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CASESTUDYwww.
nature.
com/clinicalpractice/cardioAtrialfibrillation,sleepapneaandobesityMinaKChung*,NancyFoldvary-Schaefer,VirendKSomers,PaulAFriedmanandPaulJWangThisarticleofferstheopportunitytoearnoneCategory1credittowardstheAMAPhysician'sRecognitionAward.
THECASEAnobesemanaged41yearspresentedtohisinternistwithepisodicpalpitations,dyspneaandfatigue.
ParoxysmalAFwasdiagnosedandhewastreatedwithdigoxin,verapamilandquinidine.
Atage51,AFrecurredandpersisted.
Holtermoni-toringshowedratesof18182beats/minandnocturnalpausesofupto4.
5s,consistentwithtachycardia–bradycardiasyndrome.
TwoDCcar-dioversionprocedures,onewithadjunctivequi-nidine,resultedinonlytransientsinusrhythm.
Amiodaronewasstartedandsinusrhythmwasachieved,butrecurrencesofAFandtypeIatrialflutterrequiredfurtherDCcardioversion.
Thepatientwasreferredtoacardiacelectro-physiologistforatrialflutteratage56.
Left-ventricular,right-ventricularandright-atrialsizeandsystolicfunctionwerenormalonechocardio-graphy;left-ventricularejectionfractionwas60%andmildleft-ventricularhypertrophyandmoderateleft-atrialenlargement(5.
2cm)werepresent.
Anuclearstresstestshowednomyocar-dialscarorischemia.
AnotherDCcardioversionandradiofrequencyablationoftheright-atrialisthmussuccessfullytreatedatrialflutter.
Sinusrhythmwasmaintained2monthslater,andamiodaronewasstopped.
Afteranother3months,symptomaticAFrecurredthatwasrefractorytoflecainide,propafenoneanddofetilide.
Becauseofahistoryofnocturnalbradycardia,morbidobesityandsnoring,thepatientwaseval-uatedforOSA.
Hetypicallyslept78hpernight,experiencingthreetofourunexplainedawaken-ingsnightly.
Sleepwasunrefreshinganddaytimesleepinesswasmoderate(EPWORTHSLEEPINESSSCALEscore15).
Atthistime,body-massindexwas43kg/m2.
Duringovernightpolysomnography,thepatientsleptfor196of361minobserved.
Noslow-wavesleepwasrecordedandtherewere50arousals,23APNEASandeightHYPOPNEAS(Table1).
MeanSUMMARYBackgroundA60-year-oldmalewithobesity(body-massindex43kg/m2)presentedwithrecurrentsymptomaticatrialfibrillation(AF),whichhehadhadsinceage41years.
TheAFwasrefractorytotreatmentwithantiarrhythmicdrugs.
Pacemakerimplantationfortachycardia–bradycardiasyndromewasrequiredaswellasablationforatrialflutter,andthepatientunderwentatotaloffourDCcardioversions.
Sleepstudiesshowedmildtomoderateobstructivesleepapnea,butcontinuouspositiveairwaypressurewasnottolerated.
Pacemakerinterrogationsdemonstratedmode-switchepisodes,indicatingcontinuingAF.
Hewasscheduledforcatheterablationtargetingpulmonaryveinantralisolation.
Heembarkedonaweight-lossprogram,whichsuccessfullyreducedAFburden.
InvestigationsEchocardiography,stresstesting,polysomnography,pacemakerinterrogationsandC-reactiveprotein.
DiagnosisAF,atrialflutter,tachycardia–bradycardiasyndrome,obstructivesleepapneaandmorbidobesity.
ManagementAntiarrhythmicdrugtherapy,DCcardioversion,anticoagulation,atrialflutterablation,permanentpacemakerimplantation,continuouspositiveairwaypressureandweightloss.
KEYWORDSarrhythmia,atrialfibrillation,morbidobesity,obstructivesleepapnea,weightlossMKChungisastaffcardiologist,CardiovascularMedicine,andNFoldvary-SchaeferisSectionHead,SleepMedicineSection,ClevelandClinicFoundation.
VKSomersisaProfessorandPAFriedmananAssociateProfessorofMedicine,CardiovascularDiseases,MayoClinic.
PJWangisaProfessor,CardiovascularMedicine,StanfordUniversityMedicalCenter.
Correspondence*DepartmentofCardiovascularMedicine,ClevelandClinicFoundation,9500EuclidAvenue,DeskF-15,Cleveland,OH44195,USAchungm@ccf.
orgReceived19July2004Accepted21September2004www.
nature.
com/clinicalpracticedoi:10.
1038/ncpcardio0027CME56NATURECLINICALPRACTICECARDIOVASCULARMEDICINENOVEMBER2004VOL1NO1CASESTUDYNOVEMBER2004VOL1NO1CHUNGETAL.
NATURECLINICALPRACTICECARDIOVASCULARMEDICINE57www.
nature.
com/clinicalpractice/cardiooxygensaturationwas93%(lowof76%)andwas<90%for3%oftotalsleeptime.
Loudsnoringandsnortingwerereported.
Nonotablearrhythmiaswererecorded.
Continuouspositiveairwaypres-sure(CPAP)7cmH2Owasattemptedfor2nights,butwasdiscontinuedduetodiscomfort.
ContinuingrapidAFandbradycardiawithnocturnalpauseslimiteddrugtherapy,andadual-chamberpacemakerwasimplanted.
