years

•

5iver or renal disease

• Ealignancy

• !hrombocytopenia or aspirin use

• >ypertension

• Diabetes mellitus

• Anemia

• rior stro#e

• Fall ris#

• 4enetic predisposition



• upratherapeutic I+

Alternatives to warfarin=

• If warfarin will not be used, adding clopidogrel to aspirin may be considered 2-3

• ;pdated ACC6A>A6>eart +hythm ociety (>+) guidelines on AF include a class Ib

recommendation for dabigatran 23 for preventing stro#e and systemic thromboembolismin patients with paro"ysmaltopermanent atrial fibrillation and ris# factors for stro#e or

systemic emboliation

Agents used for rate control include the following=

• Kral betabloc#ers

• ondihydropyridine calcium channel bloc#ers

• Digo"in

• Amiodarone

Agents used for rhythm control include the following=

• Flecainide

• ropafenone

• Dofetilide

• Amiodarone

• Dronedarone

• otalol

Catheter ablation performed in e"perienced centers is recommended in the '%% update to theACCF6A>A6>+ AF guidelines for the following indications2-3 =

• It is recommended as an alternative to pharmacologic therapy to prevent recurrent

paro"ysmal AF in significantly symptomatic patients with little or no structural heart

disease or severe pulmonary disease 273

• It is reasonable as a treatment for symptomatic persistent AF



• It may be reasonable as a treatment for symptomatic paro"ysmal AF in patients with

some structural heart disease

ee $reatment and #edication for more detail.

%ackround

Classification of atrial fibrillation (AF) begins with distinguishing a first detectable episode,

irrespective of whether it is symptomatic or selflimited. ublished guidelines from an American

College of Cardiology (ACC)6American >eart Association (A>A)6@uropean ociety ofCardiology (@C) committee of e"perts on the treatment of patients with atrial fibrillation

recommend classification of AF into the following & patterns (also see the image below)2*3 =

• aro"ysmal AF L @pisodes of AF that terminate spontaneously within 7 days (most

episodes last less than hours)

• ersistent AF @pisodes of AF that last more than 7 days and may re<uire either

pharmacologic or electrical intervention to terminate

• ermanent AF AF that has persisted for more than % year, either because cardioversion

has failed or because cardioversion has not been attempted

Classification scheme for patients with atrial fibrillation.

!his classification schema pertains to cases that are not related to a reversible cause of AF (eg,

thyroto"icosis, electrolyte abnormalities, acute ethanol into"ication). Atrial fibrillation secondaryto acute myocardial infarction, cardiac surgery, pericarditis, pulmonary embolism, or acute

pulmonary disease is considered separately because, in these situations, AF is less li#ely to recur

once the precipitating condition has been treated ade<uately and has resolved. ee the image

below.

Classification scheme for patients with atrial fibrillation.

Paro&!smal AF

Atrial fibrillation is considered to be recurrent when a patient has or more episodes. If recurrent

AF terminates spontaneously, it is designated as paro"ysmal.

ome patients with paro"ysmal AF, typically younger patients, have been found to have distinct

electrically active foci within their pulmonary veins. !hese patients generally have many atrial

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premature beats noted on >olter monitoring. Isolation or elimination of these foci can lead to

elimination of the trigger for paro"ysms of AF.

aro"ysmal AF may progress to permanent AF, and aggressive attempts to restore and maintainsinus rhythm may prevent comorbidities associated with AF.

Persistent AF

If recurrent AF is sustained, it is considered persistent, irrespective of whether the arrhythmia isterminated by either pharmacologic therapy or electrical cardioversion.

ersistent AF may be either the first presentation of AF or the result of recurrent episodes of

paro"ysmal AF. atients with persistent AF also include those with longstanding AF in whom

cardioversion has not been indicated or attempted, often leading to permanent AF.

atients can also have AF as an arrhythmia secondary to cardiac disease that affects the atria (eg,

congestive heart failure, hypertensive heart disease, rheumatic heart disease, coronary arterydisease). !hese patients tend to be older, and AF is more li#ely to be persistent.

ersistent AF with an uncontrolled, rapid ventricular heart rate response can cause a dilatedcardiomyopathy and can lead to electrical remodeling in the atria (atrial cardiomyopathy).

