简介：Coronaryangiographyaftercardiacarrestisimportanttoascertainpotentialtreatablecausesofcardiacarrest,salvagemyocardium,andpotentiallyincreaselong-termsurvival.Thecauseofadultout-of-hospitalcardiacarrestistypicallymyocardialischemia.Morethan50%ofsuchresuscitatedindividualswillhaveanacutelyoccludedepicardialcoronaryonemergencycoronaryangiography.ThisincludesthreeinfourwithST-segmentelevationandoneinthreewithoutSTsegmentelevation.Inthelattertheonlyreliablemethodofdetectioniscoronaryangiography.Numerouscohortstudies,nowincludingmorethan8000patients,haveshownanassociationbetweensurvivalandearlycoronaryangiographyand/orpercutaneouscoronaryintervention.Publicreportingofpercutaneouscoronaryintervention30-daymortalityrateshasbeenanimpedimentforextendingthistherapytoallresuscitatedindividualswhoexperiencedout-of-hospitalcardiacarrest,sincecurrentdatabasestodofullyrisk-adjustratesforthissubgroup.Sincereeffortsareunderwaytocorrectthissituation.

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简介：AbstractBackground:Super-responders (SRs) tocardiacresynchronization therapy (CRT) regain near-normal or normalcardiacfunction. The extent ofcardiacsynchrony of SRs and whether continuous biventricular (BIV) pacing is needed remain unknown. The aim of this study was to evaluate thecardiacelectrical and mechanical synchrony of SRs.Methods:We retrospectively analyzed CRT recipients between 2008 and 2016 in 2 centers to identify SRs, whose left ventricular (LV) ejection fraction was increased to ≥50% at follow-up.Cardiacsynchrony was evaluated in intrinsic and BIV-paced rhythms. Electrical synchrony was estimated by QRS duration and LV mechanical synchrony by single-photon emission computed tomography myocardial perfusion imaging.Results:Seventeen SRs were included with LV ejection fraction increased from 33.0 ± 4.6% to 59.3 ± 6.3%. The intrinsic QRS duration after super-response was 148.8 ± 30.0 ms, significantly shorter than baseline (174.8 ± 11.9 ms, P = 0.004, t = -3.379) but longer than BIV-paced level (135.5 ± 16.7 ms, P = 0.042, t = 2.211). Intrinsic LV mechanical synchrony significantly improved after super-response (phase standard deviation [PSD], 51.1 ± 16.5° vs. 19.8 ± 8.1°, P < 0.001, t= 5.726; phase histogram bandwidth (PHB), 171.7 ± 64.2° vs. 60.5 ± 22.9°, P < 0.001, t= 5.376) but was inferior to BIV-paced synchrony (PSD, 19.8 ± 8.1° vs. 15.2 ± 6.4°, P = 0.005, t = 3.414; PHB, 60.5 ± 22.9° vs. 46.0 ± 16.3°, P = 0.009, t = 3.136).Conclusions:SRs had significant improvements incardiacelectrical and LV mechanical synchrony. Since intrinsic synchrony of SRs was still inferior to BIV-paced rhythm, continued BIV pacing is needed to maintain longstanding and synchronized contraction.

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简介：NICFEDexpertsystem-arule-based"non-invasivecardiacfunctionevaluationandcardiacdiseasesdiagnosingexpertsystem"-isdiscussedinthispaper.Thesys-temcanberegardedasaninterpretationexpertsystemandasadiagnosticexpertsystem.Whenitisappliedtoevaluatecardiacfunction,itcanexplainmorethanonehundredparametersdetectedby"MCA-Ⅲcardiacfunctiondeviceofmulti-domainandmultidemension".Withtheseparametersthecardiacfunctionintimedomain,fre-

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简介：Positronemissiontomography(PET)isapowerfulnoninvasiveimagingtoolforphenotypingpatientsatriskoforwithknowncoronaryarterydisease(CAD).Oneofthekeyadvantagesoverotherimagingmodalitiesisitsuniqueabilitytoquantifyphysiologicprocesses,includingmyocardialbloodflow(inmillilitersperminutepergramofmyocardium),metabolism,andcardiacreceptors,anditshighsensitivityfordelineatingandquantifyingmoleculartargetsinvivousingtargetedimagingprobes.CardiacPET/CToffersopportunityforacomprehensivenoninvasiveevaluationoftheconsequencesofatherosclerosisinthecoronaryarteriesandthemyocardium.

