3/23/2017 AtrialFibrillation:PracticeEssentials,Background,Pathophysiology

Thissiteisintendedforhealthcareprofessionals

AtrialFibrillation
Updated:Jan02,2016
Author:LawrenceRosenthal,MD,PhD,FACC,FHRSChiefEditor:JeffreyNRottman,MD
more...

OVERVIEW

PracticeEssentials
Atrialfibrillation(AF)hasstrongassociationswithothercardiovasculardiseases,suchasheart
failure,coronaryarterydisease(CAD),valvularheartdisease,diabetesmellitus,andhypertension.
Itischaracterizedbyanirregularandoftenrapidheartbeat(seetheimagebelow).Theexact
mechanismsbywhichcardiovascularriskfactorspredisposetoAFarenotunderstoodfullybutare
underintenseinvestigation.Catecholamineexcess,hemodynamicstress,atrialischemia,atrial
inflammation,metabolicstress,andneurohumoralcascadeactivationareallpurportedtopromote
AF.

Ventricularratevariesfrom130168beatsperminute.Rhythmisirregularlyirregular.Pwavesarenot
discernible.
ViewMediaGallery

Signsandsymptoms
TheclinicalpresentationofAFspanstheentirespectrumfromasymptomaticAFwithrapid
ventricularresponsetocardiogenicshockordevastatingcerebrovascularaccident(CVA).Unstable
patientsrequiringimmediatedirectcurrent(DC)cardioversionincludethefollowing:

Patientswithdecompensatedcongestiveheartfailure(CHF)
Patientswithhypotension
Patientswithuncontrolledangina/ischemia

Initialhistoryandphysicalexaminationincludethefollowing:

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DocumentationofclinicaltypeofAF(paroxysmal,persistent,orpermanent)
Assessmentoftype,duration,andfrequencyofsymptoms
Assessmentofprecipitatingfactors(eg,exertion,sleep,caffeine,alcoholuse)
Assessmentofmodesoftermination(eg,vagalmaneuvers)
Documentationofprioruseofantiarrhythmicsandratecontrollingagents
Assessmentofpresenceofunderlyingheartdisease
DocumentationofanyprevioussurgicalorpercutaneousAFablationprocedures
Airway,breathing,andcirculation(ABCs)
Vitalsigns(particularlyheartrate,bloodpressure,respiratoryrate,andoxygensaturation)
Evaluationofheadandneck,lungs,heart,abdomen,lowerextremities,andnervoussystem

SeeClinicalPresentationformoredetail.

Diagnosis

Findingsfrom12leadelectrocardiography(ECG)usuallyconfirmthediagnosisofAFandinclude
thefollowing:

Typicallyirregularventricularrate
AbsenceofdiscretePwaves,replacedbyirregular,chaoticFwaves,inthesettingof
irregularQRScomplexes
AberrantlyconductedbeatsafterlongshortRRcycles(ie,Ashmanphenomenon)
Heartrate(typically110140beats/min,rarely>160170beats/min)
Preexcitation
Leftventricularhypertrophy
Bundlebranchblock
Acuteorpriormyocardialinfarction(MI)

Transthoracicechocardiography(TTE)ishelpfulforthefollowingapplications:

Toevaluateforvalvularheartdisease
Toevaluateatrialandventricularchamberandwalldimensions
Toestimateventricularfunctionandevaluateforventricularthrombi
Toestimatepulmonarysystolicpressure(pulmonaryhypertension)
Toevaluateforpericardialdisease

Transesophagealechocardiography(TEE)ishelpfulforthefollowingapplications:

Toevaluateforleftatrialthrombus(particularlyintheleftatrialappendage)
Toguidecardioversion(ifthrombusisseen,cardioversionshouldbedelayed)

SeeWorkupformoredetail.