AFbecamepersistent9monthslater.
DofetilidewaschangedtosotalolwithDCcardiover-sion,but2dayslaterAFrecurredandpersisted.
Pulmonaryveinisolationwasscheduled.
Thepatientlostweighttolessencomplica-tionsinvascularaccess,imagingandcathetermanipulation.
After1month,AFspontaneouslyconvertedtosinusrhythm.
By3months,hehadlost20.
4kg;sinusrhythmwasmaintainedataweightof125.
6kg.
Thepatientelectedtocancelpulmonaryveinisolation.
Sotalolwasreducedfrom300mgto240mgtwicedaily.
After1year,withfurtherweightlossto121.
6kg(body-massindex37kg/m2),onlytwoepisodesofbriefasymptomaticAFhadbeendetectedovertheprevious8months,andpul-monaryveinisolationwasindefinitelypost-poned.
Table2displaysthepatient'sclinicalcharacteristicsovertime.
DISCUSSIONOFDIAGNOSESAFaffectsover2millionpeopleintheUS,1andprevalenceisincreasing.
Apartfromrapidpal-pitations,symptoms,includingfatigue,dyspneaorweakness,canbesubtle.
Becauseofitsassocia-tionwiththromboemboliccomplications,docu-mentationofthearrhythmiaiscritical,eveninasymptomaticAF.
Electrocardiogramsorambu-latorymonitoringcandetectarrhythmia.
Holterandarrhythmiaeventmonitorsmightalsobeuseful.
Echocardiographyisindicatedtoassessforstructuralheartdisease,whichcanincreasetheriskofstroke.
InloneAFwithnostructuralheartdiseaseandrefractorytomultipleantiarrhythmicdrugs,thefocithatinitiateandpossiblysustainthearrhyth-miaaregenerallylocatedintheleftatriumattheostiaofthepulmonaryveins.
2AFfrequentlybecomesmorepersistentovertime,asinthecasereported.
Continuedtriggeringoffoci,electri-calandstructuralremodelingleadingtochangesinion-channelcurrentsandatrialenlargement,changesinautonomicbalanceormyocardialsenescencewithaccompanyingstructuralandelectrophysiologicalchangescanperpetuateAF.
AtrialflutteriscommoninAFtreatedwithantiarrhythmicdrugs.
Typical,ortypeI,atrialflutterisamacrore-entrantcircuitintherightatriumwithactivationthroughtheisthmusbetweenthetricuspidannulusandinferiorvenacava.
Itischaracterizedby'saw-tooth'flut-terwavesininferiorelectrocardiogramleads.
Giventhelargeexcitablegapassociatedwithtypicalatrialflutter,antiarrhythmicmedica-tionsmaystabilizere-entrantcircuits.
Atypicalatrialflutterrepresentsre-entrantcircuitsthatarenotdependentontherightatrialisthmus.
Thepatienthadclassictachycardia–bradycardiasyndromewithperiodsofrapidrateduringAFandslowratesduringsinusrhythm,sleepordrugtreatment.
OSAaffects10–15millionpeopleintheUS,andisdiagnosedbysleepstudies.
3Morbidobes-ity,historyofsnoringandnocturnalpausespos-siblyrelatedtoapnea,oxygendesaturationorhypervagaltone,ledtoOSAassessmentinthispatient.
AnassociationbetweenAFandOSAhasbeenstudied.
Acase-controlstudyreportednosignificantdifferenceinthefrequencyofsleepapneasyndromebetweenloneAFpatientsandcontrols(32%vs29%),4althoughmoredaytimefatigueandnightlyapneaoccurredintheAFgroup.
Inastudyof151patientsundergoingDCcardioversionforAFcomparedwith312patientswithoutAF,however,OSAwasdiagnosedbyquestionnaireinmoreAFpatientsthanincontrols(49%vs32%).
5OSAmayimpacttheoccurrenceofAFbyseveralmechanisms.
Repetitiveautonomic,hemodynamicandhypoxemicsurgesmightacti-vatestretch-mediatedchannels,catecholamine-GLOSSARYEPWORTHSLEEPINESSSCALEAmeasureofdaytimesleepinessbasedonaquestionnaireinwhichrespondersratethechanceofdozingineightactivitiesAPNEAAtransientabsenceofspontaneousrespirationHYPOPNEABreathingthatisshallower,slowerorboth,thannormalAROUSALINDEXThenumberofarousaleventspersleep-hourTable1Sleepdisturbancesrecordedduringovernightpolysomnography.
ParameterofsleepdisturbanceScoreAROUSALINDEX(arousals/sleep-hour)15Apneas(numberofevents)Central1Mixed4Obstructive18Total23Hypopneas(numberofevents)8Apnea–hypopneaindex(apneaandhypopneaevents/sleep-hour)Overall9.
5Supine18.
6CASESTUDY58NATURECLINICALPRACTICECARDIOVASCULARMEDICINECHUNGETAL.
NOVEMBER2004VOL1NO1www.
nature.
com/clinicalpractice/cardiosensitivechannelsorboth,leadingtogreaterfocaldischarges.
Pulmonaryorsystemichyper-tension,lungphysiologyrestrictedbymorbidobesityorbothcanelevateatrialpressuresandtriggerectopyandAF.
