简介：标题MINI研究:一个关于对比阿加曲班或肝素作为组织型纤溶酶原激活剂(tPA)的附加剂应用于急性心肌梗死患者的多中心、随机临床试验作者JangI-K,BrownDFM,GinglianoRP,etal

简介：IntroductionRecently,bonemarrowmesenchymalstemcells(MSCs)havebeenreportedtorepairchronicallyinfractedmyocardiumwithdirectinjection.However,itisverydifficulttolocalizetheinjectedcellsontotheischemicareatoregeneratesufficientcardiacmassinthethinnedscararea.Toovercometheproblem,wehaveutilizedourcellsheettechnologybasedontemperature-responsiveculturedishes.Whentheculturetemperatureisreducedfrom37℃to20℃,allcellsconnectedviacell-celljunctionproteinsareharvestedasasinglesheetwithoutusingproteolyticenzymes.Thistechnologyallowsustotransplantstemcellsinvivofortreatmentheartdiseasewithouttheproblemsmentionintheprevious.MethodsMaleClawnminipigswereusedinthisstudy.Bonemarrow(5-7mL)wascollectedundergeneralanesthesia.Histopaqe-1077(15mL),wereaddedtobonemarrowandcentrifuged.Thecellswerecollectedandculturedfor7days.Weseededthebonemarrow-derivedMSCsattheconcentrationof(6×10~5/ml)on60mmdiametertemperature-responsivedishesfor7days.Astheculturetemperaturedecreasedfrom37℃to20℃,MSCsheetdetacheditselfspon-taneouslyandfloatedupintotheculturemedium.Triplelayerswerestackedtogetherrepeatedlyformingspecialmultiplayer.Myocardialinfarctionwascreatedbytheligationoftheleftanteriordescendingbranchoftheleftcoronaryartery.Acellsheetswastransplantedontotheischemiaarea.Theechocardiographywasperformedtwoandfourweeksaftertransplantation.Thehearttissuewithcellsheetswereremovedandfixedwith10%formalinforhistologicalanalysisonemonthafterthetransplantationofcellsheets.ResultsMostMSCsarepositiveforCD29,CD90,CD146andCD73.ThesemeantheculturecellsheetswerecomposedofundifferentiatedMSCsandremainedmultipotent.Monolayers(20-30μm)andmultilayer(120μm)cellsheetswereproduced,whichretainedallcell-to-cellcontaction.Histologicalanalysesshowthecellsheetsbecomecloselycontactedwiththehearttiss

简介：SignificanceofECGChangesinAcuteMyocardialInfarctionSTsegmentelevationisconsideredbymostasasignofanoccludedcoronaryarteryandmyocardialischemia.CoronaryarteryocclusionusuallyisthecauseoftheacuteinfarctioninthepatientwiththattypeofECG.PatientswithacutemyocardialinfarctionwhodonotshowSTsegmentelevationyetleaktroponin,stillhaveamyocardialinfarction.

简介：Theriskofmyocardialinfarctionincreasesinpatientswithdiabetesmellitus.Theincidenceofmyocardialinfarctionissimilarinpatientswithtype2diabeteswithouthistoryofmyocardialinfarctionandinnon-diabeticpatientswithhistoryofmyocardialinfarction.DiabetesmellituswasconsideredasacoronarydiseaseequivalentbytheNationalCholesterolEducationProgram.Strictglycemiccontrolcanimprovethelong-termoutcomeofbothtype1andtype2diabetesmellitus.Whateverwithdiabeticornon-diabetic,strictglycemiccontrolwithintensiveinsulintherapycanreducethemortalityofcriticallyillpatientsinhospital.Aftermyocardialinfarction,therewouldbeaworseoutcomeforpatientswithpoorglycemiccontrol,whateverindiabeticornon-diabeticpatientswithstresshyperglycemia.Meanwhile,strictglycemiccontrolcanimprovetheoutcome.TheguidelineofAmericanCollegeofCardiology/AmericanHeartAssociationin2004onST-elevatedmyocardialinfarctionrecommendedinsulininfusionmaintainingtheeuglycemiaforpatientswithacutemyocardialinfarctionandcomplicatedconditions,whetherwithdiabetesmellitusornot,anditwasconsideredreasonabletoinfuseinsulinforallpatientswithhyperglycemiaduringtheperiodofacutemyocardialinfarction.Thispaperproposedaneffectiveandsafemethodforintravenousinsulininfusiontherapyfordiabeticpatientswithacutemyocardialinfarction.