Management

ThecornerstonesofAFmanagementareratecontrolandanticoagulation,[1]aswellasrhythm
controlforthosesymptomaticallylimitedbyAF.Theclinicaldecisiontousearhythmcontrolora
ratecontrolstrategyrequiresintegratedconsiderationofthefollowing:

Degreeofsymptoms
Likelihoodofsuccessfulcardioversion
Presenceofcomorbidities
CandidacyforAFablation

The2006AmericanCollegeofCardiology(ACC)/AmericanHeartAssociation(AHA)/European
SocietyofCardiology(ESC)guidelinesonanticoagulationforpatientswithnonvalvularAFinclude
thefollowing[2]:

Noriskfactors:Aspirin81325mg/day
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Noriskfactors:Aspirin81325mg/day
1moderateriskfactor:Aspirin81325mg/dayorwarfarin(internationalnormalizedratio[INR]
23)
Anyhighriskfactoror>1moderateriskfactor:Warfarin(INR23)

Riskfactorsareasfollows:

Highriskfactors:Priorstrokeortransientischemicattack(TIA),systemicthromboembolism
Moderateriskfactors:Age>75years,hypertension,heartfailure,leftventricularfunction<
35%,diabetesmellitus
Riskfactorsofunknownsignificance:Femalesex,age6574years,coronaryarterydisease,
thyrotoxicosis

NewonsetAF:

ACC/AHA/ESC2006guidelinesfornewonsetAFincludethefollowing[2]:

Aninitialratecontrolstrategyisreasonableforasymptomaticorminimallysymptomatic
olderpatientswithhypertensionandcomorbidcardiovasculardisease
Foryoungerindividuals,especiallythosewithoutsignificantcomorbidcardiovasculardisease,
aninitialrhythmcontrolstrategymaybebetter

AgentsusedforratecontrolinnewonsetAFincludethefollowing:

Diltiazem
Metoprolol
Digoxin(rarelyasmonotherapy)
Amiodarone(mainlyforpatientswhoareintolerantoforunresponsivetootheragents)

Anticoagulationisindicatedasfollows:

PatientswithnewlydiagnosedAFandthoseawaitingelectricalcardioversioncanbestarted
onintravenous(IV)heparinorlowmolecularweightheparin(LMWH)
Concomitantly,patientscanbestartedonwarfarininaninpatientsettingwhileawaitinga
therapeuticINRvalue(23)
Oraldirectthrombininhibitorsmaypresentanalternativetowarfarininahigherrisk
populationwithnonvalvularAF

NeweroralanticoagulantsthathavebeenapprovedbytheUSFoodandDrugAdministration
(FDA)andmaybeconsideredasalternativestowarfarinincludethefollowing:

Dabigatran(directthrombininhibitor)
Rivaroxaban(highlyselectivedirectfactorXainhibitor)
Apixaban(factorXainhibitor)

LongtermmanagementofAF:

OptimallongtermstrategiesforAFmanagementshouldbebasedonathoroughlyintegrated
considerationofpatientspecificfactorsandlikelihoodofsuccess.Selectionofanappropriate
antithromboticregimenshouldbebalancedbetweentheriskofstrokeandtheriskofbleeding.
Factorsthatincreasetheriskofbleedingwithwarfarintherapyincludethefollowing:

Historyofbleeding(thestrongestpredictiveriskfactor)
Ageolderthan75years
Liverorrenaldisease
Malignancy
Thrombocytopeniaoraspirinuse
Hypertension
Diabetesmellitus
Anemia
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Anemia
Priorstroke
Fallrisk
Geneticpredisposition
SupratherapeuticINR

Alternativestowarfarin:

Ifwarfarinwillnotbeused,addingclopidogreltoaspirinmaybeconsidered[3]
UpdatedACC/AHA/HeartRhythmSociety(HRS)guidelinesonAFincludeaclassIb
recommendationfordabigatran[4]forpreventingstrokeandsystemicthromboembolismin
patientswithparoxysmaltopermanentatrialfibrillationandriskfactorsforstrokeorsystemic
embolization

Agentsusedforratecontrolincludethefollowing:

Oralbetablockers
Nondihydropyridinecalciumchannelblockers
Digoxin
Amiodarone

Agentsusedforrhythmcontrolincludethefollowing:

Flecainide
Propafenone
Dofetilide
Amiodarone
Dronedarone
Sotalol

Catheterablationperformedinexperiencedcentersisrecommendedinthe2011updatetothe
ACCF/AHA/HRSAFguidelinesforthefollowingindications[3]:

Itisrecommendedasanalternativetopharmacologictherapytopreventrecurrent
paroxysmalAFinsignificantlysymptomaticpatientswithlittleornostructuralheartdisease
orseverepulmonarydisease[5]
ItisreasonableasatreatmentforsymptomaticpersistentAF
ItmaybereasonableasatreatmentforsymptomaticparoxysmalAFinpatientswithsome
structuralheartdisease

SeeTreatmentandMedicationformoredetail.

