ESC. Guidelines for the management of atrial fibrillation

62 Pages·3.432 MB·English

ESC GUIDELINES
EuropeanHeartJournal(2010)31,2369–2429
doi:10.1093/eurheartj/ehq278
Guidelines for the management of atrial
fibrillation
The Task Force for the Management of Atrial Fibrillation of the
European Society of Cardiology (ESC)
Developed with the special contribution of the European Heart Rhythm Association
(EHRA)†
Endorsed by the European Association for Cardio-Thoracic Surgery (EACTS)
Authors/Task Force Members: A. JohnCamm (Chairperson) (UK)*, PaulusKirchhof
(Germany), Gregory Y.H. Lip (UK), Ulrich Schotten (The Netherlands),
IreneSavelieva (UK), Sabine Ernst (UK), Isabelle C.Van Gelder (The Netherlands),
Nawwar Al-Attar (France), Gerhard Hindricks (Germany), Bernard Prendergast
(UK), Hein Heidbuchel (Belgium), Ottavio Alfieri (Italy), Annalisa Angelini (Italy),
Dan Atar (Norway), Paolo Colonna (Italy), Raffaele De Caterina (Italy),
Johan De Sutter (Belgium), Andreas Goette (Germany), Bulent Gorenek (Turkey),
Magnus Heldal (Norway), Stefan H. Hohloser (Germany), Philippe Kolh (Belgium),
Jean-Yves Le Heuzey (France), Piotr Ponikowski (Poland), Frans H. Rutten
(The Netherlands).
ESC Committee for Practice Guidelines (CPG): AlecVahanian (Chairperson) (France), AngeloAuricchio
(Switzerland),JeroenBax (TheNetherlands),ClaudioCeconi (Italy),VeronicaDean (France),GerasimosFilippatos
(Greece), ChristianFunck-Brentano (France), RichardHobbs (UK), PeterKearney (Ireland), TheresaMcDonagh
(UK), Bogdan A.Popescu (Romania), ZeljkoReiner (Croatia), UdoSechtem (Germany), Per AntonSirnes
(Norway), MichalTendera (Poland), Panos E.Vardas (Greece), PetrWidimsky (Czech Republic).
DocumentReviewers:PanosE.Vardas (CPGReviewCoordinator)(Greece),VazhaAgladze (Georgia),EtienneAliot
(France),ToshoBalabanski(Bulgaria),CarinaBlomstrom-Lundqvist(Sweden),AlessandroCapucci(Italy),HarryCrijns
(TheNetherlands),Bjo¨rnDahlo¨f (Sweden),ThierryFolliguet (France),MichaelGlikson (Israel),MarnixGoethals
(Belgium),DietrichC.Gulba (Germany),SiewYenHo (UK),RobertJ.M.Klautz (TheNetherlands),SedatKose
(Turkey),JohnMcMurray (UK),PasqualePerroneFilardi (Italy),PekkaRaatikainen (Finland),MariaJesusSalvador
(Spain),MartinJ.Schalij (TheNetherlands),AlexanderShpektor (RussianFederation),Joa˜oSousa (Portugal),
JaninaStepinska (Poland),HassoUuetoa (Estonia),JoseLuisZamorano (Spain),IgorZupan (Slovenia).
ThedisclosureformsoftheauthorsandreviewersareavailableontheESCwebsitewww.escardio.org/guidelines
*Correspondingauthor.A.JohnCamm,StGeorge’sUniversityofLondon,CranmerTerrace,LondonSW17ORE,UK.Tel:[phone],Fax:[phone],Email:
[email protected]
ThecontentoftheseEuropeanSocietyofCardiology(ESC)Guidelineshasbeenpublishedforpersonalandeducationaluseonly.Nocommercialuseisauthorized.Nopartofthe
ESCGuidelinesmaybetranslatedorreproducedinanyformwithoutwrittenpermissionfromtheESC.PermissioncanbeobtaineduponsubmissionofawrittenrequesttoOxford
UniversityPress,thepublisheroftheEuropeanHeartJournalandthepartyauthorizedtohandlesuchpermissionsonbehalfoftheESC.
†OtherESCentitieshavingparticipatedinthedevelopmentofthisdocument:
Associations:EuropeanAssociationofEchocardiography(EAE),EuropeanAssociationforCardiovascularPrevention&Rehabilitation(EACPR),HeartFailureAssociation(HFA).
WorkingGroups:CardiovascularSurgery,DevelopmentalAnatomyandPathology,CardiovascularPharmacologyandDrugTherapy,Thrombosis,AcuteCardiacCare,Valvular
HeartDisease.
Councils:CardiovascularImaging,CardiologyPractice,CardiovascularPrimaryCare.
Disclaimer.TheESCGuidelinesrepresenttheviewsoftheESCandwerearrivedataftercarefulconsiderationoftheavailableevidenceatthetimetheywerewritten.Health
professionalsareencouragedtotakethemfullyintoaccountwhenexercisingtheirclinicaljudgement.Theguidelinesdonot,however,overridetheindividualresponsibilityofhealth
professionalstomakeappropriatedecisionsinthecircumstancesoftheindividualpatients,inconsultationwiththatpatient,andwhereappropriateandnecessarythepatient’s
guardianorcarer.Itisalsothehealthprofessional’sresponsibilitytoverifytherulesandregulationsapplicabletodrugsanddevicesatthetimeofprescription.