简介：Managementofthrombusincoronarylesionsremainsachallengethatisfrequentlyencounteredduringprimarypercutaneouscoronaryintervention(PCI)forST-elevationmyocardialinfarction(STEMI)andisusuallyassociatedwithpoorclinicaloutcomes.Atthesametime,theoptimummanagementofsuchlesionsremainsadilemma.Multiplethrombusremovalprocedureshaveemergedwiththeshort-termaimofimprovingmyocardialperfusionandalonger-termaimofdecreasingtheincidenceofbothmajoradversecardiacevents(MACE)andall-causemortality.Inthisreview,wewillhighlightthemainproceduresutilizedforthrombusremovalduringprimaryPCIforSTEMI,withparticularemphasisonaspirationthrombectomy.Wewillalsoapproachpossibletheoriesthatmightexplaintheapparentlackofclinicalbenefitrecentlyshownwithsuchprocedures.

简介：Carvedilol,nonselectiveβ-adrenoreceptorantagonist,wasshowedprotectiveeffectsagainstacutemyocardialinfarction(AMI)-inducedmyocardialinjury,however,themechanismsunderlyingtheantifibrosiseffectofcarvedilolhasnotbeenwellknown.Theaimofthepresentstudywastoinvestigatethepotentialmechanismfortheanti-fibrosiseffectofcarvedilolagainstAMI-inducedmyocardialfibrosisinrats.MethodsMaleSDratswererandomizedintotheshamgroup,LADsurgery-AMImodelgroup,AMIpluslowdoseofcarvediloltreatmentgroup(1mg/kgperday,CAR-L),AMIplusmediumdoseofcarvediloltreatmentgroup(5mg/kgperday,CAR-M)andAMIplushighdoseofcarvediloltreatmentgroup(10mg/kgperday,CAR-H).Thepassage3neonatalSDratcardiacfibroblastswereusedforhypoxia/normoxia(2h/4h)treatmentinthepresenceofcarvedilol(0,1,2and4μM).ResultsCardiacremodelingandimpairedheartfunctionwereobservedafter14-weekLADsurgerytreatment,however,andthecardiacremodelinganddecreasedejectionfraction(EF%)andfractionalshortening(FS%)wereefficientlyrescuedintheCAR-MandCAR-Hgroups.Theup-regulatedexpressionsofCol1a1,Col3a1andα-SMAatmRNAandproteinlevelsweresignificantlyreducedintheCAR-MandCAR-Hgroups.TheinvitrostudyshowedthatCol1a1,Col3a1andαSMAexpressionsatbothmRNAandproteinlevelsweredown-regulatedbycarvedilolinratcardiacfibroblastsinadose-dependentmanner.Smad3inhibitors,SIS-3andnaringenin,couldefficientlydecreaseCol1a1,Col3a1andα-SMAexpressionsinratcardiacfibroblasts.Smad3wasshownsignificantlyinactivatedincarvedilol-treatedratcardiacfibroblasts.ConclusionCarvedilolnegativelyregulatesSmad3signalpathwayandinhibitsextracellularmatrixrelatedCol1a1,Col3a1andα-SMAexpressions,contributingtotheanti-fibrosiseffectofcarvedilolagainstAMI-inducedmyocardialfibrosisinrats.