!herapy, such as drugs or atrioventricular nodal ablation and permanent pacema#er implantation,

to control the ventricular rate can improve left ventricular function and improve <ualityoflife

scores.

Permanent AF

ermanent AF is recognied as the accepted rhythm, and the main treatment goals are ratecontrol and anticoagulation. Ghile it is possible to reverse the progression from paro"ysmal to persistent and to permanent, this tas# can be challenging.

'one atrial fibrillation

In addition to the above schema, the term Mlone atrial fibrillationM has been used to identify AF in

younger patients without structural heart disease, who are at a lower ris# for thromboembolism.

!he definition of lone AF remains controversial, but it generally refers to paro"ysmal, persistent,

or permanent AF in younger patients (9 ' y) who have normal echocardiographic findings.2N3

Pathoph!siolo!

Atrial fibrillation (AF) shares strong associations with other cardiovascular diseases, such as

heart failure, coronary artery disease (CAD), valvular heart disease, diabetes mellitus, and

hypertension.2%'3 !hese factors have been termed upstream ris# factors, but the relationship between comorbid cardiovascular disease and AF is incompletely understood and more comple"

than this terminology implies. !he e"act mechanisms by which cardiovascular ris# factors



predispose to AF are not understood fully but are under intense investigation. Catecholamine

e"cess, hemodynamic stress, atrial ischemia, atrial inflammation, metabolic stress, and

neurohumoral cascade activation are all purported to promote AF.

?ecause diabetes mellitus and obesity are increasing in prevalence and are associated with an

elevated ris# of AF, Fontes et al e"amined whether insulin resistance is an intermediate step forthe development of AF. In a communitybased cohort that included 7N patients who developed

AF within %' years of followup, no significant association was observed between insulinresistance and incident AF.2%%3

Although the precise mechanisms that cause atrial fibrillation are incompletely understood, AF

appears to re<uire both an initiating event and a permissive atrial substrate. ignificant recentdiscoveries have highlighted the importance of focal pulmonary vein triggers, but alternative and

nonmutually e"clusive mechanisms have also been evaluated. !hese mechanisms include

multiple wavelets, mother waves, fi"ed or moving rotors, and macroreentrant circuits. In a given

patient, multiple mechanisms may coe"ist at any given time. !he automatic focus theory and the

multiple wavelet hypothesis appear to have the best supporting data.

Automatic focus

A focal origin of AF is supported by several e"perimental models showing that AF persists onlyin isolated regions of atrial myocardium. !his theory has garnered considerable attention, as

studies have demonstrated that a focal source of AF can be identified in humans and that

isolation of this source can eliminate AF.

!he pulmonary veins appear to be the most fre<uent source of these automatic foci, but other

foci have been demonstrated in several areas throughout the atria. Cardiac muscle in the

pulmonary veins appears to have active electrical properties that are similar, but not identical, tothose of atrial myocytes. >eterogeneity of electrical conduction around the pulmonary veins istheoried to promote reentry and sustained AF. !hus, pulmonary vein automatic triggers may

provide the initiating event, and heterogeneity of conduction may provide the sustaining

conditions in many patients with AF.

#ultiple wa(elet

!he multiple wavelet hypothesis proposes that fractionation of wave fronts propagating through

the atria results in selfperpetuating Mdaughter wavelets.M In this model, the number of waveletsis determined by the refractory period, conduction velocity, and mass of atrial tissue. Increased

atrial mass, shortened atrial refractory period, and delayed intraatrial conduction increase thenumber of wavelets and promote sustained AF. !his model is supported by data from patientswith paro"ysmal AF demonstrating that widespread distribution of abnormal atrial electrograms

predicts progression to persistent AF.2%3 Intraatrial conduction prolongation has also been shown

to predict recurrence of AF.2%&3 !ogether, these data highlight the importance of atrial structuraland electrical remodeling in the maintenance of AFOhence the phrase Matrial fibrillation begets

atrial fibrillation.M



Etiolo!

Atrial fibrillation (AF) is strongly associated with the following ris# factors=

• >emodynamic stress

• Atrial ischemia

• Inflammation

• oncardiovascular respiratory causes

• Alcohol and drug use

• @ndocrine disorders

• eurologic disorders

• 4enetic factors

• Advancing age

)emod!namic stress

Increased intraatrial pressure results in atrial electrical and structural remodeling and

predisposes to AF. !he most common causes of increased atrial pressure are mitral or tricuspidvalve disease and left ventricular dysfunction. ystemic or pulmonary hypertension also

commonly predisposes to atrial pressure overload, and intracardiac tumors or thrombi are rare

causes.