&TheEuropeanSocietyofCardiology2010.Allrightsreserved.ForPermissionspleaseemail:[email protected]
2370 ESCGuidelines
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Keywords Atrial fibrillation † European SocietyofCardiology † Guidelines † Anticoagulation † Ratecontrol
† Rhythmcontrol † Upstreamtherapy † Pulmonary veinisolation † Left atrial ablation
Table of Contents
Abbreviationsandacronyms . . . . . . . . . . . . . . . . . . . . . . . 2370 4.1.7Cardioversion . . . . . . . . . . . . . . . . . . . . . . . . . 2391
1.Preamble. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 2372 4.1.7.1Transoesophagealechocardiogram-guided
2.Introduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 2373 cardioversion . . . . . . . . . . . . . . . . . . . . . . . . 2392
2.1Epidemiology . . . . . . . . . . . . . . . . . . . . . . . . . . . . 2373 4.1.8Non-pharmacologicalmethodstopreventstroke. . 2392
2.1.1Atrialfibrillation-relatedcardiovascularevents 4.2Rateandrhythmmanagement . . . . . . . . . . . . . . . . . 2392
(‘outcomes’) . . . . . . . . . . . . . . . . . . . . . . . . . . 2373 4.2.1Acuterateandrhythmmanagement . . . . . . . . . . 2392
2.1.2Cardiovascularandotherconditionsassociatedwith 4.2.1.1Acuteratecontrol. . . . . . . . . . . . . . . . . . . . . 2392
atrialfibrillation. . . . . . . . . . . . . . . . . . . . . . . . 2374 4.2.1.2Pharmacologicalcardioversion . . . . . . . . . . . . . 2392
2.2Mechanismsofatrialfibrillation . . . . . . . . . . . . . . . . 2375 4.2.1.3‘Pill-in-the-pocket’approach. . . . . . . . . . . . . . . 2394
2.2.1Atrialfactors. . . . . . . . . . . . . . . . . . . . . . . . . . 2375 4.2.1.4Directcurrentcardioversion . . . . . . . . . . . . . . 2395
2.2.2Electrophysiologicalmechanisms. . . . . . . . . . . . . 2375 4.3Long-termmanagement . . . . . . . . . . . . . . . . . . . . . 2396
2.2.3Geneticpredisposition . . . . . . . . . . . . . . . . . . . 2375 4.3.1Rateandrhythmcontrol. . . . . . . . . . . . . . . . . . 2397
2.2.4Clinicalcorrelates . . . . . . . . . . . . . . . . . . . . . . 2376 4.3.2Long-termratecontrol. . . . . . . . . . . . . . . . . . . 2400
3.Detection,‘natural’history,andacutemanagement. . . . . . . 2376 4.3.3Pharmacologicalratecontrol . . . . . . . . . . . . . . . 2400
3.1Definition. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 2376 4.3.4Atrioventricularnodeablationandmodification. . . 2402
3.2Detection. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 2376 4.3.5Long-termrhythmcontrol. . . . . . . . . . . . . . . . . 2403
3.3‘Natural’timecourse . . . . . . . . . . . . . . . . . . . . . . . 2377 4.3.5.1Antiarrhythmicdrugstomaintainsinusrhythm . . 2403
3.4Electrocardiogramtechniquestodiagnoseandmonitor 4.3.5.2Leftatrialcatheterablation . . . . . . . . . . . . . . . 2406
atrialfibrillation. . . . . . . . . . . . . . . . . . . . . . . . . . . 2377 4.3.5.3Surgicalablation . . . . . . . . . . . . . . . . . . . . . . 2412
3.5Typesofatrialfibrillation . . . . . . . . . . . . . . . . . . . . 2378 4.4Upstreamtherapy . . . . . . . . . . . . . . . . . . . . . . . . . 2412
3.6Initialmanagement. . . . . . . . . . . . . . . . . . . . . . . . . 2378 4.4.1Angiotensin-convertingenzymeinhibitorsand
3.7Clinicalfollow-up. . . . . . . . . . . . . . . . . . . . . . . . . . 2379 angiotensinreceptorblockers . . . . . . . . . . . . . . 2413
4.Management . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 2379 4.4.2Aldosteroneantagonists . . . . . . . . . . . . . . . . . . 2414
4.1Antithromboticmanagement . . . . . . . . . . . . . . . . . . 2379 4.4.3Statins . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 2414
4.1.1Riskstratificationforstrokeandthrombo-embolism 2381 4.4.4Polyunsaturatedfattyacids. . . . . . . . . . . . . . . . . 2415
4.1.2Antithrombotictherapy . . . . . . . . . . . . . . . . . . 2383 5.Specificpopulations . . . . . . . . . . . . . . . . . . . . . . . . . . . 2416
4.1.2.1AnticoagulationtherapywithvitaminKantagonist 5.1Heartfailure. . . . . . . . . . . . . . . . . . . . . . . . . . . . . 2416
vs.control . . . . . . . . . . . . . . . . . . . . . . . . . . 2383 5.2Athletes. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 2416
4.1.2.2Antiplatelettherapyvs.control . . . . . . . . . . . . 2383 5.3Valvularheartdisease. . . . . . . . . . . . . . . . . . . . . . . 2417
4.1.2.3AnticoagulationtherapywithvitaminKantagonist 5.4Acutecoronarysyndromes . . . . . . . . . . . . . . . . . . . 2417
vs.antiplatelettherapy . . . . . . . . . . . . . . . . . . 2383 5.5Diabetesmellitus. . . . . . . . . . . . . . . . . . . . . . . . . . 2418
4.1.2.4Otherantithromboticdrugregimens. . . . . . . . . 2383 5.6Theelderly. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 2418
4.1.2.5Investigationalagents . . . . . . . . . . . . . . . . . . . 2384 5.7Pregnancy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 2419
4.1.3Currentrecommendationsforantithrombotic 5.8Post-operativeatrialfibrillation. . . . . . . . . . . . . . . . . 2420
therapy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 2384 5.9Hyperthyroidism . . . . . . . . . . . . . . . . . . . . . . . . . . 2421
4.1.4Riskofbleeding. . . . . . . . . . . . . . . . . . . . . . . . 2385 5.10Wolff–Parkinson–Whitesyndrome. . . . . . . . . . . . . 2421
4.1.5Optimalinternationalnormalizedratio. . . . . . . . . 2386 5.11Hypertrophiccardiomyopathy . . . . . . . . . . . . . . . . 2422
4.1.6Specialsituations . . . . . . . . . . . . . . . . . . . . . . . 2386 5.12Pulmonarydisease . . . . . . . . . . . . . . . . . . . . . . . . 2423
4.1.6.1Paroxysmalatrialfibrillation. . . . . . . . . . . . . . . 2386 References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 2424
4.1.6.2Perioperativeanticoagulation . . . . . . . . . . . . . . 2386
4.1.6.3Stablevasculardisease . . . . . . . . . . . . . . . . . . 2386 Abbreviations and acronyms
4.1.6.4Acutecoronarysyndromeand/orpercutaneous
coronaryintervention. . . . . . . . . . . . . . . . . . . 2386 ACEI angiotensin-convertingenzymeinhibitor
4.1.6.5Electivepercutaneouscoronaryintervention. . . . 2387 ACS acute coronarysyndrome
4.1.6.6Non-STelevationmyocardialinfarction . . . . . . . 2387 ACTIVE Atrial fibrillation Clopidogrel Trial with Irbesar-
4.1.6.7AcuteSTsegmentelevationmyocardialinfarction tanforpreventionofVascular Events
withprimarypercutaneousintervention. . . . . . . 2388 ADONIS American–Australian–African trial with Drone-