Vagalstimulationofatrialmyocardiumshortensatrialrefractoryperiods.
VagalreflexesduringOSA,markedbybradyarrhythmias,couldalsoreducerefracto-rinessatthepulmonaryveinostia,promotingconductionoffocaldischargesfromthepul-monaryveintoleftatriumandgeneratingawindowforpulmonaryveinfocitotriggerAF.
ElevatedC-reactiveprotein(CRP)hasbeenassociatedwithobesity,metabolicsyndrome,severityofOSAandAF.
6Themajordetermi-nantofCRPelevationinobesepeoplemaybetheobesity,ratherthanOSAormetabolicsyn-drome.
7Inthepresentcase,initiallyhighlevelsofCRPreducedwithweightloss.
WhetherhighconcentrationsassociatedwithobesityindicateapredispositiontostructuralremodelingorAFitselfprovokesinflammationisunknown.
Markersofinflammationreducewithweightlossofaslittleas5%inobesesubjects,8andobesity,OSAorbothcouldpromoteatrialstruc-turalremodelingviamechanicalorinflamma-torystress.
Thelagbetweenbody-massindexreductionandCRPandAFburdenreductionobservedinthispatientsuggeststhatmorethan3monthsmightberequiredbeforeimprove-mentsinmechanical,metabolicorinflamma-torystressorsareseen.
WhetherreliefofOSAitselfwasthecriticalmechanicalfactorinthispatientcannotbedetermined,aswedidnofollow-upsleepstudyafterweightloss.
TREATMENTANDMANAGEMENTAFmanagementisaimedatreducingsymptomsandtheriskofthromboemboliccomplications.
TheAtrialFibrillationFollow-upInvestigationofRhythmManagement(AFFIRM)trial9dem-onstratednosurvivalbenefitswitharhythm-controloverrate-controlstrategy.
Theneedforcontinuedanticoagulationwasconfirmedinpatientswithriskfactorsforstroke,evenwithrhythmcontrolandapparentmaintenanceofsinusrhythm.
Warfarinanticoagulationwasindicatedforborderlinehypertensionanddiabetesmellitusinthepatientwedescribe.
Initialtreatmentcomprisedrate-controllingdigoxinandverapamilandrhythm-controllingquinidine.
First-linetherapyhassincechangedtoβ-blockers;quinidine,whichcarriesariskofproarrhythmia,isusuallyavoided.
WhenTable2Clinicalcharacteristicsrecordedfrom15December2000to4June2004.
DateWeight(kg)BMI(kg/m2)RhythmNumberofmodeswitches(%modeswitched)CRP(mg/l)Antiarrhythmicdrug15Dec2000137.
742.
3SRN/A2.
13Amiodarone11May2001145.
544.
6SR,PAFN/A4.
14None20July2001145.
544.
6AFN/A2.
80Flecainide7Sept2001N/DN/DSR,PAFN/A3.
21Dofetilide5Oct2001141.
443.
4SR,PAFN/A3.
57Dofetilide16Nov2001a138.
242.
4AF17(29.
9)3.
04Dofetilide21May2002138.
242.
4SR,PAF84(15.
8)2.
79Dofetilide8July2002N/DN/DAFN/D3.
20None15July2002N/DN/DAFN/D3.
14Sotalol18Oct2002143.
243.
9AF137(65.
3)2.
34Sotalol24Jan2003144.
144.
2AF15(69.
7)1.
90Sotalol6June2003bc146.
444.
9AFN/D2.
70Sotalol19Sept2003d125.
938.
6SRN/D2.
80Sotalol4June2004e121.
837.
4SR21(16)0.
90Sotalola1monthafterPPMimplant.
bStartofweight-lossprogram.
cPVIscheduled.
d20.
5kgweightloss.
eTwoepisodessinceOctober2003,longest7h.
AF,atrialfibrillation(atvisit);BMI,body-massindex;CRP,ultrasensitiveC-reactiveprotein;N/A,notapplicable;N/D,notdone;PAF,paroxysmalatrialfibrillation;PPM,permanentpacemaker;PVI,pulmonaryveinantralisolation;SR,sinusrhythm.
GLOSSARYAPNEA–HYPOPNEAINDEXThenumberofrespiratoryevents(apneasandhypopneas)persleep-hourCASESTUDYNOVEMBER2004VOL1NO1CHUNGETAL.
NATURECLINICALPRACTICECARDIOVASCULARMEDICINE59www.
nature.
com/clinicalpractice/cardioAFbecamemorepersistent,amiodaronewasstarted.
AlthougheffectiveforAF,amiodaronecanhavetoxiceffects.
Otherfirst-linedrugsforloneAFareflecainideandpropafenone.
Whiletakingamiodarone,thepatientdevelopedatrialflutter.
Ablationoftheposteriorcorridorthatformsthecircuitofatrialfluttermaybeusedinconjunctionwithantiarrhythmicdrugs.
Sinusrhythmwasmaintainedafterablationonamiodar-one,butwhenamiodaronewasstoppedtoavoidlong-termtoxiceffects,AFrecurredasexpected.
Flecainide,propafenoneanddofetilidehadnoeffect.
DCcardioversionsarehelpfulforpersistentAFandcanbeperformedmultipletimes.
Pacemakerimplantationwaschosenforsymp-tomatictachycardia–bradycardiasyndrometofacilitaterate-controllingmedications.