Atrial ischemia

Coronary artery disease infre<uently leads directly to atrial ischemia and AF. Eore commonly,

severe ventricular ischemia leads to increased intraatrial pressure and AF.

*nflammation

Eyocarditis and pericarditis may be idiopathic or may occur in association with collagen

vascular diseases8 viral or bacterial infections8 or cardiac, esophageal, or thoracic surgery.

+oncardio(ascular respirator! causes

ulmonary embolism, pneumonia, lung cancer, and hypothermia have been associated with AF.

http://emedicine.medscape.com/article/300901-overview




Dru and alcohol use

timulants, alcohol, and cocaine can trigger AF. Acute or chronic alcohol use (ie, holiday oraturday night heart, also #nown as alcoholrelated cardiomyopathy) and illicit drug use (ie,

stimulants, methamphetamines, cocaine) have been specifically found to be related to AF.

Endocrine disorders

>yperthyroidism, diabetes, and pheochromocytoma have been associated with AF.

+euroloic disorders

Intracranial processes such as subarachnoid hemorrhage or stro#e can precipitate AF.

Familial AF

A history of parental AF appears to confer increased li#elihood of AF (and occasional family pedigrees of AF are associated with defined ion channel abnormalities, especially sodium

channels).2%3 Kne cohort study suggests that familial AF is associated with an increased ris# of

AF. !his increase was not lessened by ad0ustment for genetic variants and other AF ris# factors.2%-3

Ad(ancin ae

AF is strongly agedependent, affecting H of individuals older than ' years and *H of personsolder than *' years.

Epidemiolo!

Atrial fibrillation affects more than . million persons in the ;nited tates. AF is strongly age

dependent, affecting H of individuals older than ' years and *H of persons older than *'years. Appro"imately -H of individuals aged ' years and older will develop AF during their

lifetime.2%3

!he prevalence of AF is '.%H in persons younger than -- years, &.*H in persons ' years or

older, and %'H in persons *' years or older. Gith the pro0ected increase in the elderly populationin the ;nited tates, the prevalence of AF is e"pected to more than double by the year '-'. AF

is uncommon in childhood e"cept after cardiac surgery.2%73

!he incidence of AF is significantly higher in men than in women in all age groups. AF appears

to be more common in whites than in blac#s, with blac#s have less than half the agead0usted ris# of developing AF.

In %'%-H of cases of AF, the disease occurs in the absence of comorbidities (lone atrial

fibrillation). >owever, AF is often associated with other cardiovascular diseases, including



hypertension8 heart failure8 diabetesrelated heart disease8 ischemic heart disease8 and valvular,

dilated, hypertrophic, restrictive, and congenital cardiomyopathies.2%3 !he Atherosclerosis +is# in

Communities (A+IC) tudy suggests reduced #idney function and presence of albuminuria arestrongly associated with AF.2%*3

!he rate of ischemic stro#e in patients with nonrheumatic AF averages -H a year, which issomewhere between and 7 times the rate of stro#e in patients without AF. !he ris# of stro#e is

not due solely to AF8 it increases substantially in the presence of other cardiovascular diseases.2%N3

!he prevalence of stro#e in patients younger than ' years is less than '.-H8 however, in those

older than 7' years, the prevalence doubles with each decade.2'3 !he attributable ris# of stro#e

from AF is estimated to be %.-H for those aged -'-N years, and it approaches &'H for thoseaged *'*N years. Gomen are at a higher ris# of stro#e due to AF than men and some have

suggested this may be due to undertreatment with warfarin. >owever, one study of patients -

years or older with recently diagnosed AF found warfarin use played no part in the increased ris# of stro#e among female patients.2%3

Pronosis

AF is associated with a %.- to %.Nfold higher ris# of death, which is in part due to the strong

association between AF and thromboembolic events, according to data from the Framinghamheart study.23

Eedical therapies aimed at rhythm control offered no survival advantage over rate control and

anticoagulation, according to the Atrial Fibrillation Followup Investigation of +hythm