4.1.6.8Acutestroke . . . . . . . . . . . . . . . . . . . . . . . . 2388 darONe In atrial fibrillation or flutter for the
4.1.6.9Atrialflutter . . . . . . . . . . . . . . . . . . . . . . . . . 2391 maintenanceofSinusrhythm
ESCGuidelines 2371
AF-CHF Atrial Fibrillation andCongestiveHeartFailure EAPCI European Association of Percutaneous Cardio-
AFFIRM Atrial Fibrillation Follow-up Investigation of vascularInterventions
Rhythm Management EHRA European HeartRhythmAssociation
ANDROMEDA ANtiarrhythmic trial with DROnedarone in ECG electrocardiogram
Moderate-to-severe congestive heart failure EMA European MedicinesAgency
Evaluating morbidity DecreAse EURIDIS EURopean trial In atrial fibrillation or flutter
AP accessorypathway patientsreceivingDronedaroneforthemaInten-
APAF Ablation forParoxysmal Atrial Fibrillationstudy anceofSinus rhythm
ARB angiotensin receptorblocker GISSI-AF Gruppo Italiano per lo Studio della Sopravvi-
ARMYDA Atorvastatin for Reduction of MYocardial Dys- venzanell’InsufficienzacardiacaAtrialFibrillation
rhythmia Aftercardiacsurgery GPI glycoproteininhibitor
ATHENA A placebo-controlled, double-blind, parallel arm GRACE Global RegistryofAcute Coronary Events
Trial to assess the efficacy of dronedarone HAS-BLED hypertension, abnormal renal/liver function (1
400mgb.i.d.forthepreventionofcardiovascular pointeach),stroke,bleedinghistoryorpredispo-
Hospitalisation or death from any cause in sition, labile INR, elderly (.65), drugs/alcohol
patiENts with Atrial fibrillation/atrial flutter concomitantly (1pointeach)
ATRIA AnTicoagulation and Risk factors In Atrial HOPE HeartOutcomes PreventionEvaluation
fibrillation HOTCAFE How to TreatChronic AtrialFibrillation
AVRO A Phase III prospective, randomized, double- HR hazardratio
blind, Active-controlled,multicentre,superiority HT hypertension
study of Vernakalant injection vs. amiodarone INR international normalizedratio
insubjects with Recent Onset atrial fibrillation i.v. intravenous
AVERROES Apixaban VERsus acetylsalicylic acid to pRevent J-RHYTHM Japanese Rhythm Management Trial for Atrial
strOkES Fibrillation
BAFTA Birmingham Atrial Fibrillation Treatment of the LA leftatrial
Aged LAA leftatrialappendage
b.i.d. bis indie (twicedaily) LIFE LosartanInterventionForEndpointreductionin
bpm beats perminute hypertension
CABG coronaryarterybypassgraft LMWH low molecularweightheparin
CACAF CatheterAblationfortheCureofAtrialFibrilla- LoE level ofevidence
tionstudy LV leftventricular
CFAE complex fractionatedatrial electrogram LVEF leftventricularejectionfraction
CHA DS -VASc cardiacfailure,hypertension,age≥75(doubled), o.d. omnidie (every day)
2 2
diabetes, stroke (doubled)-vascular disease, age OAC oral anticoagulant
65–74andsexcategory (female) OR odds ratio
CHADS cardiac failure, hypertension, age, diabetes, MRI magneticresonanceimaging
2
stroke(doubled) NYHA New YorkHeartAssociation
CHARISMA ClopidogrelforHighAthero-thromboticRiskand PAD peripheral arterydisease
IschemicStabilisation,Management,andAvoidance PCI percutaneousintervention
CHARM Candesartan in Heart failure: Assessment of PIAF PharmacologicalInterventioninAtrialFibrillation
Reductionin Mortalityandmorbidity PPI protonpump inhibitor
CI confidenceinterval PROTECT-AF System for Embolic PROTECTion in patients
COPD chronic obstructivepulmonarydisease withAtrial Fibrillation
CPG clinicalpractice guidelines PUFA polyunsaturatedfattyacid
CRT cardiacresynchronizationtherapy PV pulmonaryvein
CT computed tomography PVI pulmonaryveinisolation
CV cardioversion RACE RAteControlversusElectricalcardioversionfor
DAFNE DronedaroneAtrialFibrillatioNstudyafterElec- persistentatrialfibrillation
trical cardioversion RACE II RAte Control Efficacy in permanent atrial
DCC direct currentcardioversion fibrillation
DIONYSOS Randomized Double blind trIal to evaluate effi- RAAFT RadiofrequencyAblation AtrialFibrillation Trial
cacy and safety of drOnedarone [400mg b.i.d.] RE-LY RandomizedEvaluationofLong-termanticoagu-
versus amiodaroNe [600mg q.d. for 28 daYS, lant therapY withdabigatranetexilate
then 200mg qd thereafter] for at least 6 RIKS-HIA Register of Information and Knowledge about
mOnths for the maintenance of Sinus rhythm SwedishHeartIntensivecareAdmissions
inpatientswithatrial fibrillation RR relative risk
2372 ESCGuidelines
SAFE-T Sotalol, Amiodarone, atrial Fibrillation Efficacy
Table1 Classesofrecommendations
Trial
SAFE Screening forAF intheElderly
Classes of Definition
SCD suddencardiacdeath
recommendations
SPAF StrokePrevention inAtrial Fibrillation
STAF Strategies ofTreatment ofAtrial Fibrillation Class I Evidence and/or general agreement
STEMI STsegmentelevation myocardial infarction that a given treatment or procedure is
beneficial, useful, effective.
STOP-AF Sustained Treatment Of Paroxysmal Atrial
Fibrillation Class II Conflicting evidence and/or a
TIA transientischaemic attack divergence of opinion about the
usefulness/efficacy of the given
t.i.d. ter indie (three times daily)
treatment or procedure.
TIMI ThrombolysisIn Myocardial Infarction
TOE transoesophagealechocardiogram Class IIa Weight of evidence/opinion is in favour
of usefulness/efficacy.
TRANSCEND Telmisartan Randomized AssessmeNt Study in
aCE iNtolerant subjects with cardiovascular Class IIb Usefulness/efficacy is less well
Disease established by evidence/opinion.
UFH unfractionatedheparin
Class III Evidence or general agreement that
VALUE Valsartan Antihypertensive Long-term Use the given treatment or procedure is
Evaluation not useful/effective, and in some cases
may be harmful.
VKA vitamin Kantagonist
WASPO WarfarinversusAspirinforStrokePreventionin
Octogenarianswith AF
1. Preamble Table2 Levelsofevidence
Guidelinessummarizeandevaluateallcurrentlyavailableevidence
onaparticularissuewiththeaimofassistingphysiciansinselecting Level of Data derived from multiple randomized
evidence A clinical trials or meta-analyses.
the best management strategy for an individual patient suffering
from a given condition, taking into account the impact on
outcome, as well astherisk–benefit ratio of particular diagnostic Level of Data derived from a single randomized
evidence B clinical trial or large non-randomized studies.
ortherapeuticmeans.Guidelinesarenosubstitutesfortextbooks.
The legal implications of medical guidelines have been discussed
Level of Consensus of opinion of the experts and/or
previously.
evidence C small studies, retrospective studies, registries.