简介：ObjectivesToevaluateretrospectivelythepotentialbenefitsofcombinedutilizationofvariousassistedcirculationdevicesincardiacarrestpatientswhodidnotrespondtoconventionalcardiopulmonarycerebralresuscitation(CPCR).MethodsAssistedcirculationdevices,includingemergencycardiopulmonarybypass(ECPB),intra-aorticballoonpump(IABP),andleftventricularassistdevice(LVAD),wereappliedto16adultpatientswhohadcardiacarrest82min-56hafteropenheartsurgeryanddidnotrespondto20minorlongerconventionalCPCR.ECPBwasappliedto2patients,ECPBplusIABPto8patients,ECPBplusIABPandLVADto6patients.ResultsOnepatientrecoveredfullyandonepatientdied.Oftheother14patients,13resumedspontaneouscardiacrhythmandonedidnot;noneofthemcouldbeweanedfromECPB.Furthertreatmentofthe14patientswithcombinationsofassistedcirculationdevicesenabled6patientstorecover.Oneofthe7recoveredpatientsdiedofreoccurringcardiacarrestafter11days;theother6weredischargedingoodconditionandwerefollowedupfor3-49months(mean=22months).Ofthe6dischargedpatientsonesufferedcerebralembolismduringLVADtreatment,resultinginmildlimitationofmobilityoftherightlimbs;theother5nevermanifestedanycentralnervoussystemcomplications.Therewasnolatedeathsgivinga37.5%(6/16)long-termsurvivalrate.ConclusionsECPBcouldeffectivelyreestablishbloodcirculationandoxygensupply,rectifyacidosis,andimproveinternalmilieu.ThecombinedutilizationofECPB,IABP,andLVADreducesthedurationofECPB,improvestheincidenceofrecovery,andoffersbeneficialalternativestorefractorycardiacarrestpatients.

简介：BackgroundThevideo-assistedthoracoscopicsurgicaltechniquesarewidelyusedinthetreatmentofpatientswithcongenitalheartdiseaseswithgoodoutcomes.However,thefeasibilityandsignificanceofnursebasedearlycardiacrehabilitationincardiacintensivecareunit(ICU)forpatientswithtotallythoracoscopiccardiacoperationhasbeenseldomstudied.MethodsThirty-sixpatientswithtotallythoracoscopiccardiacoperationundertheconditionofthecardiacICUinGuangdongGeneralHospitalwererandomallocatedtotheinterventiongroupandthecontrolgroupbetweenJanuary2012toDecember2014.Thecontrolgroupreceivedstandardnursingcare,andtheinterventiongroupreceivedearlycardiacrehabilitationnursingcareinadditiontostandardcare.Theoutcomemeasuresincludedtheoxygensaturation(SpO2%),vitalcapacity,forcedexpiratoryvolumein1second(FEV1),andpaininthethoracicwound(visualanaloguescale,VAS),whichweremeasuredatthebaselineandwithin2-dayafter4-weeknursingcare.Forsafetyreason,wealsomonitoredtherateofperceivedexertion(RPE),heartrate,systemicbloodpressure.ResultsTherewerenon-significantdifferencesbetweenthegroupsinage,sex,totalnumberofcomorbidconditions,totalnumberofmedications,surgicaltime,andanesthetictime(P>0.05).Following4weekstreatment,thecardiopulmonaryfunctionsandVASscorewereimproved(P<0.05)inallgroups.Inaddition,theimprovementsweremoreintheearlycardiacrehabilitationnursecaregroupthaninthecontrolgroup(P<0.05).ConclusionTheearlycardiacrehabilitationnursingcareincardiacICUissafe,feasibleandbeneficialforpatientswithtotallythoracoscopiccardiacoperation.

简介：CASEREPORTA43-year-oldChinesemalefarmerpresentedtothehospitalwithcomplaintsofexertionalpalpitationanddyspneafor2months.Hehadhisdiscomfortsoftentogetherwithdrycough,andgraduallyappearedparoxys-

简介：Theconnexin43(Cx43)proteins,whichisthepredominantproteinthatcanformgapjunctionsandnon-junctionalhemichannelsinventricularmyocardium,arecentraltothecardioprotectionaffordedbyischemicpreconditioning(IP)andmaybeischemicpostconditioning(PC)too.RecentstudiesshowedthatrecruitmentofCx43tothemitochondriainIPmightplayaroleintheproductionofreactiveoxygenspecies(ROS)thatmediatesIP.ThelocalizationofCx43atmitochondriaappearstobeimportantfortheachievedcardioprotectionandopensanewdoorforustorevealtheexactmechanismsofischemia/reperfusion(I/R)injuryandcardioprotection,anditmightbenewtargetsofpharmacologicalmodulatortoachievedcardioprotection.