PacemakersmayalsobebeneficialforOSA.
10Mode-switchlogsenableassessmentofAFburden.
Becauseofthepersistenceofthepatient'sAF,catheter-basedpulmonaryveinisolationwasrecommended.
Thismethodissuccessfulin60–85%ofpatients,withhighersuccessratesinloneAF.
Obesitycanraisevascularaccessrisks,suchasinadvertentarterialcannulationorhematomaformation;dosesofanticoagulationhigherthannormalmightberequired.
Inaddi-tion,weightlimitsof135–160kgoftenapplytocatheterizationtables,andfluoroscopyintensitycanberaised.
Weightlossis,therefore,advisableinobesepatientsscheduledforthisprocedure.
MildOSA(APNEA–HYPOPNEAINDEX<20,withoutsignificantsleepcomplaints)canbemanagedconservativelywithweightlossandavoidanceofcentralnervoussystemdepres-sants,sleepdeprivationandsleepingsupine.
Evenmodestweightcontrolhasbeenshowntoimprovesleep-disorderedbreathing.
11CPAPshouldbeofferedasinitialtherapyinmoder-atetoseverediseaseormilddiseasewithseveredaytimesleepiness.
Variousinterfacesshouldbetriedfortolerabilityandcomfort.
SurgeryshouldbeconsideredifCPAPisnottoleratedorfails.
WhenOSAandAFcoexist,treatmentforOSAmightassistmanagementofAF.
Althoughareductioninapneicepisodes,bradyarrhyth-miasorbothhasbeenseenwithatrialpacingorCPAP,supraventriculararrhythmias10,12arenotreduced.
Nevertheless,asignificantlyraisedriskofrecurrentAFafterDCcardioversionhasbeenreportedinuntreatedcomparedwithtreatedpatientswithOSA.
3RiskofAFrecur-rencewasparticularlyevidentamonguntreatedOSApatientswithseverenocturnaloxygenAcknowledgmentsWrittenconsentforpublicationwasobtainedfromthepatientreportedinthiscasestudy.
CompetinginterestsTheauthorsdeclaredtheyhavenocompetinginterests.
desaturation,asinthepatientwesaw.
TreatmentorresolutionofOSAcouldreversethemilieuthatpromotesAFandpulmonaryveintoleft-atrialconnections.
Whetherpulmonaryveintriggeringfocibecomesuppressed,latentorlesspronetoconducttotheleftatriumwithweightlossorOSAtherapyrequiresfurtherstudy.
CONCLUSIONSInpatientswithAFandobesity,weightlossandscreeningforOSAshouldbepursued.
WeightlossandtreatmentofOSAarelikelytoreducemechan-ical,inflammatoryandelectricalstressorsthatpro-moteAF.
Equallyimportantly,screeningforAFandappropriatetreatmentmayhelptoreducetheriskofthromboemboliccomplicationsinOSA.
References1FusterVetal.
(2001)ACC/AHA/ESCGuidelinesfortheManagementofPatientsWithAtrialFibrillation:ExecutiveSummaryAReportoftheAmericanCollegeofCardiology/AmericanHeartAssociationTaskForceonPracticeGuidelinesandtheEuropeanSocietyofCardiologyCommitteeforPracticeGuidelinesandPolicyConferences(CommitteetoDevelopGuidelinesfortheManagementofPatientsWithAtrialFibrillation)DevelopedinCollaborationWiththeNorthAmericanSocietyofPacingandElectrophysiology.
Circulation104:2118–21502HaissaguerreMetal.
(1998)Spontaneousinitiationofatrialfibrillationbyectopicbeatsoriginatinginthepulmonaryveins.
NEnglJMed339:659–6663KanagalaRetal.
(2003)Obstructivesleepapneaandtherecurrenceofatrialfibrillation.
Circulation107:2589–25944PorthanKMetal.
(2004)Prevalenceofsleepapneasyndromeinloneatrialfibrillation:acase-controlstudy.
Chest125:879–8855GamiASetal.
(2004)Associationofatrialfibrillationandobstructivesleepapnea.
Circulation110:364–3676ChungMKetal.
(2001)C-reactiveproteinelevationinpatientswithatrialarrhythmias:inflammatorymechanismsandpersistenceofatrialfibrillation.
Circulation104:2886–28917AronsonDetal.
(2004)ObesityisthemajordeterminantofelevatedC-reactiveproteininsubjectswiththemetabolicsyndrome.
IntJObesRelatMetabDisord28:674–6798ValsamakisGetal.
(2004)Modestweightlossandreductioninwaistcircumferenceaftermedicaltreatmentareassociatedwithfavorablechangesinserumadipocytokines.
Metabolism53:430–4349WyseDGetal.
(2002)Acomparisonofratecontrolandrhythmcontrolinpatientswithatrialfibrillation.
NEnglJMed347:1825–183310GarrigueSetal.
(2002)Benefitofatrialpacinginsleepapneasyndrome.
NEnglJMed346:404–41211PeppardPEetal.
(2000)Longitudinalstudyofmoderateweightchangeandsleep-disorderedbreathing.
JAMA284:3015–302112SimantirakisENetal.
(2004)Severebradyarrhythmiasinpatientswithsleepapnoea:theeffectofcontinuouspositiveairwaypressuretreatment;Along-termevaluationusinganinsertablelooprecorder.