Background
Classificationofatrialfibrillation(AF)beginswithdistinguishingafirstdetectableepisode,
irrespectiveofwhetheritissymptomaticorselflimited.PublishedguidelinesfromanAmerican
CollegeofCardiology(ACC)/AmericanHeartAssociation(AHA)/EuropeanSocietyofCardiology
(ESC)committeeofexpertsonthetreatmentofpatientswithatrialfibrillationrecommend
classificationofAFintothefollowing3patterns(alsoseetheimagebelow)[6]:

ParoxysmalAFEpisodesofAFthatterminatespontaneouslywithin7days(mostepisodes
lastlessthan24hours)
PersistentAFEpisodesofAFthatlastmorethan7daysandmayrequireeither
pharmacologicorelectricalinterventiontoterminate
PermanentAFAFthathaspersistedformorethan1year,eitherbecausecardioversionhas
failedorbecausecardioversionhasnotbeenattempted

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Classificationschemeforpatientswithatrialfibrillation.
ViewMediaGallery

ThisclassificationschemapertainstocasesthatarenotrelatedtoareversiblecauseofAF(eg,
thyrotoxicosis,electrolyteabnormalities,acuteethanolintoxication).Atrialfibrillationsecondaryto
acutemyocardialinfarction,cardiacsurgery,pericarditis,pulmonaryembolism,oracutepulmonary
diseaseisconsideredseparatelybecause,inthesesituations,AFislesslikelytorecuroncethe
precipitatingconditionhasbeentreatedadequatelyandhasresolved.Seetheimagebelow.

Classificationschemeforpatientswithatrialfibrillation.
ViewMediaGallery

ParoxysmalAF

Atrialfibrillationisconsideredtoberecurrentwhenapatienthas2ormoreepisodes.Ifrecurrent
AFterminatesspontaneously,itisdesignatedasparoxysmal.

SomepatientswithparoxysmalAF,typicallyyoungerpatients,havebeenfoundtohavedistinct
electricallyactivefociwithintheirpulmonaryveins.Thesepatientsgenerallyhavemanyatrial
prematurebeatsnotedonHoltermonitoring.Isolationoreliminationofthesefocicanleadto
eliminationofthetriggerforparoxysmsofAF.

ParoxysmalAFmayprogresstopermanentAF,andaggressiveattemptstorestoreandmaintain
sinusrhythmmaypreventcomorbiditiesassociatedwithAF.

PersistentAF

IfrecurrentAFissustained,itisconsideredpersistent,irrespectiveofwhetherthearrhythmiais
terminatedbyeitherpharmacologictherapyorelectricalcardioversion.

PersistentAFmaybeeitherthefirstpresentationofAFortheresultofrecurrentepisodesof
paroxysmalAF.PatientswithpersistentAFalsoincludethosewithlongstandingAFinwhom
cardioversionhasnotbeenindicatedorattempted,oftenleadingtopermanentAF.

PatientscanalsohaveAFasanarrhythmiasecondarytocardiacdiseasethataffectstheatria(eg,
congestiveheartfailure,hypertensiveheartdisease,rheumaticheartdisease,coronaryartery
disease).Thesepatientstendtobeolder,andAFismorelikelytobepersistent.

PersistentAFwithanuncontrolled,rapidventricularheartrateresponsecancauseadilated
cardiomyopathyandcanleadtoelectricalremodelingintheatria(atrialcardiomyopathy).Therapy,
suchasdrugsoratrioventricularnodalablationandpermanentpacemakerimplantation,tocontrol
theventricularratecanimproveleftventricularfunctionandimprovequalityoflifescores.

