fibrillation心房纤颤（英文版）课件

AtrialFibrillation BeyondCardizemandCoumadin WilliamR Colyer Jr MDResidentGroundRoundsFebruary23 1999 CasePresentation HPI 47yoWMpresentedwithpalpitationsfor12hours Begansuddenlyandremainedconstant Nopriorsymptoms Denieddizziness CPorSOB Noothercomplaints Allergies NKDAMedications None CasePresentation PMH H OparoxysmalAF8yearsagoperPCP FH NoncontributorySH Smoked1ppdfor27years SocialEtOH NorecentincreasedEtOHconsumption ROS Unremarkable CasePresentation VS Afebrile HR110 RR14 BP128 76Gen WDWNWMNADHEENT NC AT PERRLA EOMI OPclearNeck Supple 2 upstrokesbilaterally noJVDorbruits CasePresentation CV S1S2irregular NoS3S4murmursorrubsPulm LungsCTAbilaterallyAbdomen Soft NT ND BSpositiveExtremities Noclubbing cyanosisoredema CasePresentation ECG AF NoacuteSTsegmentorTwavechanges CXR NormalLabs BMPnormal TSH2 3Echo EF55 noSWMA allvalvespliable noMR LAsize39 CasePresentation Impression Atrialfibrillationwithoutevidenceofstructuralheartdiseaseorobviousmetaboliccause Overview MainGoal Tohelpphysiciansbecomemorecomfortablewithtreatmentsdesignedtoachievesinusrhythm EpidemiologyandpathophysiologyWhytotreatAFDrugtherapyinAFConclusions Introduction AFisacommonclinicalcondition Notahomogeneouscondition Characterizedbyanirregularlyirregularrhythmonexam NopwavesonECG RRintervaloftenirregular NotetheRRintervalmayberegularifAVblockorconductionsystemdiseasepresent Introduction Introduction AnAHAreportin1996statedthreemaingoalsinmanagementofAF 1 Controlofventricularrate2 Preventionofthromboembolism3 Maintainingsinusrhythm Epidemiology Currentestimateof2 2millionAmericanswithAF Prevalencevariesbyage Feinbergetal Epidemiology Epidemiology AFresultsinasignificantnumberofhospitalizationseachyear AFaccountedfor0 52 ofdischargediagnosesin1990 176 460patients Bialyetal Pathophysiology MultiplewavelettheoryfirstproposedbyMoe NonuniformdistributionofrelativelybriefrefractoryperiodsandrelativelyslowimpulseconductionleadstothedevelopmentofAF Morelikelytooccurwithincreasedtissuemass Pathophysiology Theseconditionsresultinself sustainedturbulentactivityandirregularimpulsepropagationinanirregularpattern Onceinitiatedtheactivityisindependentofinitiatingevent Pathophysiology AvarietyofclinicalconditionsassociatedwithAF AcuteEtOHingestion HolidayHeart AcuteMIAcutepericarditisAcutemyocarditisAcutePEHyperthyroidism Pathophysiology HypertrophiccardiomyopathyDilatedcardiomyopathyCOPDAtrialmyxomaASDandothercongenitaldefectsAmyloidosisHemochromotosisPheochromocytoma Pathophysiology EndomyocardialfibrosisWPWLGLSicksinusElectrocution Pathophysiology AFmaybeassociatedwithorganicheartdisease70 80 ofthetimeAFassociatedwithvalvularheartdisease20 23 ofthetime CHFispredictiveforthedevelopmentofAFinthissetting Levy Pathophysiology AFintheabsenceofunderlyingconditionsiscalledloneAF LoneAFaccountsfor10 30 ofcases LoneAFhasabetterprognosisbutisnotabenignclinicalcondition WhytoTreatAF Avoidhemodynamiccompromise AFwithWPWleadstoVRVRand COMSanddiastolicdysfunctionimpairLVfilling Atrial kick neededtomaintainCO WhytoTreatAF CASSdatashowAFtoberiskfactorforincreasedmortality AF1 982 95 CI1 496 2 626 p 0 0001 RRofdeathcomparedtopatientsinNSR WhytoTreatAF MayresultinLVdysfunction FirstreportedbyPhillipsandLevinein1949 AlsoreportedbyPetersandKienzle