EurHeartJ25:1070–1076
nature.
com/clinicalpractice/cardioAtrialfibrillation,sleepapneaandobesityMinaKChung*,NancyFoldvary-Schaefer,VirendKSomers,PaulAFriedmanandPaulJWangThisarticleofferstheopportunitytoearnoneCategory1credittowardstheAMAPhysician'sRecognitionAward.
THECASEAnobesemanaged41yearspresentedtohisinternistwithepisodicpalpitations,dyspneaandfatigue.
ParoxysmalAFwasdiagnosedandhewastreatedwithdigoxin,verapamilandquinidine.
Atage51,AFrecurredandpersisted.
Holtermoni-toringshowedratesof18182beats/minandnocturnalpausesofupto4.
5s,consistentwithtachycardia–bradycardiasyndrome.
TwoDCcar-dioversionprocedures,onewithadjunctivequi-nidine,resultedinonlytransientsinusrhythm.
Amiodaronewasstartedandsinusrhythmwasachieved,butrecurrencesofAFandtypeIatrialflutterrequiredfurtherDCcardioversion.
Thepatientwasreferredtoacardiacelectro-physiologistforatrialflutteratage56.
Left-ventricular,right-ventricularandright-atrialsizeandsystolicfunctionwerenormalonechocardio-graphy;left-ventricularejectionfractionwas60%andmildleft-ventricularhypertrophyandmoderateleft-atrialenlargement(5.
2cm)werepresent.
Anuclearstresstestshowednomyocar-dialscarorischemia.
AnotherDCcardioversionandradiofrequencyablationoftheright-atrialisthmussuccessfullytreatedatrialflutter.
Sinusrhythmwasmaintained2monthslater,andamiodaronewasstopped.
Afteranother3months,symptomaticAFrecurredthatwasrefractorytoflecainide,propafenoneanddofetilide.
Becauseofahistoryofnocturnalbradycardia,morbidobesityandsnoring,thepatientwaseval-uatedforOSA.
Hetypicallyslept78hpernight,experiencingthreetofourunexplainedawaken-ingsnightly.
Sleepwasunrefreshinganddaytimesleepinesswasmoderate(EPWORTHSLEEPINESSSCALEscore15).
Atthistime,body-massindexwas43kg/m2.
Duringovernightpolysomnography,thepatientsleptfor196of361minobserved.
Noslow-wavesleepwasrecordedandtherewere50arousals,23APNEASandeightHYPOPNEAS(Table1).
MeanSUMMARYBackgroundA60-year-oldmalewithobesity(body-massindex43kg/m2)presentedwithrecurrentsymptomaticatrialfibrillation(AF),whichhehadhadsinceage41years.
TheAFwasrefractorytotreatmentwithantiarrhythmicdrugs.
Pacemakerimplantationfortachycardia–bradycardiasyndromewasrequiredaswellasablationforatrialflutter,andthepatientunderwentatotaloffourDCcardioversions.
Sleepstudiesshowedmildtomoderateobstructivesleepapnea,butcontinuouspositiveairwaypressurewasnottolerated.
Pacemakerinterrogationsdemonstratedmode-switchepisodes,indicatingcontinuingAF.
Hewasscheduledforcatheterablationtargetingpulmonaryveinantralisolation.
Heembarkedonaweight-lossprogram,whichsuccessfullyreducedAFburden.
InvestigationsEchocardiography,stresstesting,polysomnography,pacemakerinterrogationsandC-reactiveprotein.
DiagnosisAF,atrialflutter,tachycardia–bradycardiasyndrome,obstructivesleepapneaandmorbidobesity.
ManagementAntiarrhythmicdrugtherapy,DCcardioversion,anticoagulation,atrialflutterablation,permanentpacemakerimplantation,continuouspositiveairwaypressureandweightloss.
KEYWORDSarrhythmia,atrialfibrillation,morbidobesity,obstructivesleepapnea,weightlossMKChungisastaffcardiologist,CardiovascularMedicine,andNFoldvary-SchaeferisSectionHead,SleepMedicineSection,ClevelandClinicFoundation.
VKSomersisaProfessorandPAFriedmananAssociateProfessorofMedicine,CardiovascularDiseases,MayoClinic.
PJWangisaProfessor,CardiovascularMedicine,StanfordUniversityMedicalCenter.
Correspondence*DepartmentofCardiovascularMedicine,ClevelandClinicFoundation,9500EuclidAvenue,DeskF-15,Cleveland,OH44195,USAchungm@ccf.
orgReceived19July2004Accepted21September2004www.
nature.
com/clinicalpracticedoi:10.
1038/ncpcardio0027CME56NATURECLINICALPRACTICECARDIOVASCULARMEDICINENOVEMBER2004VOL1NO1CASESTUDYNOVEMBER2004VOL1NO1CHUNGETAL.
NATURECLINICALPRACTICECARDIOVASCULARMEDICINE57www.
nature.
com/clinicalpractice/cardiooxygensaturationwas93%(lowof76%)andwas<90%for3%oftotalsleeptime.
Loudsnoringandsnortingwerereported.
Nonotablearrhythmiaswererecorded.
Continuouspositiveairwaypres-sure(CPAP)7cmH2Owasattemptedfor2nights,butwasdiscontinuedduetodiscomfort.
ContinuingrapidAFandbradycardiawithnocturnalpauseslimiteddrugtherapy,andadual-chamberpacemakerwasimplanted.