PermanentAF

PermanentAFisrecognizedastheacceptedrhythm,andthemaintreatmentgoalsareratecontrol5/17
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PermanentAFisrecognizedastheacceptedrhythm,andthemaintreatmentgoalsareratecontrol
andanticoagulation.Whileitispossibletoreversetheprogressionfromparoxysmaltopersistent
andtopermanent,thistaskcanbechallenging.

Loneatrialfibrillation

Inadditiontotheaboveschema,theterm"loneatrialfibrillation"hasbeenusedtoidentifyAFin
youngerpatientswithoutstructuralheartdisease,whoareatalowerriskforthromboembolism.
ThedefinitionofloneAFremainscontroversial,butitgenerallyreferstoparoxysmal,persistent,or
permanentAFinyoungerpatients(<60y)whohavenormalechocardiographicfindings.[7]

Pathophysiology
Atrialfibrillation(AF)sharesstrongassociationswithothercardiovasculardiseases,suchasheart
failure,coronaryarterydisease(CAD),valvularheartdisease,diabetesmellitus,andhypertension.
[8] Thesefactorshavebeentermedupstreamriskfactors,buttherelationshipbetweencomorbid
cardiovasculardiseaseandAFisincompletelyunderstoodandmorecomplexthanthisterminology
implies.TheexactmechanismsbywhichcardiovascularriskfactorspredisposetoAFarenot
understoodfullybutareunderintenseinvestigation.Catecholamineexcess,hemodynamicstress,
atrialischemia,atrialinflammation,metabolicstress,andneurohumoralcascadeactivationareall
purportedtopromoteAF.

Becausediabetesmellitusandobesityareincreasinginprevalenceandareassociatedwithan
elevatedriskofAF,Fontesetalexaminedwhetherinsulinresistanceisanintermediatestepforthe
developmentofAF.Inacommunitybasedcohortthatincluded279patientswhodevelopedAF
within10yearsoffollowup,nosignificantassociationwasobservedbetweeninsulinresistance
andincidentAF.[9]

Althoughtheprecisemechanismsthatcauseatrialfibrillationareincompletelyunderstood,AF
appearstorequirebothaninitiatingeventandapermissiveatrialsubstrate.Significantrecent
discoverieshavehighlightedtheimportanceoffocalpulmonaryveintriggers,butalternativeand
nonmutuallyexclusivemechanismshavealsobeenevaluated.[10]Thesemechanismsinclude
multiplewavelets,motherwaves,fixedormovingrotors,andmacroreentrantcircuits.[10]Ina
givenpatient,multiplemechanismsmaycoexistatanygiventime.Theautomaticfocustheoryand
themultiplewavelethypothesisappeartohavethebestsupportingdata.

Automaticfocus

AfocaloriginofAFissupportedbyseveralexperimentalmodelsshowingthatAFpersistsonlyin
isolatedregionsofatrialmyocardium.Thistheoryhasgarneredconsiderableattention,asstudies
havedemonstratedthatafocalsourceofAFcanbeidentifiedinhumansandthatisolationofthis
sourcecaneliminateAF.

Thepulmonaryveinsappeartobethemostfrequentsourceoftheseautomaticfoci,butotherfoci
havebeendemonstratedinseveralareasthroughouttheatria.Cardiacmuscleinthepulmonary
veinsappearstohaveactiveelectricalpropertiesthataresimilar,butnotidentical,tothoseofatrial
myocytes.Heterogeneityofelectricalconductionaroundthepulmonaryveinsistheorizedto
promotereentryandsustainedAF.Thus,pulmonaryveinautomatictriggersmayprovidethe
initiatingevent,andheterogeneityofconductionmayprovidethesustainingconditionsinmany
patientswithAF.

Multiplewavelet

Themultiplewavelethypothesisproposesthatfractionationofwavefrontspropagatingthroughthe
atriaresultsinselfperpetuating"daughterwavelets."Inthismodel,thenumberofwaveletsis
determinedbytherefractoryperiod,conductionvelocity,andmassofatrialtissue.Increasedatrial
mass,shortenedatrialrefractoryperiod,anddelayedintraatrialconductionincreasethenumberof6/17
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mass,shortenedatrialrefractoryperiod,anddelayedintraatrialconductionincreasethenumberof
waveletsandpromotesustainedAF.Thismodelissupportedbydatafrompatientswith
paroxysmalAFdemonstratingthatwidespreaddistributionofabnormalatrialelectrogramspredicts
progressiontopersistentAF.[11]Intraatrialconductionprolongationhasalsobeenshownto
predictrecurrenceofAF.[12]Together,thesedatahighlighttheimportanceofatrialstructuraland
electricalremodelinginthemaintenanceofAF[10]hencethephrase"atrialfibrillationbegets
atrialfibrillation."