A largenumberofGuidelineshavebeenissuedin recentyears
by the European Society of Cardiology (ESC) as wellas byother
societiesandorganizations.Becauseoftheimpactonclinicalprac-
tice,qualitycriteriafordevelopmentofguidelineshavebeenestab-
lishedinordertomakeall decisionstransparenttotheuser.The ESC and was developed without any involvement of the pharma-
recommendations for formulating and issuing ESC Guidelines can ceutical, device, orsurgical industry.
be found on the ESC Web Site (http://www.escardio.org/ The ESC Committee for Practice Guidelines (CPG) supervises
knowledge/guidelines/rules). and coordinates the preparation of new Guidelines produced by
Inbrief,expertsinthefield are selectedandundertake acom- TaskForces,expertgroups,orconsensuspanels.TheCommittee
prehensivereviewofthepublishedevidenceformanagementand/ is also responsible for the endorsement process of these Guide-
orpreventionofagivencondition.Acriticalevaluationofdiagnos- lines or statements. Once the document has been finalized and
ticandtherapeuticproceduresisperformed,includingassessment approved by all the experts involved in the Task Force, it is sub-
of the risk–benefit ratio. Estimates of expected health outcomes mitted tooutside specialists forreview. Thedocumentisrevised,
forlargersocietiesareincluded,wheredataexist.Thelevelofevi- finallyapprovedby theCPG,andsubsequentlypublished.
denceandthestrengthofrecommendationofparticulartreatment Afterpublication,disseminationofthemessageisofparamount
optionsareweighedandgradedaccordingtopre-definedscales,as importance. Pocket-sized versions and personal digital assistant-
outlinedin Tables 1and2. downloadable versions are useful at the point of care. Some
The experts of the writing panels have provided disclosure surveys have shown that the intended users are sometimes
statements of all relationships they may have that might be per- unawareoftheexistenceofguidelines,orsimplydonottranslate
ceived as real or potential sources of conflicts of interest. These them into practice. Thus, implementation programmes for new
disclosure forms are kept on file at the European Heart House, guidelinesformanimportantcomponentofknowledgedissemina-
headquarters of the ESC. Any changes in conflict of interest that tion.MeetingsareorganizedbytheESC,anddirectedtowardsits
arise during the writing period must be notified to the ESC. The member National Societies and key opinion leaders in Europe.
Task Force report received its entire financial support from the Implementation meetings can also be undertaken at national
ESCGuidelines 2373
levels, once the guidelines have been endorsed by the ESC TheproblemofearlyrecognitionofAFisgreatlyaggravatedby
member societies, and translated into the national language. the often ‘silent’ nature of the rhythm disturbance. In about
Implementation programmes are needed because it has been one-third of patients with this arrhythmia, the patient is not
shown thatthe outcome of disease may be favourablyinfluenced aware of so-called ‘asymptomatic AF’. Much earlier detection of
bythethoroughapplication ofclinicalrecommendations. the arrhythmia might allow the timely introduction of therapies
Thus, the task of writing Guidelines covers not only the inte- to protect the patient, not only from the consequences of the
grationofthemostrecentresearch,butalsothecreationofedu- arrhythmia, but also from progression of AF from an
cational tools and implementation programmes for the easily treated condition to an utterly refractory problem.
recommendations. The loop between clinical research, writing of Monitoring and screening as advocated in this guideline may help
guidelines, and implementing them into clinical practice can then to dothis.
only be completed if surveys and registries are performed to Non-pharmacological interventions to control the occurrence
verify that real-life daily practice is in keeping with what is rec- ofAFortolimititsexpressionhavebeeneagerlyandsubstantially
ommended in the guidelines. Such surveys and registries also developed in the past decade. Ablation techniques, usually done
make it possible to evaluate the impact of implementation of the percutaneously using a catheter, have proved successful in the
guidelinesonpatientoutcomes.Guidelinesandrecommendations treatment of AF, particularly by reducing the symptomatic
shouldhelpthephysicianstomakedecisionsintheirdailypractice; burden associated with the arrhythmia, to such an extent that a
however,theultimatejudgementregardingthecareofanindivid- ‘cure’maybeachievedinsomepatients.Thenewguidelinesrecog-
ualpatientmustbemadebythephysicianinchargeoftheircare. nizetheseadvances.Whenappliedinconcertwithmajornewdrug
developments such as novel antithrombotic agents and emerging
2. Introduction safer antiarrhythmic drugs, these therapeutic options should help
to improve outcomesin AFpatients.
Atrial fibrillation (AF) is the most common sustained cardiac The expanding and diversifying possibilities and restraints of
arrhythmia, occurring in 1–2% of the general population. Over 6 medicalcarewithinEuropemakeitdifficulttoformulateguidelines
million Europeans suffer from this arrhythmia, and its prevalence thatarevalidthroughoutEurope.Therearedifferencesintheavail-
is estimated to at least double in the next 50 years as the popu- ability of therapies, delivery of care, and patient characteristics in
lation ages. It is now 4 yearssince the last AF guidelinewaspub- Europeandinotherpartsoftheworld.Therefore,theseEuropean
lished,anda newversionis now needed. guidelines,thoughbasedlargelyongloballyacquireddata,arelikely
AFconfersa5-foldriskofstroke,andoneinfiveofallstrokesis torequiresomemodificationswhenappliedtomultiplehealthcare
attributedtothisarrhythmia.Ischaemicstrokesinassociationwith settings.
AFareoftenfatal,andthosepatientswhosurviveareleftmoredis-
abled by their stroke and more likely to suffer a recurrence than
2.1 Epidemiology
patients with other causes of stroke. In consequence, the risk of
death from AF-related stroke is doubled and the cost of care is AF affects 1–2% of the population, and this figure is likely to
increased1.5-fold.Therehasbeenmuchresearchintostrokepre- increaseinthenext50years.1–2Inacutestrokepatients,systema-
vention, whichhas influencedthis guideline. tic electrocardiographic (ECG) monitoring would identify AF in 1
In the majority of patients there appears to be an inexorable in 20 subjects, a far greater number than would have been
progression of AF to persistent or permanent forms, associated detected by standard 12-lead ECG recordings. AF may long
with further development of the disease that may underlie the remain undiagnosed (silent AF),3 and many patients with AF will
arrhythmia. Some advance has been made in the understanding never present to hospital.4 Hence, the ‘true’ prevalence of AF is
of the dynamic development of AF from its preclinical state as probably closer to 2%of thepopulation.3
an ‘arrhythmia-in-waiting’ to its final expression as an irreversible TheprevalenceofAFincreaseswithage,from,0.5%at40–50
and end-stage cardiac arrhythmia associated with serious adverse years,to 5–15%at80 years.1–2,5–7 Men are moreoften affected
cardiovascular events. Much recent therapeutic effort with than women. The lifetime risk of developing AF is (cid:3)25% in
‘upstream therapies’ has been expended to slow or halt the pro- thosewho havereached theageof40.8 Theprevalenceandinci-
gression of AF due to underlying cardiovascular disease and to denceofAFinnon-Caucasianpopulationsislesswellstudied.The
AF itself. Limited success has been achieved and is recognized in incidence of AF appears to be increasing (13% in the past two
this guideline. decades).