简介：ObjectiveTofurtherimprovetherateofreperfusionofinfarctionrelatedarteryinAMI,removethestricture,rescueischemicmyocardium,protectcardiacfunctionandamelioratethelong-termprognosis.MethodAmong73patientswithA-MI,50underwentdirectPICA,15immediatePICA,8rescuePTCAand20braceswereimplanted.ResultTheproportionofrecanalizationis94.5%(69/73).Thegradeofbloodflow(TIMI)improvedtograde3in20patientswithbraceimplantation,while44tograde3and5tograde2among49patientswithsimplePTCA.Residualstenosisinvesselwas1.8±5.9(-10-10)%inpatientswithbraceimplantationversus15.4±11.(0-30)%withsimplePTCA.Theincidenceofreperfusivecardiacarrythmiawas18.1%(10/62).Therewasmainlyfrequentventricularprematurebeatandshortparoxysmalventriculartachycardia,ifleftanteriordecendingbranchwasreopened,whilebradycardiaandatrialventricularblockusuallyoccurredafterrightcoronaryreperfused.ConclusionEmergencyP

简介：ObjectiveFortycasesofIAMIwereexaminedwithcoronaryangiographyinordertostudytherelationshipofthevesselswiththeECGofIAMI.MethodsForcoronaryangiographyJudkin’smethodwasused;IAMIwasdiagnosedbythe1979WHO’sstandardofISHDandECGwasseparatelymeasuredbytwodoctors.ResultsMostofIAMIwithpolybranchcoronaryoritscollateraldisease(32.5%and42.5%)andonly10cases(25%)withsinglebranchcoronarydisease,whoseECGswereuntypical.ConclusionIAMIwithsingle-branchcoronarydiseasemightexpressasmildsymptomsandhavenotypicalECGchange.WhiletypicalECGchangeemerges,thecoronaryarteryalwaysshowedpoly-branchdiseaseorcollateralbranchobstructionandthediseasewouldbeadvanced.ItisimportanttopaymoreattentiontothecasesofIAMIwithoutclassicECGchangesoastogivediagnosisandtreatmentthemintime.

简介：ObjectivesToinvestigatetheeffectsofadrenergicreceptorantagonist(metoprololorprazosin)onmyocardialα1-ARdensityandthechangesofventriculareffectiverefractoryperioddispersion(VERP-D)inrabbitsaftermyocardialinfarction.Methodstwenty-fouradultmaleNewZealandrabbitsweredividedintofourgroupsatrandom:controlgroup(n=6);MIwithplacebogroup(n=6);MIwithmetoprololgroup(n=6);MIwithprazosingroup(n=6).Therabbitsreceivedcorrespondingdrugsforsevendays,beginningatthefirstdayafterMIandmyocardialα1-ARdensityweremeasuredandmeanwhile,myocardialβ-ARwasalsomeasured.ResultsIntheplacebogroup,thedensityofventricularα1-ARwasincreasedincomparisonwithcontrolgroup(α1-ARinnormalregion36.9±0.2vs27.3±0.9fmolmg-1Pro-1,p＜0.01;α1-ARinischemicregion33.0±0.9vs26.6±0.4fmolmg-1pro-1P＜0.01).Inthemetoprololgroup,itwasalsoincreasedincomparisonwithcontrolgroup(α1-ARinnormalregion44.7±1.5vs27.3±0.9fmolmg-1pro-1,P＜0.01;α1-ARinischemicregion33.6±0.5vs26.6±0.4fmolmg-1pro-1,P＜0.01).Meanwhilethedensityofventricularα1-ARinnormalregioninthemetoprololgroupwasincreasedincomparisonwithplacebogroup(44.7±1.5vs36.9±0.2fmolmg-1pro-1,P＜0.01).Whileitdecreasedintheprazosingroupincomparisonwithcontrolgroup(α1-ARinnormalregion22.5±0.6vs27.3±0.9fmolmg-1pro-1,P＜0.01;α1-ARinischemicregion20.9±0.4vs26.6±0.4fmolmg-1pro-1,P＜0.01).VERP-DwasincreasedafterMI(P＜0.01).Aftertreatmentwithmetoprololorprazosin,VERP-Dwasdecreased(P＜0.01).ConclusionsAfteracuteMI,α1-ARofventricularmyocardiumwasupregulated,whichmaybeaccompaniedbyitsactivitation.Thedensityofmyocardialα1-ARbecameupregulatedmoredramaticallytreatedwithmetoprololanddownregulatedwithprazosin.Whentreatedwithmetoprololorprazosin,VERP-Ddecreased.