Etiology
Atrialfibrillation(AF)isstronglyassociatedwiththefollowingriskfactors:

Hemodynamicstress
Atrialischemia
Inflammation
Noncardiovascularrespiratorycauses
Alcoholanddruguse
Endocrinedisorders
Neurologicdisorders
Geneticfactors
Advancingage

Hemodynamicstress
Increasedintraatrialpressureresultsinatrialelectricalandstructuralremodelingandpredisposes
toAF.Themostcommoncausesofincreasedatrialpressurearemitralortricuspidvalvedisease
andleftventriculardysfunction.Systemicorpulmonaryhypertensionalsocommonlypredisposes
toatrialpressureoverload,andintracardiactumorsorthrombiarerarecauses.

Atrialischemia

CoronaryarterydiseaseinfrequentlyleadsdirectlytoatrialischemiaandAF.Morecommonly,
severeventricularischemialeadstoincreasedintraatrialpressureandAF.

Inflammation
Myocarditisandpericarditismaybeidiopathicormayoccurinassociationwithcollagenvascular
diseasesviralorbacterialinfectionsorcardiac,esophageal,orthoracicsurgery.

Noncardiovascularrespiratorycauses

Pulmonaryembolism,pneumonia,lungcancer,andhypothermiahavebeenassociatedwithAF.

Drugandalcoholuse

Stimulants,alcohol,andcocainecantriggerAF.Acuteorchronicalcoholuse(ie,holidayor
Saturdaynightheart,alsoknownasalcoholrelatedcardiomyopathy)andillicitdruguse(ie,
stimulants,methamphetamines,cocaine)havebeenspecificallyfoundtoberelatedtoAF.

Endocrinedisorders

Hyperthyroidism,diabetes,andpheochromocytomahavebeenassociatedwithAF.

Neurologicdisorders
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IntracranialprocessessuchassubarachnoidhemorrhageorstrokecanprecipitateAF.

FamilialAF
AhistoryofparentalAFappearstoconferincreasedlikelihoodofAF(andoccasionalfamily
pedigreesofAFareassociatedwithdefinedionchannelabnormalities,especiallysodium
channels).[13]OnecohortstudysuggeststhatfamilialAFisassociatedwithanincreasedriskof
AF.ThisincreasewasnotlessenedbyadjustmentforgeneticvariantsandotherAFriskfactors.
[14]

Advancingage

AFisstronglyagedependent,affecting4%ofindividualsolderthan60yearsand8%ofpersons
olderthan80years.

Other
Ina15yearprospectivecohortstudyof132,250Japanesesubjects,Xuetalfoundthatanemia
andchronickidneydisease,aloneandincombination,wereassociatedwithanincreasedriskof
newonsetAF.[15,16]Duringameanfollowupof13.8yearsin1232patientswithnewonsetAF,
multivariateanalysisshowedthatthosewithanestimatedglomerularfiltrationrate(eGFR)lower
than60mL/min/1.73m2were2.56timesmorelikelytoexperiencenewonsetAFcomparedwith
patientswithnormalkidneyfunctionthosewhosehemoglobinlevelswerelowerthan13g/dLhad
a1.5timesincreasedriskofnewonsetAFrelativetopatientswithnormalhemoglobinlevels(P<
0.0001forbothanalyses).[15,16]PatientswithCKDandanemiahadathreefoldhigherincidence
ofAF.[16]

Epidemiology
Atrialfibrillationsthemostfrequentlyencounteredcardiacarrhythmia.[10]Itaffectsmorethan2.2
millionpersonsintheUnitedStates.AFisstronglyagedependent,affecting4%ofindividuals
olderthan60yearsand8%ofpersonsolderthan80years.Approximately25%ofindividualsaged
40yearsandolderwilldevelopAFduringtheirlifetime.[17]