Clinical frustration has been fuelled by numerous clinical trials
that have demonstrated that the strategic aim of maintaining 2.1.1 Atrial fibrillation-relatedcardiovascularevents
sinus rhythm has no demonstrable value when compared with (‘outcomes’)
the laissez-faire approach of leaving AF unchecked apart from AF is associated with increased rates of death, stroke and other
restriction of the ventricular rate. No advantage from strict rate thrombo-embolic events, heart failure and hospitalizations,
control has been established. These sobering findings are clearly degradedqualityoflife,reducedexercisecapacity,andleftventri-
at odds with the severe complications associated with AF in cular (LV) dysfunction (Table 3).
surveysandepidemiologicalstudies.However,newantiarrhythmic DeathratesaredoubledbyAF,independentlyofotherknown
approachesmayofferaddedvalueandhavestimulatedadditionsto predictors of mortality.3,9 Only antithrombotic therapy has been
theseguidelines. shownto reduceAF-relateddeaths.10
2374 ESCGuidelines
Ageing increases the risk of developing AF, possibly through
Table3 Clinicalevents(outcomes)affectedbyAF
age-dependentlossandisolationofatrialmyocardiumandassoci-
ated conductiondisturbances (seeSection 2.2).
Relative change in AF
Outcome parameter Hypertensionisariskfactorforincident (firstdiagnosed)AF
patients
and for AF-related complications such as stroke and systemic
1. Death Death rate doubled.
thrombo-embolism.
2. Stroke (includes haemorrhagic Stroke risk increased; AF is Symptomatic heart failure [New York Heart Association
stroke and cerebral bleeds) associated with more severe (NYHA) classes II–IV] is found in 30% of AF patients,14,15 and
stroke.
AF is found in up to 30–40% of heart failure patients, depending
Hospitalizations are frequent in
on the underlying cause and severity of heart failure. Heart
3. Hospitalizations AF patients and may contribute to
reduced quality of life. failurecanbebothaconsequenceofAF(e.g.tachycardiomyopathy
ordecompensationinacuteonsetAF)andacauseofthearrhyth-
Wide variation, from no effect to
major reduction. mia due to increased atrial pressure and volume overload,
4. Quality of life and exercise
AF can cause marked distress secondary valvular dysfunction, or chronic neurohumoral
capacity
through palpitations and other stimulation.
AF-related symptoms.
Tachycardiomyopathy should be suspected when LV dys-
Wide variation, from no change to
function is found in patients with a fast ventricular rate but no
5. Left ventricular function tachycardiomyopathy with acute
signs of structural heart disease. It is confirmed by normalization
heart failure.
or improvement of LV function when good AF rate control or
reversionto sinus rhythm isachieved.
AF¼atrialfibrillation.
Valvular heart diseases are found in (cid:3)30% of AF
Outcomesarelistedinhierarchicalordermodifiedfromasuggestionputforward
inarecentconsensusdocument.3Thepreventionoftheseoutcomesisthemain patients.14,15 AF caused by left atrial (LA) distension is an
therapeuticgoalinAFpatients. early manifestation of mitral stenosis and/or regurgitation. AF
occurs in later stages of aortic valve disease. While ‘rheumatic
AF’ was a frequent finding in the past, it is now relatively rare in
Europe.
StrokeinAFisoftensevereandresultsinlong-termdisability
Cardiomyopathies, including primary electrical cardiac dis-
or death. Approximately every fifth stroke is due to AF; further-
eases,16carryanincreasedriskforAF,especiallyinyoungpatients.
more,undiagnosed‘silentAF’isalikelycauseofsome‘cryptogenic’
strokes.3,11 ParoxysmalAFcarriesthesamestroke riskasperma- Relatively rare cardiomyopathies are found in 10% of AF
nent orpersistent AF.12 patients.14,15 A small proportion of patients with ‘lone’ AF carry
knownmutations for‘electrical’ cardiomyopathies.
HospitalizationsduetoAFaccountforone-thirdofalladmis-
Atrial septal defect is associated with AF in 10–15% of
sions for cardiac arrhythmias. Acute coronary syndrome (ACS),
patients in older surveys. This association has important clinical
aggravation of heart failure, thrombo-embolic complications, and
implications for the antithrombotic management of patients with
acutearrhythmiamanagement are the maincauses.
previous stroke or transient ischaemic attack (TIA) and an atrial
Cognitive dysfunction, including vascular dementia, may be
septal defect.
related to AF. Small observational studies suggest that asympto-
OthercongenitalheartdefectsatriskofAFincludepatients
matic embolic events may contribute to cognitive dysfunction in
AF patients inthe absenceof anovertstroke.11 withsingleventricles,afterMustardoperationfortranspositionof
the greatarteries, orafterFontan surgery.
Qualityoflifeandexercisecapacityareimpairedinpatients
Coronaryarterydiseaseispresentin≥20%oftheAFpopu-
withAF.PatientswithAFhaveasignificantlypoorerqualityoflife
lation.14,15Whetheruncomplicatedcoronaryarterydiseaseperse
compared with healthy controls, the general population, or
patientswithcoronary heart disease insinusrhythm.13 (atrial ischaemia) predisposes to AF and how AF interacts with
coronary perfusion17 areuncertain.
Leftventricular(LV)functionisoftenimpairedbytheirre-
Overt thyroid dysfunction can be the sole cause of AF and
gular,fastventricularrateandbylossofatrialcontractilefunction
may predispose to AF-related complications. In recent surveys,
and increased end-diastolic LV filling pressure. Both rate control
hyperthyroidism or hypothyroidism was found to be relatively
and maintenance of sinus rhythm can improve LV function in AF
uncommoninAFpopulations,14,15butsubclinicalthyroiddysfunc-
patients.
tionmay contributeto AF.
Obesity is found in 25% of AF patients,15 and the mean body
2.1.2Cardiovascularandotherconditionsassociatedwith mass indexwas27.5kg/m2ina large, GermanAFregistry (equiv-
atrialfibrillation alent to moderatelyobese).
AF is associated with a variety of cardiovascular conditions.14,15 Diabetesmellitusrequiringmedicaltreatmentisfoundin20%
Concomitant medical conditions have an additive effect on the ofAF patients,andmay contributeto atrial damage.
perpetuation of AF by promoting a substrate that maintains AF Chronicobstructivepulmonarydisease(COPD)isfound
(see Section 2.2). Conditions associated with AF are also in 10–15% of AF patients, and is possibly more a marker for
markers for global cardiovascular risk and/or cardiac damage cardiovascular risk in general than a specific predisposing factor
rather than simplycausative factors. for AF.
ESCGuidelines 2375
Sleepapnoea,especiallyinassociationwithhypertension,dia- normal atrial refractorinessoccurs within afewdays after restor-
betesmellitus,andstructuralheartdisease,maybeapathophysio- ationof sinusrhythm.
logicalfactorforAFbecauseofapnoea-inducedincreasesinatrial Perturbationofatrialcontractilefunctionalsooccurswithindays
pressureandsize, orautonomicchanges. of AF. The main cellular mechanisms of atrial contractiledysfunc-
Chronic renal disease is present in 10–15% of AF patients. tion are down-regulation of the Ca2+ inward current, impaired
Renal failure may increase the risk of AF-related cardiovascular release of Ca2+ from intracellular Ca2+ stores, and alterations of
complications, although controlled data are sparse. myofibrillarenergetics.