简介：Cholesterolcrystalshavelongbeenrecognizedaspartofatheroscleroticplaques.Theyhavebeenvisualizedbylightmicroscopyasemptyspacesorimprintswherecrystalswereoncepresentandthendissolvedbytissueprocessing.Thus,untilnow,theirroleinatherosclerosisandplaquerupturehadbeenconsideredtobeinert.However,bytheprocessingoftissuewithoutethanolitwaspossibletovisualizetheirextensivenessandpotentialroleintissueinjury.Also,itwasdemonstratedthatcholesterolexpandsinvolumewhencrystallizingfromtheliquidtothesolidstate,whichisthepresumedcauseofplaquerupturebysharp-tippedcrystalsgrowingoutoftheplaque'snecroticcore.Specifically,inpatientswhodiedofmyocardialinfarction,allculpritcoronarylesionshadextensivecholesterolcrystalsperforatingthefibrouscapandintima,whilethosepatientswhodiedofothercausesandhadplaquesdidnothavecrystalsperforatingthecapandintima.Additionally,cholesterolcrystalstravelingdownstreamfromtheplaquerupturesitecanscrapetheendotheliumandpromotevasospasm.Moreover,cholesterolcrystalslodgingintothemusclecantriggeraninflammationwithnecrosisindependentofcirculatorycompromiseorischemia.Thesefindingssuggestthatcholesterolcrystalscouldplayacriticalroleinplaquerupture,aswellasvascularandmyocardialinjury.

简介：CLINICALMATERIALSThepatientwas7year-oldboy,bodyweight20kg.HewasadmittedonMay10th,2002becauseoffever,rashes,enlargedlymphnodes,conjunctivaeinjection,strawberrytongue,edemaanderythemaofthehandsandfeet.Laboratorydataasfollow:1.Prominentincreaseinwhitebloodcell(WBC)14.3-22.7×109.2.Anemia,hemoglobin(Hb)121→103g/L.

简介：ObjectivesLittleisknownaboutthemechanismofexercise-indueedangiogenieresponseinisehemicmyoeardium.Thisstudywasdesignedtoinvestigatetheeffeetsofexercisetrainingonexpressionofvaseularendothelialgrowthfaetorandangiogenesisininfarctedheart.MethodsFiftymaleFVBmiceweredividedintothreesubgroupstotestvariousresponsestoexercise,includingtimedependentresponseofangiogenicfactorstoexercisetraininginintactheart(n=10)andinfarctedheart(n=10),aswellasexercise-inducedangiogenieresponseinheartwithmyocardialinfarction(MI)(n=30).Themiceintheexercise-traininggroupswereallowedtoexercisedailyat1hourperdayfor7days.ResultsVEGFproteinexpressionwasup-regulatedbyexercisetrainingintimedependentfashioninmicewithMI.AngiogenesiswasevidentbyincreasedmyocardialmicrovesselsobservedbyPECAM-1immunohistoc-hemicalstaininginpost-MIexercisegroup(16.5±3.4)/0.4mm^2versuspost-MIsedentarymice(10±2.1)/0.4mm^2(P<0.05).Cellproliferationassessmentshowedsignificantlyhigher(P<0.05)numberofBrdUpositivecellsinpostMImiceinexerciseerouoasopposedtosedentarypostMImice.2%TTCstainingdisclosedaprofounddifferenceinthesizeofMI(18.25±2.93)%inexercisegroupvssedentarygroup(29.26±7.64)%(P<0.05).ConclusionsActivationandup-regulationofVEGFininfarctedmiceheartmaycontributestheangiogenicresponsetoexercisetrainingattheearlystageofmyocardialinfarction.Thisunderscorestheimpactofexerciseonangiogenesisinpostmyocardialinfarctionsetting.