简介：在心肌层的重入的推动被认为是支持electrophysiological畸形或甚至导致室的心悸亢进(vt)和室的纤维性颤动(VF)的一个主要因素。重入的波浪的尖端轨道能反映重入的运动的电的繁殖和区域的稳定性，从而在在VT/VF期间学习电的活动被看作大多数担心的参数之一。现在的学习的目的是建议一个实际方法用一条计算途径发现尖端轨道。在室的房间的这个学习Luo-Rudy1991数学模型被使用。切开方法的操作员被利用在二维的织物集成部分微分方程。并且螺线波浪被切割波浪前面技术开始。通过我们发现了它的实验是困难的由发现在大多数报纸求婚了的二根isovoltage线的交叉发现尖端。因此，我们建议尖端点被寻求二根邻近的isovoltage轮廓线的最短的距离检测。结果证明以我们的方法发现的这些螺线波浪的尖端轨道很接近观察的尖端，暗示我们在测量在心脏的再废的尖端轨道的方法的确认。

简介：Thetechniqueofcomputersimulationsisaveryefficientmethodininvestigatingmechanismsofmanydiseases.Thispaperreviewshowthesimulationsofthehumanheartstartedasasimplemathematicalmodelsinthepastanddevelopedtothepointwheregeneticinformationisneededtodosuitableworklikefindingoutnewmedicamentsagainstheartdiseases.AlsotheInfluenceofthedevelopmentofcomputerperformanceinthefutureaswellasthedatapresentationisdescribed.

简介：Inthelastseveralyears,therateofinnovationincardiacimagingtechniqueshasacceleratedsignificantly.Advanceshavebeenseeninall4majormodalities;echocardiography,nuclear(positronemissiontomography(PET)andsinglephotonemissioncomputedtomography(SPECT),cardiacmagneticresonanceimaging(CMR),andcomputedtomographicangiography(CTA).ThisissueofCardiovascularInnovationsandApplicationswillhighlightmanyoftheseadvances.

简介：RecentstudiesrevealingtheimportantrolesofmicroRNAs（miRNAs）inregulatingexpressionofionchannelgeneshaveopeneduparesearchfieldforextendinganddeepeningourinvesti-gationintothecardiacexcitabilityandtheassociatedarrhythmogenesis.Cardiacexcitability,thefundamentalpropertyofthecardiacmyocytes,definesthecardiacconduction,repolarization,automaticity,intracellularcalciumhandling,andtheirregionalheterogeneity.OurpreviousandongoingstudiesandtheworkfromotherlaboratorieshavedemonstratedthesignificantinvolvementofmiRNAsinregulatingeveryaspectsofcardiacexcitability.Wehavefoundearlierthatthemuscle-specificmiRNAmiR-1boostsupthearrhythmogenicpotentialthroughtargetinggapjunctionchannelconnexin43inmyocardialinfarction.AsubsequentstudyrevealedthatmiR-1canalsocausearrhythmiasbyimpairingCa2+handlingbytargetingphosphatase.Wethenidentifiedanothermuscle-specificmiRNAmiR-133promotesabnormalQTprolongationbyrepressingHERGK+channelexpressionindiabeticcardiomyopathy.Subsequently,wediscoveredthatbothmiR-1andmiR-133areinvolvedinthereexpressionofpacemakerchannelsHCN2/HCN4toenhanceabnormalautomaticityincardiachypertrophy.Recently,wefurtheridentifiedmiR-328asanimportantdeterminantforatrialfibrillation（AF）andtheassociatedadverseatrialelectricalremodelingviatargetingL-typeCa2+channels.Whilealltheabove-mentionedmiRNAsareproarrhythmic,wehavenewlyidentifiedforthefirsttimeanaturalantiarrhythmicmiRNAmiR-26.WefoundthatallthreemembersofthemiR-26familyisdownregulatedintheirexpressioninAFtissuesandthisdownregulationincreasesAFvulnerabilityasaresultofremovalofanendogenousantiarrhythmicfactor.miR-26downregulationshortensatrialactionpotentialfavoringAFbyincreasinginwardrectifierK+current（IK1）density.ThisiscausedbyanupregulationofKir2.1K+channelsu

简介：Inanerawhencardiactransplantpatientsaresurvivingmoreimmediateissuesofrejectionandinfection,theprevalenceofmorechronicissuessuchascardiacallograftvasculopathy(CAV)isrising.Thiscasedescribesaman20yearsaftercardiactransplantwithhisfirstpresentationofCAV.Acutemyocardialinfarctionwasdiagnosedonthebasisofsymptomsandbiochemicalmarkersandoncoronaryangiography,andhewasfoundtohaveacriticalstenosisofthemidportionoftheleftanteriordescendingartery.Itwaselectedtotreatthispercutaneouslywithafullybioresorbablevascularscaffold(BVS)becauseofthediffusenatureofthediseaseprocess.Thiswassuccessfullyperformedwithopticalcoherencetomographyguidance.TheuseofBVSinCAVhasnotbeenwellstudied.ThisisoneoffewcasereportsdescribingtheuseofBVSinCAV.