Groganetal reportedon10patientswithAFand idiopathic cardiomyopathy InitiallymedianEF25 range12 30 AftertreatmentmedianEF52 range40 64 WhytoTreatAF PossiblecausesofAFinducedLVdysfxn DepletionofhighenergyPO4storesDepletionofANFSympatheticnervoussystemactivationReninangiotensinactivationMyocardialischemiaLVH diastolicdysfunctionandLVremodelinghavebeenseeninanimalmodels WhytoTreatAF Avoidanceofemboliccomplications Occurinupto70 ofpatientswithAFAccordingtoAHAreport attributableriskforstrokewithAF1 5 forpatientsage50 59 Thisincreasesto30 forpatientsage80 89 Framinghamstudyfoundthatbyage80onlyAFwasastatisticallysignificantriskfactorforstroke CAD HTNandCHFnotsignificantriskfactorsinthisagegroup WhytoTreatAF Avoidanceofembolicevents Con t AnticoagulationusedforthispurposeSPAFshowedareductioninstrokefrom7 4 to2 3 peryear p 0 01 PatientsmusthaveblooddrawntomonitoranticoagulationComplicationsassociatedwithanticoagulation WhytoTreatAF Improvementinqualityoflife Reductioninpalpitations dizziness dyspneaandfatigue Hardertoquantify butimportanttopatients WhytoTreatAF AFbegetsAF Increasedatrialpressuresleadtoincreasedatrialsize Increasedatrialsizeassociatedwithdecreasedsuccessofconversion Maybeduetoincreasedwaveletactivity WhytoTreatAF AFbegetsAF EPremodelingWijfellsetal demonstratedEPremodelingingoatsmaintainedinAF After24hoursmeanfibrillationintervaldecreasedfrom145 18msto108 8ms AlsoAERPdecreasedfrom146 19msto95 20ms WhytoTreatAF AFbegetsAF After24hoursAFinducibilitybyasingleprematurestimulusincreasedfrom24 to76 GoatskeptinAF2 4weeksthensinusrhythmrestored WhytoTreatAF AFbegetsAF Sixhoursaftercardioversion meanfibrillationintervalincreasedfrom105 10msto139 7ms After24hoursithadincreasedtobaselineof151 25ms AERPbegantoimprovewithin24hoursandnormalizedwithinoneweek WhytoTreatAF AFbegetsAF SinglestimulusinducibilityofAFdecreasedto46 within24hoursofconversionandto29 withinoneweek WhytoTreatAF Directevidenceformaintainingsinusrhythmisscarce Threetrialscurrentlyinvestigatingthis 1 RACE2 PIAF3 AFFIRM WhytoTreatAF RACE RateControlversusElectricalCardioversion StudyinTheNetherlands500patientsrandomizedtoratecontrolversuselectricalcardioversionPrimaryendpointcombinedmorbidityandmortality WhytoTreatAF PIAF PharmacologicInterventioninAtrialFibrillation StudyinGermany252patientswithsymptomaticpersistentAFof7to360daysdurationrandomizedtoratecontrolversuspharmacologicconversion Patientstobefollowedfor12months WhytoTreatAF PIAF Con t PrimaryendpointofrecurrenttachycardiainratecontrolarmandrecurrentAFinconversionarm Secondaryendpointsofqualityoflife assessedbyastructuredquestionnaire hemodynamicconsequencesoftherapy thromboemboliccomplicationsandmortalitywillalsobeevaluated WhytoTreatAF AFFIRM AtrialFibrillationFollow upofRhythmManagement SponsoredbyNHLBI5 300patientsathighriskforstroketoberandomizedtoratecontrolorrhythmcontrol allpatientstobeanticoagulated Drugchoicetobeleftuptotreatingphysician WhytoTreatAF AFFIRM Con t Patientstobefollowedaminimumoftwoyearsandanaverageof3 5years Endpointstobeevaluatedincludetotalmortality disablingstroke disablinganoxicencephalopathy intracranialbleeding majorextracranialbleeding cardiacarrest qualityoflifeandcostoftherapy WhytoTreatAF WhytoTreatAF DrugTherapyinAF