简介：ObjectivesToexaminepatientdelay(PD)inseekingtreatmentamongpatientswithST-elevationmyocardialinfarction(STEMI)andtoidentifyfactorsinfluencingPD.MethodspatientswithSTEMIweredividedintotwogroupsbasedonPD:ShortPDgroup(PD≤60minutesafteronsetofsymptoms)andlongPDgroup(>60minutesaftersymptomonset).Aquestionnairedevelopedtoassessdemographiccharacteristics,clinicalfactorsandpsychologicalfactors.Patientswereinterviewedwithin72hoursofadmissionto2hospitals.Results329consecutiveconfirmedSTEMIpatients(Meanage61years;72.5%men)withamedianPDof90minandapre-hospitaldelaytime170minwerestudied,PDwaslessthan1hoursin47.4%ofpatients,whilemorethan1hoursin52.6%,Inunivariateanalyses,patientswithshortPDwerewitnessonset,progresscourseofsymptom,severepain,deathanxiety,knowingAMIasadeadlydiseaseanditspresentation,takingthesymptomseriously.PatientswithlongerPDwereage≥65year,nocturnalonset,experiencedtheirsymptomsathome,gradualonset,’waitedtoseewhethersymptomsdisappeared’,’worriedabouttroublingothers’,’tookpainmedication’andpreinfarctionangina.Astepwisemultipleregressionanalysisfurthersuggestedthatthefollowinginde-pendentcontributorstoalatedecisiontoseekmedicalhelp(relativerisk,95%confidenceinterval):takingpainmedication(15.97;1.70～149.8),wantingtowaitandsee(6.46;1.92～21.74),notwantingtobotheranybody(6.42;2.87～14.34),preinfarctangina(2.73;1.20～6.19),age≥65years(2.51;1.15～5.48),gradualonset(2.40;1.05～5.44),severepain(0.38,0.17～0.85),witnessonset(0.27,0.10～0.70),takingsymptomsseriously(0.019;0.08～0.46).ConclusionsAge≥65years,gradualonset,witnessonset,severepain,preinfarctangina,emotionalresponsesandcopingstrategiesaretheindependentfactorsassociatedwithpatientdelayordecisiontimeinpatientswithAMI.Emotionalresponsesandcopin

简介：ObjectivesTodetectwhetherpersistingortransientglucosemetabolismdisorderisresponsibleforadmissionhyperglycemiainpatientswithacutemyocardicinfarction(AMI).MethodsTwogroupsofpatientswereenrolled:AMIgroupandcontrolgroup.Fastingplasmaglucose,2hoursplasmaglucose,glycatedalbumin(GA)andglycatedhaemoglobin(HbA1c)weremeasuredatbaselineinbothgroupsand30daysafterAMIattackinAMIgroup.Results(1)Therewerenosignificantdifferencesinbaselinecharacteristicsbetweenbothgroups;(2)Comparedwiththecontrolgroup,thelevelsofGAandHbAlcinAMIgroupatbaselineweresignificantlyhigher.(3)At30dayfollow-upinAMIgroup,bothFBGand2hPGdecreasedtonormalvalues,HbAlcdidnotchange,butonlyGAkeptonincreasing.ConclusionsHyperglycemiaonadmissioninpatientswithAMIresultedfrombothpreexistingmetabolicdisorderandstressreactionaswell.GAistheonlyindicatorthatcouldrecalltheexaggerationofglucosemetabolicdisorderduringAMIattackat30dayfollow-up.

简介：BackgroundThecombinationofglycoproteinⅡb/Ⅲainhibitorsandheparinhasnotbeencomparedwithbivalirudininstudiesspecificallyinvolvingpatientswithnon-ST-segmentelevationmyocardialinfarctionundergoingpercutaneouscoronaryintervention(PCI).Wecomparedthetwotreatmentsinthispatientpopulation.MethodsImmediatelybeforePCI,werandomlyassigned,inadouble-blindmanner,1721patientswithacutenon-ST-segmentelevationmyocardialinfarctiontoreceiveabciximabplusunfractionatedheparin(861patients)orbivalirudin(860patients).Thestudytestedthehypothesisthatabciximabandheparinwouldbesuperiortobivalirudinwithrespecttotheprimarycompositeendpointofdeath,largerecurrentmyocardialinfarction,urgenttarget-vesselrevascularization,ormajorbleedingwithin30days.Secondaryendpointsincludedthecompositeofdeath,anyrecurrentmyocardialinfarction,orurgenttarget-vesselrevascularization(efficacyendpoint)andmajorbleeding(safetyendpoint)within30days.ResultsTheprimaryendpointoccurredin10.9%ofthepatientsintheabciximabgroup(94patients)andin11.0%inthebivalirudingroup(95patients)(relativeriskwithabciximab,0.99;95%confidenceinterval[CI],0.74to1.32;P=0.94).Death,anyrecurrentmyocardialinfarction,orurgenttarget-vesselrevascularizationoccurredin12.8%ofthepatientsintheabciximabgroup(110patients)andin13.4%inthebivalirudingroup(115patients)(relativerisk,0.96;95%CI,0.74to1.25;P=0.76).Majorbleedingoccurredin4.6%ofthepatientsintheabciximabgroup(40patients)ascomparedwith2.6%inthebivalirudingroup(22patients)(relativerisk,1.84;95%CI,1.10to3.07;P=0.02).ConclusionsAbciximabandunfractionatedheparin,ascomparedwithbivalirudin,failedtoreducetherateoftheprimaryendpointandincreasedtheriskofbleedingamongpatientswithnon-ST-segmentelevationmyocardialinfarctionwhowereundergoingPCI.(FundedbyNycomedPharmaandothers;