AFbecamepersistent9monthslater.
DofetilidewaschangedtosotalolwithDCcardiover-sion,but2dayslaterAFrecurredandpersisted.
Pulmonaryveinisolationwasscheduled.
Thepatientlostweighttolessencomplica-tionsinvascularaccess,imagingandcathetermanipulation.
After1month,AFspontaneouslyconvertedtosinusrhythm.
By3months,hehadlost20.
4kg;sinusrhythmwasmaintainedataweightof125.
6kg.
Thepatientelectedtocancelpulmonaryveinisolation.
Sotalolwasreducedfrom300mgto240mgtwicedaily.
After1year,withfurtherweightlossto121.
6kg(body-massindex37kg/m2),onlytwoepisodesofbriefasymptomaticAFhadbeendetectedovertheprevious8months,andpul-monaryveinisolationwasindefinitelypost-poned.
Table2displaysthepatient'sclinicalcharacteristicsovertime.
DISCUSSIONOFDIAGNOSESAFaffectsover2millionpeopleintheUS,1andprevalenceisincreasing.
Apartfromrapidpal-pitations,symptoms,includingfatigue,dyspneaorweakness,canbesubtle.
Becauseofitsassocia-tionwiththromboemboliccomplications,docu-mentationofthearrhythmiaiscritical,eveninasymptomaticAF.
Electrocardiogramsorambu-latorymonitoringcandetectarrhythmia.
Holterandarrhythmiaeventmonitorsmightalsobeuseful.
Echocardiographyisindicatedtoassessforstructuralheartdisease,whichcanincreasetheriskofstroke.
InloneAFwithnostructuralheartdiseaseandrefractorytomultipleantiarrhythmicdrugs,thefocithatinitiateandpossiblysustainthearrhyth-miaaregenerallylocatedintheleftatriumattheostiaofthepulmonaryveins.
2AFfrequentlybecomesmorepersistentovertime,asinthecasereported.
Continuedtriggeringoffoci,electri-calandstructuralremodelingleadingtochangesinion-channelcurrentsandatrialenlargement,changesinautonomicbalanceormyocardialsenescencewithaccompanyingstructuralandelectrophysiologicalchangescanperpetuateAF.
AtrialflutteriscommoninAFtreatedwithantiarrhythmicdrugs.
Typical,ortypeI,atrialflutterisamacrore-entrantcircuitintherightatriumwithactivationthroughtheisthmusbetweenthetricuspidannulusandinferiorvenacava.
Itischaracterizedby'saw-tooth'flut-terwavesininferiorelectrocardiogramleads.
Giventhelargeexcitablegapassociatedwithtypicalatrialflutter,antiarrhythmicmedica-tionsmaystabilizere-entrantcircuits.
Atypicalatrialflutterrepresentsre-entrantcircuitsthatarenotdependentontherightatrialisthmus.
Thepatienthadclassictachycardia–bradycardiasyndromewithperiodsofrapidrateduringAFandslowratesduringsinusrhythm,sleepordrugtreatment.
OSAaffects10–15millionpeopleintheUS,andisdiagnosedbysleepstudies.
3Morbidobes-ity,historyofsnoringandnocturnalpausespos-siblyrelatedtoapnea,oxygendesaturationorhypervagaltone,ledtoOSAassessmentinthispatient.
AnassociationbetweenAFandOSAhasbeenstudied.
Acase-controlstudyreportednosignificantdifferenceinthefrequencyofsleepapneasyndromebetweenloneAFpatientsandcontrols(32%vs29%),4althoughmoredaytimefatigueandnightlyapneaoccurredintheAFgroup.
Inastudyof151patientsundergoingDCcardioversionforAFcomparedwith312patientswithoutAF,however,OSAwasdiagnosedbyquestionnaireinmoreAFpatientsthanincontrols(49%vs32%).
5OSAmayimpacttheoccurrenceofAFbyseveralmechanisms.
Repetitiveautonomic,hemodynamicandhypoxemicsurgesmightacti-vatestretch-mediatedchannels,catecholamine-GLOSSARYEPWORTHSLEEPINESSSCALEAmeasureofdaytimesleepinessbasedonaquestionnaireinwhichrespondersratethechanceofdozingineightactivitiesAPNEAAtransientabsenceofspontaneousrespirationHYPOPNEABreathingthatisshallower,slowerorboth,thannormalAROUSALINDEXThenumberofarousaleventspersleep-hourTable1Sleepdisturbancesrecordedduringovernightpolysomnography.
ParameterofsleepdisturbanceScoreAROUSALINDEX(arousals/sleep-hour)15Apneas(numberofevents)Central1Mixed4Obstructive18Total23Hypopneas(numberofevents)8Apnea–hypopneaindex(apneaandhypopneaevents/sleep-hour)Overall9.
5Supine18.
6CASESTUDY58NATURECLINICALPRACTICECARDIOVASCULARMEDICINECHUNGETAL.
NOVEMBER2004VOL1NO1www.
nature.
com/clinicalpractice/cardiosensitivechannelsorboth,leadingtogreaterfocaldischarges.
Pulmonaryorsystemichyper-tension,lungphysiologyrestrictedbymorbidobesityorbothcanelevateatrialpressuresandtriggerectopyandAF.
Vagalstimulationofatrialmyocardiumshortensatrialrefractoryperiods.