TheprevalenceofAFis0.1%inpersonsyoungerthan55years,3.8%inpersons60yearsor
older,and10%inpersons80yearsorolder.Withtheprojectedincreaseintheelderlypopulation
intheUnitedStates,theprevalenceofAFisexpectedtomorethandoublebytheyear2050.AFis
uncommoninchildhoodexceptaftercardiacsurgery.[18]

TheincidenceofAFissignificantlyhigherinmenthaninwomeninallagegroups.AFappearsto
bemorecommoninwhitesthaninblacks,withblackshavelessthanhalftheageadjustedriskof
developingAF.

In1015%ofcasesofAF,thediseaseoccursintheabsenceofcomorbidities(loneatrial
fibrillation).However,AFisoftenassociatedwithothercardiovasculardiseases,including
hypertensionheartfailurediabetesrelatedheartdiseaseischemicheartdiseaseandvalvular,
dilated,hypertrophic,restrictive,andcongenitalcardiomyopathies.[17]TheAtherosclerosisRiskin
Communities(ARIC)Studysuggestsreducedkidneyfunctionandpresenceofalbuminuriaare
stronglyassociatedwithAF.[19]

TherateofischemicstrokeinpatientswithnonrheumaticAFaverages5%ayear,whichis
somewherebetween2and7timestherateofstrokeinpatientswithoutAF.Theriskofstrokeis
notduesolelytoAFitincreasessubstantiallyinthepresenceofothercardiovasculardiseases.
[20] Theprevalenceofstrokeinpatientsyoungerthan60yearsislessthan0.5%however,in

thoseolderthan70years,theprevalencedoubleswitheachdecade.[21]Theattributableriskof
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thoseolderthan70years,theprevalencedoubleswitheachdecade.[21]Theattributableriskof
strokefromAFisestimatedtobe1.5%forthoseaged5059years,anditapproaches30%for
thoseaged8089years.WomenareatahigherriskofstrokeduetoAFthanmenandsomehave
suggestedthismaybeduetoundertreatmentwithwarfarin.However,onestudyofpatients65
yearsorolderwithrecentlydiagnosedAFfoundwarfarinuseplayednopartintheincreasedriskof
strokeamongfemalepatients.[22]

Prognosis
AFisassociatedwitha1.5to1.9foldhigherriskofdeath,whichisinpartduetothestrong
associationbetweenAFandthromboembolicevents,accordingtodatafromtheFraminghamheart
study.[23]

Medicaltherapiesaimedatrhythmcontrolofferednosurvivaladvantageoverratecontroland
anticoagulation,accordingtotheAtrialFibrillationFollowupInvestigationofRhythmManagement
(AFFIRM)trial.Thestudyaddressedwhetherratecontrolandanticoagulationaresufficientgoals
forasymptomatic,elderlypatients.[24]

Atrialfibrillation(AF)isassociatedwithincreasedmorbidityandmortality,inpartduetotheriskof
thromboembolicdisease,particularlystroke,inAFandinpartduetoitsassociatedriskfactors.
StudieshaveshownthatindividualsinsinusrhythmlivelongerthanindividualswithAF.Disruption
ofnormalatrialelectromechanicalfunctioninAFleadstobloodstasis.This,inturn,canleadto
developmentofthrombus,mostcommonlyintheleftatrialappendage.Dislodgementor
fragmentationofaclotcanthenleadtoembolicphenomena,includingstroke.

DevelopmentofAFpredictsheartfailureandisassociatedwithaworseNewYorkHeart
AssociationHeartFailureclassification.AFmayalsoworsenheartfailureinindividualswhoare
dependentontheatrialcomponentofthecardiacoutput.Thosewithhypertensiveheartdisease
andthosewithvalvularheartdiseaseareparticularlyathighriskfordevelopingheartfailurewhen
AFoccurs.Inaddition,AFmaycausetachycardiamediatedcardiomyopathyifadequaterate
controlisnotestablished.