In patients with ‘lone’ AF, fibrosis and inflammatory changes
have been documented.20
2.2 Mechanisms of atrial fibrillation
2.2.1Atrial factors 2.2.2 Electrophysiological mechanisms
Pathophysiological changespreceding atrial fibrillation Theinitiationandperpetuationofatachyarrhythmiarequiresboth
Any kind of structural heart disease may trigger a slow but pro- triggers for its onset and a substrate for its maintenance. These
gressive process of structural remodelling in both the ventricles mechanisms are not mutually exclusive and are likely to co-exist
andtheatria.Intheatria,proliferationanddifferentiationoffibro- atvarioustimes.
blasts into myofibroblasts and enhanced connective tissue depo-
sition and fibrosis are the hallmarks of this process. Structural Focalmechanisms
remodelling results in electrical dissociation between muscle Focalmechanismspotentiallycontributingtotheinitiationandper-
bundles and local conduction heterogeneities facilitating the petuationofAFhaveattractedmuchattention.21Cellularmechan-
initiationandperpetuationofAF.Thiselectroanatomicalsubstrate isms of focal activity might involve both triggered activity and
permits multiple small re-entrant circuits that can stabilize the re-entry. Because of shorter refractory periods as well as abrupt
arrhythmia. Structural abnormalities reported in patients with AF changes in myocyte fibre orientation, the pulmonary veins (PVs)
are summarized inTable 4. have a stronger potential to initiate and perpetuate atrial
tachyarrhythmias.
Ablationofsiteswithahighdominantfrequency,mostlylocated
Pathophysiological changesas aconsequence ofatrialfibrillation
at or close to the junction between the PVs and the left atrium,
AftertheonsetofAF,changesofatrialelectrophysiologicalprop-
resultsinprogressiveprolongationoftheAFcyclelengthandcon-
erties, mechanical function, and atrial ultrastructure occur with
version to sinus rhythm in patients with paroxysmal AF, while in
differenttimecoursesandwithdifferentpathophysiologicalconse-
persistent AF, sites with a high dominant frequency are spread
quences.18 Shortening of the atrial effective refractory period
throughout the entire atria, and ablation or conversion to sinus
within the first days of AF has been documented in humans.19
rhythm is more difficult.
The electrical remodelling process contributes to the increasing
stabilityofAFduringthefirstdaysafteritsonset.Themaincellular
Themultiplewavelethypothesis
mechanismsunderlyingtheshorteningoftherefractoryperiodare
down-regulation of the L-type Ca2+ inward current and Accordingtothemultiplewavelethypothesis,AFisperpetuatedby
+ continuousconductionofseveralindependentwaveletspropagat-
up-regulation of inward rectifier K currents. Recovery of
ing throughthe atrial musculature in a seemingly chaotic manner.
Fibrillationwavefrontscontinuouslyundergowavefront–waveback
Table4 StructuralabnormalitiesassociatedwithAF interactions, resulting in wavebreak and the generation of new
wavefronts, while block, collision, and fusion of wavefronts tend
Extracellular matrix alterations to reduce their number. As long as the number of wavefronts
does not decline below a critical level, the multiple wavelets will
Interstitial and replacement fibrosis
sustain the arrhythmia. While in most patients with paroxysmal
Inflammatory changes
AF localized sources of the arrhythmia can be identified, such
Amyloid deposit
attempts are often not successful in patients with persistent or
Myocyte alterations permanent AF.
Apoptosis
Necrosis 2.2.3 Geneticpredisposition
AFhasafamilialcomponent,especiallyAFofearlyonset.22During
Hypertrophy
the past years, numerous inherited cardiac syndromes associated
Dedifferentiation
withAFhavebeenidentified.BothshortandlongQTsyndromes
Gap junction redistribution
and Brugada syndrome are associated with supraventricular
Intracellular substrate accumulation (haemocromatosis, glycogen) arrhythmias, often including AF.23 AF also frequently occurs in a
Microvascular changes varietyofinheritedconditions,includinghypertrophiccardiomyo-
Endocardial remodelling (endomyocardial fibrosis) pathy, a familial form of ventricular pre-excitation, and abnormal
LV hypertrophy associated with mutations in the PRKAG gene.
Other familial forms of AF are associated with mutations in the
AF¼atrialfibrillation.
gene coding for atrial natriuretic peptide,24 loss-of-function
2376 ESCGuidelines
mutationsinthecardiacsodiumchannelgeneSCN5A,25orgainof Thrombo-embolism
function in a cardiac potassium channel.26 Furthermore, several RiskofstrokeandsystemicembolisminpatientswithAFislinked
genetic loci close to the PITX2 and ZFHX3 genes associate with toanumberofunderlyingpathophysiologicalmechanisms.29‘Flow
AF and cardioembolic stroke in population-wide studies.27 The abnormalities’inAFareevidencedbystasiswithintheleftatrium,
pathophysiological role of other genetic defects in the initiation withreducedleftatrialappendage(LAA)flowvelocities,andvisu-
andperpetuationof AFiscurrentlyunknown.23 alizedasspontaneousecho-contrastontransoesophagealechocar-
diography (TOE). ‘Endocardial abnormalities’ include progressive
atrial dilatation, endocardial denudation, and oedematous/fibroe-
2.2.4 Clinical correlates lasticinfiltrationoftheextracellularmatrix.TheLAAisthedomi-
Atrioventricularconduction nant source of embolism (.90%) in non-valvular AF.29
In patients with AF and a normal conduction system [in the
‘Abnormalities of blood constituents’ are well described in AF
absence of accessory pathways (APs) or His–Purkinje dysfunc-
and include haemostatic and platelet activation, as well as inflam-
tion],theatrioventricularnodefunctionsasafrequencyfilterpre- mationandgrowthfactorabnormalities.29
venting excessive ventricular rates. The main mechanisms limiting
atrioventricularconductionareintrinsicrefractorinessoftheatrio-
3. Detection, ‘natural’ history, and
ventricular node and concealed conduction. Electrical impulses
reaching the atrioventricular node may not be conducted to the acute management
ventricles, but may alter atrioventricular node refractoriness,
slowingorblocking subsequentatrial beats. 3.1 Definition
Fluctuations in sympathetic and parasympathetic tone result in
AF is defined as a cardiac arrhythmia with the following
variability of the ventricular rate during the diurnal cycle or
characteristics:
during exercise. The high variability of the ventricular rate is
oftenatherapeuticchallenge.Digitalis,whichslowsdowntheven- (1) ThesurfaceECGshows‘absolutely’irregularRRintervals(AF
tricularratebyanincreaseinparasympathetictone,iseffectivefor is therefore sometimes known as arrhythmia absoluta), i.e. RR
controllingheartrateatrest,buttoalesserextentduringexercise. intervalsthatdonotfollowa repetitivepattern.
b-Blockers and non-dihydropyridine calcium channel antagonists (2) There are no distinct P waves on the surface ECG. Some
reducetheventricular rateduringboth restandexercise. apparently regular atrial electrical activity may be seen in
In patients with pre-excitation syndromes, fast and potentially some ECGleads,mostoften inleadV1.
life-threatening ventricular rates may occur. In patients with AF (3) Theatrialcyclelength(whenvisible),i.e.theintervalbetween
and pre-excitation syndromes, administration of compounds that two atrial activations, is usually variable and ,200ms
slow atrioventricular nodal conduction without prolonging atrial/ (.300bpm).