VagalreflexesduringOSA,markedbybradyarrhythmias,couldalsoreducerefracto-rinessatthepulmonaryveinostia,promotingconductionoffocaldischargesfromthepul-monaryveintoleftatriumandgeneratingawindowforpulmonaryveinfocitotriggerAF.
ElevatedC-reactiveprotein(CRP)hasbeenassociatedwithobesity,metabolicsyndrome,severityofOSAandAF.
6Themajordetermi-nantofCRPelevationinobesepeoplemaybetheobesity,ratherthanOSAormetabolicsyn-drome.
7Inthepresentcase,initiallyhighlevelsofCRPreducedwithweightloss.
WhetherhighconcentrationsassociatedwithobesityindicateapredispositiontostructuralremodelingorAFitselfprovokesinflammationisunknown.
Markersofinflammationreducewithweightlossofaslittleas5%inobesesubjects,8andobesity,OSAorbothcouldpromoteatrialstruc-turalremodelingviamechanicalorinflamma-torystress.
Thelagbetweenbody-massindexreductionandCRPandAFburdenreductionobservedinthispatientsuggeststhatmorethan3monthsmightberequiredbeforeimprove-mentsinmechanical,metabolicorinflamma-torystressorsareseen.
WhetherreliefofOSAitselfwasthecriticalmechanicalfactorinthispatientcannotbedetermined,aswedidnofollow-upsleepstudyafterweightloss.
TREATMENTANDMANAGEMENTAFmanagementisaimedatreducingsymptomsandtheriskofthromboemboliccomplications.
TheAtrialFibrillationFollow-upInvestigationofRhythmManagement(AFFIRM)trial9dem-onstratednosurvivalbenefitswitharhythm-controloverrate-controlstrategy.
Theneedforcontinuedanticoagulationwasconfirmedinpatientswithriskfactorsforstroke,evenwithrhythmcontrolandapparentmaintenanceofsinusrhythm.
Warfarinanticoagulationwasindicatedforborderlinehypertensionanddiabetesmellitusinthepatientwedescribe.
Initialtreatmentcomprisedrate-controllingdigoxinandverapamilandrhythm-controllingquinidine.
First-linetherapyhassincechangedtoβ-blockers;quinidine,whichcarriesariskofproarrhythmia,isusuallyavoided.
WhenTable2Clinicalcharacteristicsrecordedfrom15December2000to4June2004.
DateWeight(kg)BMI(kg/m2)RhythmNumberofmodeswitches(%modeswitched)CRP(mg/l)Antiarrhythmicdrug15Dec2000137.
742.
3SRN/A2.
13Amiodarone11May2001145.
544.
6SR,PAFN/A4.
14None20July2001145.
544.
6AFN/A2.
80Flecainide7Sept2001N/DN/DSR,PAFN/A3.
21Dofetilide5Oct2001141.
443.
4SR,PAFN/A3.
57Dofetilide16Nov2001a138.
242.
4AF17(29.
9)3.
04Dofetilide21May2002138.
242.
4SR,PAF84(15.
8)2.
79Dofetilide8July2002N/DN/DAFN/D3.
20None15July2002N/DN/DAFN/D3.
14Sotalol18Oct2002143.
243.
9AF137(65.
3)2.
34Sotalol24Jan2003144.
144.
2AF15(69.
7)1.
90Sotalol6June2003bc146.
444.
9AFN/D2.
70Sotalol19Sept2003d125.
938.
6SRN/D2.
80Sotalol4June2004e121.
837.
4SR21(16)0.
90Sotalola1monthafterPPMimplant.
bStartofweight-lossprogram.
cPVIscheduled.
d20.
5kgweightloss.
eTwoepisodessinceOctober2003,longest7h.
AF,atrialfibrillation(atvisit);BMI,body-massindex;CRP,ultrasensitiveC-reactiveprotein;N/A,notapplicable;N/D,notdone;PAF,paroxysmalatrialfibrillation;PPM,permanentpacemaker;PVI,pulmonaryveinantralisolation;SR,sinusrhythm.
GLOSSARYAPNEA–HYPOPNEAINDEXThenumberofrespiratoryevents(apneasandhypopneas)persleep-hourCASESTUDYNOVEMBER2004VOL1NO1CHUNGETAL.
NATURECLINICALPRACTICECARDIOVASCULARMEDICINE59www.
nature.
com/clinicalpractice/cardioAFbecamemorepersistent,amiodaronewasstarted.
AlthougheffectiveforAF,amiodaronecanhavetoxiceffects.
Otherfirst-linedrugsforloneAFareflecainideandpropafenone.
Whiletakingamiodarone,thepatientdevelopedatrialflutter.
Ablationoftheposteriorcorridorthatformsthecircuitofatrialfluttermaybeusedinconjunctionwithantiarrhythmicdrugs.
Sinusrhythmwasmaintainedafterablationonamiodar-one,butwhenamiodaronewasstoppedtoavoidlong-termtoxiceffects,AFrecurredasexpected.
Flecainide,propafenoneanddofetilidehadnoeffect.
DCcardioversionsarehelpfulforpersistentAFandcanbeperformedmultipletimes.
Pacemakerimplantationwaschosenforsymp-tomatictachycardia–bradycardiasyndrometofacilitaterate-controllingmedications.