Inasystematicreview(13studies)andmetaanalysis(10eligiblestudies)ofdeathandadverse
outcomesin54,587patientswithAFandconcomitantheartfailure,investigatorsreporteda
significantlyhigherallcausemortalityinAFpatientswithreducedejectionfractioncomparedto
thosewithpreservedejectionfraction.[25]However,theratesofstrokeandhospitalizationswere
similarbetweenthegroups.

TheriskofstrokefromAFthatlastslongerthan24hoursisamajorconcernandisusually
addressedbyprescribingabloodthinner(Coumadinordabigatran).Prognosticscoresystems,
suchasCHADS2,appeartounderestimatetheriskofembolicstrokeinpatientsolderthan75
yearsthus,somestudiesrecommendtreatingallpatientsolderthan75yearsunlessacompelling
contraindicationisnoted.[26]TheCHADS2scorepredictsischemicstrokenotonlyforpatientswith
ahistoryofatrialfibrillationbutalsoforpatientswithoutatrialfibrillationwhohaveahistoryof
coronaryheartdisease.[27]Inthelattergroup,netbenefitofprophylacticanticoagulationhasyetto
beestablished.

AnanalysisoftheAFNET(CentralRegistryoftheGermanCompetenceNETworkonAtrial
Fibrillation)registryof8847patientswithnonvalvularatrialfibrillationindicatedthattheCHA2DS2
VAScscoreismoresensitivethantheCHADS2scoreforriskstratificationofthromboembolic
events(ischemicstroke,transientischemicattack[TIA],systemicembolism),particularlyin
patientsatloworintermediateriskforstroke(CHADS2scoreof0or1)whothereforedonot
requireoralanticoagulation.[28,29]

Duringameanfollowupof5years,theinvestigatorsfound36.5%(144of395)ofstrokesorother
thromboemboliceventsoccurredinpatientsgivenaCHADS2scoreof0or1,groupsinwhichthere
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thromboemboliceventsoccurredinpatientsgivenaCHADS2scoreof0or1,groupsinwhichthere
isnodefinitiverecommendationfororalanticoagulation.[28,29]However,CHA2DS2VAScscoring
whichaddsage6574years,vasculardisease,andfemalesexasstrokeriskfactorstothe
CHADS2score[29]placed30.3%ofthoseclassifiedasCHADS20or1intoCHA2DS2VASc1
or2andhigher,groupsinwhichoralanticoagulationisrecommended.[28]

AposthocanalysisoftheONTARGETandTRENDstudies,whichevaluatedtheefficacyof
treatmentwithramiprilplustelmisartanortelmisartanaloneinreducingcardiovasculardisease,
usedtheMiniMentalStateExamination(MMSE)tomeasurethecognitivefunctionofparticipants
atbaselineandaftertwoandfiveyears.ResultsshowthatAFisassociatedwithanincreasedrisk
ofcognitivedecline,newdementia,lossofindependenceinperformingactivitiesofdailylivingand
admissiontolongtermcarefacilities.[30]

Atrialfibrillationinassociationwithacutemyocardialinfarction

AFisacommonfindinginpatientspresentingwithanacutemyocardialinfarction.Ametaanalysis
pooleddatafrom43studiesandmorethan278,800patients.[31]ThestudyfoundthatAFinthe
settingofacutemyocardialinfarctionwasassociatedwith40%increaseinmortalitycomparedto
patientsinsinusrhythmwithacutemyocardialinfarction.Thecausesofdeathwereunclear,but
mayberelatedtotripleanticoagulationtherapywithaspirin,clopidogrel,andwarfarin,ormaybe
relatedtohemodynamicconsequencesassociatedwiththelossofatrialcontraction.WhetherAF
isacomplicationofmyocardialinfarctionoramarkerformyocardialinfarctionseverityisunclear.

PatientEducation
AstudybyvanDiepenetalsuggeststhatpatientswithheartfailureoratrialfibrillationhavea
significantlyhigherriskofnoncardiacpostoperativemortalitythanpatientswithcoronaryartery
diseasethus,patientsandphysiciansshouldconsiderthisrisk,evenifaminorprocedureis
planned.[32]

Forpatienteducationresources,seeHeartCenterandStrokeCenter.Also,seepatienteducation
articlesAtrialFibrillation,HeartRhythmDisorders,Stroke,andSupraventricularTachycardia.

ClinicalPresentation

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