AP refractory periods (e.g. verapamil, diltiazem, and digitalis) can
accelerate conductionviathe AP. Differential diagnosis
Severalsupraventriculararrhythmias,mostnotablyatrialtachycar-
diasandatrialflutter,butalsorareformsoffrequentatrialectopy
Haemodynamic changes or even dual antegrade atrioventricular nodal conduction, may
Factors affecting haemodynamic function in patients with AF present with rapid irregular RR intervals and mimic AF. Most
involve loss of coordinated atrial contraction, high ventricular atrial tachycardias and flutters show longer atrial cycle lengths
rates,irregularityoftheventricularresponse,anddecreaseinmyo- ≥200ms. Patients on antiarrhythmic drugs may have slower
cardial blood flow, as well as long-term alterations such as atrial atrial cycle lengths duringAF.
andventricularcardiomyopathy. An ECG recording during the arrhythmia is usually needed to
Acute loss of coordinated atrial mechanical function after the differentiate the common diagnosis of AF from other rare supra-
onset of AF reduces cardiac output by 5–15%. This effect is ventricular rhythms with irregular RR intervals, or the common
morepronouncedinpatientswithreducedventricularcompliance occurrenceofventricularextrasystoles.Anyepisodeofsuspected
in whom atrial contraction contributes significantly to ventricular AFshouldberecordedbya12-leadECGofsufficientdurationand
filling. High ventricular rates limit ventricular filling due to the qualitytoevaluateatrialactivity.Occasionally,whentheventricular
shortdiastolicinterval.Rate-relatedinterventricularorintraventri- rate is fast, atrioventricular nodal blockade during the Valsalva
cularconductiondelaymayleadtodyssynchronyoftheleftventri- manoeuvre, carotid massage, or intravenous (i.v.) adenosine
cle andreduce cardiac outputfurther. administration30 canhelp to unmaskatrialactivity.
Inaddition,irregularityoftheventricularratecanreducecardiac
output.Becauseofforce–intervalrelationships,fluctuationsofthe 3.2 Detection
RRintervalscausealargevariabilityinthestrengthsofsubsequent
Anirregularpulseshouldalwaysraisethesuspicion ofAF,butan
heart beats, often resultingin pulsedeficit.
ECG recording is necessary to diagnose AF. Any arrhythmia that
Persistent elevation of ventricular rates above 120–130bpm
has the ECG characteristics of AF and lasts sufficiently long for a
may produce ventricular tachycardiomyopathy.28 Reduction of
12-lead ECG to be recorded, or at least 30 s on a rhythm strip,
the heart rate may restore normal ventricular function and
shouldbeconsideredasAF.3,31TheheartrateinAFcanbecalcu-
preventfurther dilatationanddamageto theatria.
lated from a standard 12-lead ECG by multiplying the number of
ESCGuidelines 2377
RR intervals on the 10 s strip (recorded at 25mm/s) by six. The
risk of AF-related complications is not different between short
AF episodes and sustained forms of the arrhythmia.12 It is there- ‘Upstream’ therapy of concomitant conditions
fore important to detect paroxysmal AF in order to prevent
Anticoagulation
AF-relatedcomplications(e.g.stroke).However,short‘atrialhigh-
Rate control
rateepisodes’,e.g.detectedbypacemakers,defibrillators,orother
icSmoecpmtlaiponlnitcea3dt.i4od)n.esvicuensle,smsatyheniortdbueraatsiosoncieaxtecdeewdsithsetvherroaml bhoo-uermsb(oseliec first documented CAarndtiioarvreAhrybstiloahtmnioicn drugs
AFmaymanifestinitiallyasanischaemicstrokeorTIA,anditis AF
reasonabletoassumethatmostpatientsexperienceasymptomatic, silent paroxysmal persistent long-standing permanent
persistent
oftenself-terminating,arrhythmiaepisodesbeforeAFisfirstdiag-
nosed.TherateofAFrecurrenceis10%inthefirstyearafterthe
initial diagnosis, and (cid:3)5% per annum thereafter. Co-morbidities Figure 1 ‘Natural’ time course of AF. AF¼atrial fibrillation.
and age significantly accelerate both the progression of AF and The dark blue boxes show a typical sequence of periods in AF
thedevelopment ofcomplications.3,23 against a background of sinus rhythm, and illustrate the pro-
gression of AF from silent and undiagnosed to paroxysmal and
3.3 ‘Natural’ time course chronic forms, at times symptomatic. The upper bars indicate
therapeutic measures that could be pursued. Light blue boxes
AFprogressesfromshort,rareepisodes,tolongerandmorefre-
indicate therapies that have proven effects on ‘hard outcomes’
quent attacks. Over time (years), many patients will develop sus-
in AF, such as stroke or acute heart failure. Red boxes indicate
tained forms of AF (Figure 1). Only a small proportion of therapiesthatarecurrentlyusedforsymptomrelief,butmayin
patients without AF-promoting conditions (see Section 2.1.2) will the future contribute to reduction of AF-related complications.
remain in paroxysmal AF over several decades (2–3% of AF Rate control (grey box) is valuable for symptom relief and may
patients).32 The distribution of paroxysmal AF recurrences is not improvecardiovascularoutcomes.
random, but clustered.3 ‘AF burden’ can vary markedly over
months or even years in individual patients.3 Asymptomatic AF is
Holter recordings or external event recorders should be con-
common even in symptomatic patients, irrespective of whether
sidered. In patients with rhythm or rate control treatment and
the initial presentation was persistent or paroxysmal. This has
without further arrhythmia- or therapy-related symptoms, a
important implications for (dis)continuation of therapies aimed at
12-lead ECG should be recorded at regular intervals. In patients
preventingAF-relatedcomplications.
receiving antiarrhythmic drug therapy, the frequency of 12-lead
3.4 Electrocardiogram techniques to ECGrecordingdependsonthetypeofantiarrhythmicdrugtreat-
diagnose and monitor atrial fibrillation ment, the potential side effects, complications, and risks of
proarrhythmia.