PacemakersmayalsobebeneficialforOSA.
10Mode-switchlogsenableassessmentofAFburden.
Becauseofthepersistenceofthepatient'sAF,catheter-basedpulmonaryveinisolationwasrecommended.
Thismethodissuccessfulin60–85%ofpatients,withhighersuccessratesinloneAF.
Obesitycanraisevascularaccessrisks,suchasinadvertentarterialcannulationorhematomaformation;dosesofanticoagulationhigherthannormalmightberequired.
Inaddi-tion,weightlimitsof135–160kgoftenapplytocatheterizationtables,andfluoroscopyintensitycanberaised.
Weightlossis,therefore,advisableinobesepatientsscheduledforthisprocedure.
MildOSA(APNEA–HYPOPNEAINDEX<20,withoutsignificantsleepcomplaints)canbemanagedconservativelywithweightlossandavoidanceofcentralnervoussystemdepres-sants,sleepdeprivationandsleepingsupine.
Evenmodestweightcontrolhasbeenshowntoimprovesleep-disorderedbreathing.
11CPAPshouldbeofferedasinitialtherapyinmoder-atetoseverediseaseormilddiseasewithseveredaytimesleepiness.
Variousinterfacesshouldbetriedfortolerabilityandcomfort.
SurgeryshouldbeconsideredifCPAPisnottoleratedorfails.
WhenOSAandAFcoexist,treatmentforOSAmightassistmanagementofAF.
Althoughareductioninapneicepisodes,bradyarrhyth-miasorbothhasbeenseenwithatrialpacingorCPAP,supraventriculararrhythmias10,12arenotreduced.
Nevertheless,asignificantlyraisedriskofrecurrentAFafterDCcardioversionhasbeenreportedinuntreatedcomparedwithtreatedpatientswithOSA.
3RiskofAFrecur-rencewasparticularlyevidentamonguntreatedOSApatientswithseverenocturnaloxygenAcknowledgmentsWrittenconsentforpublicationwasobtainedfromthepatientreportedinthiscasestudy.
CompetinginterestsTheauthorsdeclaredtheyhavenocompetinginterests.
desaturation,asinthepatientwesaw.
TreatmentorresolutionofOSAcouldreversethemilieuthatpromotesAFandpulmonaryveintoleft-atrialconnections.
Whetherpulmonaryveintriggeringfocibecomesuppressed,latentorlesspronetoconducttotheleftatriumwithweightlossorOSAtherapyrequiresfurtherstudy.
CONCLUSIONSInpatientswithAFandobesity,weightlossandscreeningforOSAshouldbepursued.
WeightlossandtreatmentofOSAarelikelytoreducemechan-ical,inflammatoryandelectricalstressorsthatpro-moteAF.
Equallyimportantly,screeningforAFandappropriatetreatmentmayhelptoreducetheriskofthromboemboliccomplicationsinOSA.
References1FusterVetal.
(2001)ACC/AHA/ESCGuidelinesfortheManagementofPatientsWithAtrialFibrillation:ExecutiveSummaryAReportoftheAmericanCollegeofCardiology/AmericanHeartAssociationTaskForceonPracticeGuidelinesandtheEuropeanSocietyofCardiologyCommitteeforPracticeGuidelinesandPolicyConferences(CommitteetoDevelopGuidelinesfortheManagementofPatientsWithAtrialFibrillation)DevelopedinCollaborationWiththeNorthAmericanSocietyofPacingandElectrophysiology.
Circulation104:2118–21502HaissaguerreMetal.
(1998)Spontaneousinitiationofatrialfibrillationbyectopicbeatsoriginatinginthepulmonaryveins.
NEnglJMed339:659–6663KanagalaRetal.
(2003)Obstructivesleepapneaandtherecurrenceofatrialfibrillation.
Circulation107:2589–25944PorthanKMetal.
(2004)Prevalenceofsleepapneasyndromeinloneatrialfibrillation:acase-controlstudy.
Chest125:879–8855GamiASetal.
(2004)Associationofatrialfibrillationandobstructivesleepapnea.
Circulation110:364–3676ChungMKetal.
(2001)C-reactiveproteinelevationinpatientswithatrialarrhythmias:inflammatorymechanismsandpersistenceofatrialfibrillation.
Circulation104:2886–28917AronsonDetal.
(2004)ObesityisthemajordeterminantofelevatedC-reactiveproteininsubjectswiththemetabolicsyndrome.
IntJObesRelatMetabDisord28:674–6798ValsamakisGetal.
(2004)Modestweightlossandreductioninwaistcircumferenceaftermedicaltreatmentareassociatedwithfavorablechangesinserumadipocytokines.
Metabolism53:430–4349WyseDGetal.
(2002)Acomparisonofratecontrolandrhythmcontrolinpatientswithatrialfibrillation.
NEnglJMed347:1825–183310GarrigueSetal.
(2002)Benefitofatrialpacinginsleepapneasyndrome.
NEnglJMed346:404–41211PeppardPEetal.
(2000)Longitudinalstudyofmoderateweightchangeandsleep-disorderedbreathing.
JAMA284:3015–302112SimantirakisENetal.
(2004)Severebradyarrhythmiasinpatientswithsleepapnoea:theeffectofcontinuouspositiveairwaypressuretreatment;Along-termevaluationusinganinsertablelooprecorder.
EurHeartJ25:1070–1076
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