简介：BackgroundToinvestigatetheassociationbetweenleftventricularremodelingandstresshyperglycemia(SH)inpatientswithacuteanteriorwallmyocardialInfarction.MethodsPatientswithacuteanteriormyocardialinfarctionandasuccessfulprimarypercutaneouscoronaryintervention(PCI)wereenrolledanddividedintotwogroupsaccordingtothepresenceorabsenceofSH.Patientswithdiabetesmellituswereexcluded.Echocardiographicstudieswereperformedondischargeandat6monthfollow-up.Leftventricular(LV)ejectionfractions(EF),LVend-diastolicvolume(EDV)andLVend-systolicvolume(ESV)wereobtainedatbaselineandat6month.DifferencesbetweenchangesofESV(ΔESV)andchangesofEDV(ΔEDV)inthetwogroupsaswellasEFimprovementrate(ΔEF%)oversixmonthwereobtained.CorrelationbetweenSHandLVremodelingwasinvestigated.Results(1)Atbaseline,thelevelofhemoglobinA1cwassignificantlyhigherinSHgroup(6.9±1.4vs6.2±0.8P=0.04).Otherbaselinecharacteristics,includingpeakserumcreatinekinaseMBandLVfunction,weresimilarbetweentwogroups;(2)EFincreasedsignificantlyover6monthsinbothgroupwithSH((41.1±7.2)%vs(52.7±8.4)%,P=0.02)andgroupwithoutSH.((43.6±8.7)%vs(54.5±9.3)%,P=0.03)(3)OnlyinSHgroup,EDVincreasedsignificantlyat6month(139.6±26.7vs126.1±26.7P=0.04);(4)TherewasaweakcorrelationbetweenΔEDVandtheleveloffastingplasmaglucoseonadmission.(Pearson'sr=0.35,P<0.01).Conclusions(1)Previousglucosemetabolismdisorderisatleastpartiallyresponsibleforhyperglycemiaonadmission;(2)GivensuccessfulprimaryPCIwithinrecommendedtimeinterval,leftventricularfunctionimprovedregardlessofwhetherSHispresentornot;(3)Thedegreeofglucosemetabolicdysfunctiononadmissionisweaklyassociatedwiththeremodelingprocessin6months

简介：

简介：ObjectivesTostudytherelationshipbetweenplasmaBNPandcardiacstructural,functionalchangesafterAMI,andtoevaluatetheapplicationofplasmaBNPdeterminationinpredictingtheearlyphaseofventricleremodelingafterAMI.MethodsAMIgroupincluded37patients,allpatientunderwentstrictmedicaltreatment;32healthyindividualswereenrolledascontrols.PlasmaBNPwasdeterminatedbyimmunofluorescence.EchocardiogramexaminationwasusedtodeterminateLVEF,V_E,V_A,V_E/V_A,LVEDd,LVEDV;Allpatientsunderwenttheexaminationsat72h,30daysand90daysafterAMIoccurred,respectively,andwerecomparedwithhealthycontrols.ResultsIncomparingtocontrols,PlasmaBNPinAMI72h,30daysand90dayselevatedsignificantly.LVEDdandLVEDVwereincreasedsignificantlyinall3phasesofAMI,andEF,V_E/V_Aweresignificantlylowerthanincontrols.CorrelationanalysisrevealedthatplasmaBNPlevelin72hafterAMIwaspositivelycorrelatedtoLVEDd,LVEDV,andwaspositivelycorrelatedtoEF,V_E/V_Ain30daysand90daysafterAMI.ConclusionsPlasmaBNPlevelin72hafterAMIisapowerfulindextopredictleftventricleremodelingandventriclefunctionasplasmBNPlevelispositivelycorrelatedtoventricleremodeling;loweringtheplasmBNPlevelmightbeusedasanendpointfortreatmentofheartfailure.