Eanagement (AFFI+E) trial. !he study addressed whether rate control and anticoagulation aresufficient goals for asymptomatic, elderly patients.2&3

Atrial fibrillation (AF) is associated with increased morbidity and mortality, in part due to theris# of thromboembolic disease, particularly stro#e, in AF and in part due to its associated ris#

factors. tudies have shown that individuals in sinus rhythm live longer than individuals with AF.Disruption of normal atrial electromechanical function in AF leads to blood stasis. !his, in turn,

can lead to development of thrombus, most commonly in the left atrial appendage. Dislodgement

or fragmentation of a clot can then lead to embolic phenomena, including stro#e.

Development of AF predicts heart failure and is associated with a worse ew Por# >eartAssociation >eart Failure classification. AF may also worsen heart failure in individuals who are

dependent on the atrial component of the cardiac output. !hose with hypertensive heart disease

and those with valvular heart disease are particularly at high ris# for developing heart failure

when AF occurs. In addition, AF may cause tachycardiamediated cardiomyopathy if ade<uaterate control is not established.

!he ris# of stro#e from AF that lasts longer than hours is a ma0or concern and is usually

addressed by prescribing a blood thinner (Coumadin or dabigatran). rognostic score systems,such as C>AD, appear to underestimate the ris# of embolic stro#e in patients older than 7-

years8 thus, some studies recommend treating all patients older than 7- years unless a compelling

contraindication is noted.23 !he C>AD score predicts ischemic stro#e not only for patients





with a history of atrial fibrillation but also for patients without atrial fibrillation who have a

history of coronary heart disease.2-3 In the latter group, net benefit of prophylactic

anticoagulation has yet to be established.

An analysis of the AF@! (Central +egistry of the 4erman Competence @!wor# on Atrial

Fibrillation) registry of **7 patients with nonvalvular atrial fibrillation indicated that the C>A D $Ac score is more sensitive than the C>AD score for ris# stratification of

thromboembolic events (ischemic stro#e, transient ischemic attac# 2!IA3, systemic embolism), particularly in patients at low or intermediate ris# for stro#e (C>AD score of ' or %)Owho

therefore do not re<uire oral anticoagulation.2, 73

During a mean followup of - years, the investigators found &.-H (% of &N-) of stro#es orother thromboembolic events occurred in patients given a C>AD score of ' or %, groups in

which there is no definitive recommendation for oral anticoagulation. 2, 73 >owever, C>A D

$Ac scoringOwhich adds age -7 years, vascular disease, and female se" as stro#e ris#

factors to the C>AD score273 Oplaced &'.&H of those classified as C>AD ' or % into C>A

D $Ac % or and higher, groups in which oral anticoagulation is recommended.

23

A posthoc analysis of the K!A+4@! and !+@D studies, which evaluated the efficacy of

treatment with ramipril plus telmisartan or telmisartan alone in reducing cardiovascular disease,

used the EiniLEental tate @"amination (EE@) to measure the cognitive function of participants at baseline and after two and five years. +esults show that AF is associated with an

increased ris# of cognitive decline, new dementia, loss of independence in performing activities

of daily living and admission to longterm care facilities.2*3

Atrial fibrillation in association with acute m!ocardial infarction

AF is a common finding in patients presenting with an acute myocardial infarction. A metaanalysis pooled data from & studies and more than 7*,*'' patients.2N3 !he study found that AFin the setting of acute myocardial infarction was associated with 'H increase in mortality

compared to patients in sinus rhythm with acute myocardial infarction. !he causes of death were

unclear, but may be related to triple anticoagulation therapy with aspirin, clopidogrel, andwarfarin, or may be related to hemodynamic conse<uences associated with the loss of atrial

contraction. Ghether AF is a complication of myocardial infarction or a mar#er for myocardial

infarction severity is unclear.

Patient Education

A study by van Diepen et al suggests that patients with heart failure or atrial fibrillation have asignificantly higher ris# of noncardiac postoperative mortality than patients with coronary artery

disease8 thus, patients and physicians should consider this ris#, even if a minor procedure is planned.2&'3

For patient education resources, see >eart Center and tro#e Center . Also, see patient education

articles Atrial Fibrillation, >eart +hythm Disorders, tro#e, and upraventricular !achycardia.

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