简介：RecentnovelapproachesinmyocardialperfusionsinglephotonemissionCT(SPECT)havebeenfacilitatedbynewdedicatedhigh-efficiencyhardwarewithsolid-statedetectorsandoptimizedcollimators.Newprotocolsincludeverylow-dose(1mSv)stress-only,two-positionimagingtomitigateattenuationartifacts,andsimultaneousdual-isotopeimaging.Attenuationcorrectioncanbeperformedbyspecializedlow-dosesystemsorbypreviouslyobtainedCTcoronarycalciumscans.HybridprotocolsusingCTangiographyhavebeenproposed.Imagequalityimprovementshavebeendemonstratedbynovelreconstructionsandmotioncorrection.FastSPECTacquisitionfacilitatesdynamicflowandearlyfunctionmeasurements.Imageprocessingalgorithmshavebecomeautomatedwithvirtuallyunsupervisedextractionofquantitativeimagingvariables.Thisautomationfacilitatesintegrationwithclinicalvariablesderivedbymachinelearningtopredictpatientoutcomeordiagnosis.Inthisreview,wedescribenewimagingprotocolsmadepossiblebythenewhardwaredevelopments.WealsodiscussseveralnovelsoftwareapproachesforthequantificationandinterpretationofmyocardialperfusionSPECTscans.

简介：Over20yearsofresearchhasledtothenowwidelyacceptedroleofcardiacresynchronizationtherapy(CRT)inmedicallyrefractory,mildtoseveresystolicheartfailure(HF)withincreasedQRSduration.Inadditiontoconferringamortalitybenefit,CRThasbeenshowntoreduceHFhospitalizationratesandimprovefunctionalstatusinthispopulation.However,notallpatientsconsistentlydemonstrateapositiveresponsetoCRT.EffortstoimproveresponsetoCRThavefocusedonimprovingpatientselectionandoptimizingdeviceimplantationandfollow-up,therebycorrectingelectricalandmechanicaldyssynchrony.Inthisarticlewereviewthepathobiologyofcardiacdyssynchrony,therationalefortheuseofCRT,thehistoryandthestateoftheartofCRT,andguidelinesandrecommendationsforCRT,whilealsofocusingontheareasofcontroversyandpotentialfutureapplications.

简介：Oxidativestressplaysanessentialroleinregulatinggrowthanddeathofcardiacmyocytes.ClassⅡhistonedeacetylases（cⅡ-HDACs）arelocalizedprimarilyinthenucleusinunstimulatedcardiacmyocytesandnegativelyregulatecardiachypertrophybyinteractingwithpro-hypertrophictranscriptionfactors,includingmyocyteenhancerfactor2（MEF2）,calmodulin-bindingtranscriptionactivator（CAMTA）,andnuclearfactoractivatedTcells（NFATs）.NuclearlocalizationofcII-HDACsisregulatednotonlybyphosphorylationbutalsothroughoxidationofconservedcysteineresidues（Agoetal2007）,suggestingthatposttranslationalmodulationplaysanimportantroleinmediatingpathologicalcardiachypertrophyandheartfailure.Inthispresentation,Iwilldiscusshowreactiveoxygenspecies（ROS）areproducedintheheartunderstressandhowROSregulatethesubcellularlocalizationofcII-HDACs,therebycausingpathologicalhypertrophy.TheNADPHoxidasefamilyisagroupoftransmembraneproteinsproducingsuperoxideandhydrogenperoxide.Nox4islocalizedprimarilyinmitochondria,endoplasmicreticulum,andnucleus,whoseexpressionisupregulatedbypressureoverloadandheartfailure.Nox4playsanessentialroleinmediatingincreasesinROSinthefailingheart.IncreasedoxidativestressinducesoxidationofcysteineresidesincⅡ-HDACs,suchasC667andC669inHDAC4,whichinturncausesnuclearexitofcⅡ-HDACs.ThecⅡ-HDACsarefurtherphospho-rylatedbytheHDACkinases,includingCa2+calmodulinkinaseandPKD,leadingtoprolongedcytoplasmiclocalizationofcⅡ-HDACsandconsequentcardiachypertrophy.Thioredoxin1（Trx1）,ananti-oxidant,reducesthecriticalcysteineresiduesincⅡ-HDACs,therebyrestoringthenuclearlocalizationofcⅡ-HDACsandinhibitingpathologicalhypertrophy.DownregulationofNox4enhancesnuclearlocalizationofHDAC4,therebyinhibitingcardiachypertrophy,suggestingthatendogenousNox4mediatesoxidationofHDAC4.Insummary,oxidatives

简介：Theearlydiagnosisofcardiacruptureisoneofthekeyfactorsforasuccessfuloutcome.However,theaccuratediagnosisisoftendifficultintheearlystageofinjury,especiallywhensomeobviousseverewoundsarefoundinotherregionsofthebody,1,2fortheyareeasytodisguisethesymptomoftheheart.Wereportacasewithcardiacruptureandlivertraumacausedbytrafficaccident.