Theintensityanddurationofmonitoringshouldbedeterminedby
the clinical need to establish the diagnosis, and should be driven
Toolsfornon-continuous ECGmonitoring
mainly by the clinical impact of AF detection. More intense AF
Available non-continuous ECG methods include scheduled or
recording is usually necessary in clinical trials than in clinical
symptom-activatedstandardECGs,Holter(24hto7days)moni-
practice.3,33
toring and transtelephonic recordings, patient- and automatically
activateddevices, andexternal loop recorders. If AF ispresentat
Patientswithsuspectedbutundiagnosedatrialfibrillation
thetimeofrecording,useofthestandard12-leadECGissufficient
InpatientswithsuspectedAF,a12-leadECGisrecommendedas
to confirm the diagnosis. In paroxysmal AF, prolonged non-
thefirststeptoestablishthediagnosis.Clinicalsymptomssuchas
continuous recording will facilitate AF detection. It has been esti-
palpitations or dyspnoea should trigger ECG monitoring to
mated that 7 day Holter ECG recording or daily and
demonstrate AF, or to correlate symptoms with the underlying
symptom-activated event recordings may document the arrhyth-
rhythm.Thereareonlylimiteddatacomparingthevalueofdiffer-
ent monitoring strategies.3,34–37 More intense and prolonged mia in (cid:3)70% of AF patients, and that their negative predictive
valuefortheabsenceofAFisbetween30and50%.3Instrokesur-
monitoring is justified in highly symptomatic patients [European
vivors,astep-wiseadditionoffivedailyshort-termECGs,one24h
Heart Rhythm Association IV (EHRA IV)—see Section 3.6],
HolterECG,andanother7dayHolterECGwilleachincreasethe
patientswithrecurrentsyncope,andpatientswithapotentialindi-
cationforanticoagulation(especiallyaftercryptogenicstroke).34,38 detection rateofAFbya similarextent.34
In selected patients, implantation of a leadless AF monitoring
devicemaybe considered to establish the diagnosis.39 Toolsforcontinuous ECGmonitoring
Implantable devices capable of intracardiac atrial electrogram
Patientswith known atrial fibrillation recording such as dual-chamber pacemakers and defibrillators
IndicationsforAFmonitoringinpatientswithpreviouslydiagnosed candetectAFappropriately,particularlywhenanarrhythmiadur-
AFdiffercomparedwithundiagnosedpatients.Whenarrhythmia- ation ≥5minisusedasacut-offvalue.Longeratrialhigh-rateepi-
or therapy-related symptoms are suspected, monitoring using sodes (e.g. .5.5h) may be associated with thrombo-embolic
2378 ESCGuidelines
events.35,36 Leadless implantable loop recorders provide continu- strategy be adopted, the arrhythmia is redesignated as ‘long-
ousAFmonitoringovera2yearperiodwithautomaticAFdetec- standingpersistent AF’.
tionbasedonRRintervalanalysis.Preliminaryclinicaldataindicate
ThisclassificationisusefulforclinicalmanagementofAFpatients
good sensitivity but less specificity for AF detection.40 No data
(Figure 2), especially when AF-related symptoms are also con-
exist on the implementation of such devices in the clinical
sidered. Many therapeutic decisions require careful consideration
routineofAFmonitoring.
ofadditionalindividual factors andco-morbidities.
SilentAF(asymptomatic)maymanifestasanAF-relatedcom-
plication (ischaemic stroke or tachycardiomyopathy) or may be
3.5 Types of atrial fibrillation diagnosed by an opportunistic ECG. Silent AF may present as
anyofthetemporalformsofAF.
Clinically, itisreasonabletodistinguishfivetypes of AFbasedon
the presentation and duration of the arrhythmia: first diagnosed,
3.6 Initial management
paroxysmal, persistent, long-standing persistent, and permanent
A thorough medical history should be obtained from the patient
AF (Figure2).
with suspected or known AF (Table 5). The acute management
(1) Every patient who presents with AF for the firsttime is con-
of AF patients should concentrate on relief of symptoms and
sidered a patient with first diagnosed AF, irrespective of
assessment of AF-associated risk. Clinical evaluation should
the duration of the arrhythmia or the presence and severity include determination of the EHRA score (Table 63), estimation
ofAF-relatedsymptoms.
ofstrokerisk(seeSection4.1),andsearchforconditionsthatpre-
(2) Paroxysmal AF is self-terminating, usually within 48h.
dispose to AF (see Section 2.1.2) and for complications of the
Although AF paroxysms may continue for up to 7 days, the
arrhythmia (see Section 2.1.1). The 12-lead ECG should be
48htimepointisclinicallyimportant—afterthisthelikelihood
ofspontaneousconversionislowandanticoagulationmustbe
considered (see Section4.1). Table5 Relevantquestionstobeputtoapatientwith
(3) Persistent AF is present when an AF episode either lasts suspectedorknownAF
longer than7 days or requires termination by cardioversion,
eitherwithdrugsorbydirectcurrentcardioversion(DCC). Does the heart rhythm during the episode feel regular or irregular?
(4) Long-standingpersistentAFhaslastedfor ≥1yearwhen Is there any precipitating factor such as exercise, emotion, or alcohol
itisdecided toadopt arhythm controlstrategy. intake?
(5) Permanent AF is said to exist when the presence of the Are symptoms during the episodes moderate or severe—the severity
arrhythmia is accepted by the patient (and physician). Hence, may be expressed using the EHRA score,3 which is similar to the
CCS-SAF score.41
rhythm control interventions are, by definition, not pursued
in patients with permanent AF. Should a rhythm control Are the episodes frequent or infrequent, and are they long or short
lasting?
Is there a history of concomitant disease such as hypertension,
coronary heart disease, heart failure, peripheral vascular disease,
cerebrovascular disease, stroke, diabetes, or chronic pulmonary disease?
First diagnosed episode of atrial fibrillation
Is there an alcohol abuse habit?
Is there a family history of AF?
Paroxysmal
(usually <48 h)
AF¼atrialfibrillation;CCS-SAF¼CanadianCardiovascularSocietySeverityin
AtrialFibrillation;EHRA¼EuropeanHeartRhythmAssociation.
Persistent
(>7 days or requires CV)
Long-standing
Persistent (>1 year)
Table6 EHRAscoreofAF-relatedsymptoms
Permanent
Classification of AF-related symptoms (EHRA score)
(accepted)
EHRA class Explanation
EHRA I ‘No symptoms’
Figure 2 Different types of AF. AF¼atrial fibrillation; CV¼
EHRA II ‘Mild symptoms’; normal daily activity not affected
cardioversion.Thearrhythmiatendstoprogressfromparoxysmal
EHRA III ‘Severe symptoms’; normal daily activity affected
(self-terminating,usually,48h)topersistent[non-self-terminating
orrequiring cardioversion(CV)],long-standing persistent (lasting ‘Disabling symptoms’; normal daily activity
EHRA IV
longer than 1 year) and eventually to permanent (accepted) AF. discontinued
First-onsetAFmaybethefirstofrecurrentattacksoralreadybe
deemedpermanent. AF¼atrialfibrillation;EHRA¼EuropeanHeartRhythmAssociation.