FourclassesofantiarrhythmicagentsinVaughanWilliamsclassification ClassIa classIcandclassIIIdrugsusedtotreatAF DrugTherapyinAF ClassIdrugsblockfastNa channelsClassIadrugsreduceVmaxandprolongactionpotentialduration Procainamide QuinidineandDisopyramideClassIcdrugsreduceVmax primarilyslowconductionandminimallyprolongtherefractoryperiod Flecainide PropafenoneandMoricizine DrugTherapyinAF ClassIIIdrugsblockK channelsandprolongrepolarizationAmiodaroneandSotalolIbutilideforacuteconversionbutnotmaintenanceofsinusrhythmNotethatNAPAalsoworksbyclassIIIaction DrugTherapyinAF Onlyquinidine flecainideandpropafenoneareFDAapprovedforconversionandmaintenancetherapy IbutilideisFDAapprovedforacuteconversiontherapy DrugTherapyinAF ElectrophysiologicmechanismsAllesieetal demonstratedclassIdrugsrestoresinusrhythmbyprolongationofAFCLsecondarytowideningoftheexcitablegap Capuccietal showedthatclassIIIdrugsareaheterogeneousgroup Amiodaronehaspropertiesofallfourdrugclasses RacemicsotalolhasclassII blocker andclassIIIproperties DrugTherapyinAF Electrophysiologicmechanismsd sotalolhas pure classIIIactivity Morethan98 ofclassIIactivityinracemicsotalolcomesfroml isomer Other pure classIIIagentsincludeibutilide dofetilide azimilide andexperimentalagentssuchastedisamil DrugTherapyinAF ClassIaandclassIIIagentsreducedefibrillationthresholds ClassIcagentsincreasedefibrillationthresholds DrugTherapyinAF Iskosetal demonstrateddecreaseddefibrillationthresholdswithd sotalolindogs DogsinAFcardiovertedwithintraatrialshocksbeforeandaftertreatmentwithd sotalolat5mg kg Defibrillationthresholdsdecreasedfrom1 72 1 12joulesto0 59 0 60joulesafterd sotaloladministration DrugTherapyinAF AvoidClassIcagentsinpatientswithknownCAD BasedonCASTdata DrugTherapyinAF AmiodaronepreferredinpatientswithLVdysfunction BasedonGESICAdata DrugTherapyinAF ProcainamidedrugofchoicewhenAFpresentwithpre excitation Thisisbecauseitblockstheaccessorypathway TypicalAVnodalblockingdrugsdonotblocktheaccessorypathwayandmayenhanceconductionacrossit DrugTherapyinAF Limitedstudiescomparingantiarrhythmicagents DrugTherapyinAF Lparedtolerabilityandefficacyofquinidineandflecainide 10patientsrandomizedtoflecainideand9toquinidine After8weeksoftherapypatientscrossed overtoothertreatment FlecainidereducedrecurrencesofAFcomparedtoquinidine DrugTherapyinAF Lauetal Con t Meanof21daystofirstrecurrencewithflecainideversus15dayswithquinidine DrugTherapyinAF Naccarellietal alsocomparedflecainideandquinidine Openlabel randomized comparativetrial 239patientsrandomized 122toflecainide 117toquinidine Patientsfollowedfor12months 70 5 ofpatientsonflecainideeffectivelytreatedversus55 4 onquinidine p 0 007 DrugTherapyinAF FAPIScomparedflecainideandpropafenone Randomized openlabel comparativetrial 200patientsrandomized 97toflecainide 103topropafenone Patientsfollowedforoneyear DrugTherapyinAF FAPIS Con t Intentiontotreatanalysisrevealedsuccessfultreatmentin77 offlecainidegroupand75 ofpropafenonegroup 2proarrhythmiceventswithflecainideand1withpropafenone Nostatisticallysignificantdifferencesnotedbetweenthetwodrugs DrugTherapyinAF Kparedamiodaroneandsotalol Randomized doubleblindstudy 70patientsrandomized 35toeachdrug Patientsfollowedupat1 2 4 6 9 12months DrugTherapyinAF DrugTherapyinAF Kochiadakisetal Con t Attheendof12months71