简介：BackgroundIt'saneffectivetreatmenttoachievepercutaneouscoronaryinterventioninAMIpatients,whichrapidlyimprovesthebloodsupplyofcoronaryartery.StudieshaveshownthatdifferentmodesofPCItherapyhavedifferenteffectsinAMIpatients.TheaimofthisstudywastoexploretheeffectsandclinicalsignificancesofemergencyorlatePCItherapyonleftventricularremodelingandcardiacautonomicfunctioninacutemyocardialinfarction(AMI)patients.MethodsOnehundredandfiftycasesofAMIpatientswererandomlydividedintothreegroups,whichallweregiventheroutinemedicine.ThetwotherapygroupsweretheemergencyPCIgroup(n=60)andthelatePCIgroup(n=50).Thevariationsofheartrateturbulence(HRT)andheartratevariability(HRV)parameterswereobservedafter2weeksoftreatmentby24-hourambulatoryECG.ResultsComparedwiththecontrolgroup,after2weeksoftreatment,thelevelsofTS,SDNNandSDANNoftwoPCI-treatedgroupwassignificantlyhigher(P<0.01),TOwerelower(P<0.01)thanwhichinthecontrolgroup.ThereweresignificantdifferencesinTS,SDNN,SDANNandTObetweenthetwoPCItreatmentgroup(P<0.05).ConclusionEmergencyPCIorlatePCImaygivecoronaryeffectivereperfusion,improveleftventricularfunctionandautonomicnervousfunction,andpreventmalignantarrhythmiastooccur.ThetreatmentofprimaryPCIissuperiortodelayedPCI.

简介：BackgroundTheremaybedysregulationofcirculatingmicroRNAsinacutemyocardialinfarction(AMI),whichisanaging-relatedprocess.However,thedifferencebetweenyoungandelderlypeopleinexpressionlevelofcirculatingmiR-21inAMIpatientshasnotbeeninvestigated.MethodsThestudyincluded72consecutivepatientswithAMI.ThegroupIconsistedof43patientsagedequaltoorabove65yearsandthegroupIIconsistedof29patientsagedequaltoorbelow45years.Real-timeRT-PCRwasappliedtodetectserummiR-21expressionlevelsatthetimeofmechanicalreperfusionand12h,D1,D3andD7afterPCI,respectively.ResultsTheexpressionlevelofmiR-21inAMIpatientsincreasedmarkedly12hafterPCIandreachedthepeakatD1afterPCIinbothgroups.TherewasnodifferenceofmiR-21expressionbetweenGroupⅠandⅡatthetimeofmechanicalreperfusion(5.12±0.73vs.4.98±0.87)andD7afterPCI(1.28±0.75vs.1.94±0.89),However,groupⅠpatientsexhibitedhighermiR-21expressionlevelthangroupⅡat12h(7.96±0.78vs.4.23±0.77,P<0.05),D1(9.32±0.89vs.6.12±0.92,P<0.05)andD3(4.78±0.91vs.2.97±0.77,P<0.05)afterPCI,respectively.ConclusionOurdatarevealanincreaseofmiR-21inpatientswithAMImaybeamechanismofmyocardialischemiareperfusioninjury.TheexpressionofmiR-21wasrelatedtothedevelopmentandprogressionofAMI,andthereisanage-relatedchangeintheexpressionofmiR-21inacutemyocardialinfarctionpatients.