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：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

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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：BackgroundAsforthepatientswithcoronaryarteriosclerosis,thepresenceofischemicmyocardialsurvivalissignificantforthetreatmentandprognosis.Gated13N-NH3and18F-FDGPET/CTimagingprovidesmyocardialperfusion,metabolismandcardiacfunctionwhichcanvaluatemyocardialviabilityaccuratelyandnoninvasively.MethodsFourpigsweresubjectedtobilateralinternalmammaryarteryY-bypassoperationinoperatingroom.ThepigsundertheanesthetizedstateweresenttoPETcenterwhentheoperationfinished.Then13N-NH3gated-PET/CTand18F-FDGgated-PET/CTwereperformed.ResultsThemyocardialperfusionandmyocardialmetabolismiswell-distributedofleftventricularwall.Themotionofthewallwasnormal.Theejectionfunctionwasgreaterthan50%.ConclusionGated-PET/CTcanbeusedfornoninvasiveevaluationofmyocardialperfusion,myocardialmetabolismandleftventriclefunction.

简介：BackgroundMyocardialbloodflow(MBF)canbequantifiedwithmyocardialcontrastechocardiography(MCE)duringavenousinfusionofmicrobubble.AminimalMBFisrequiredtomaintaincellmembraneintegrityandmyocardialviabilityinischemiccondition.Thus,wehypothesizedthatMCEcouldbeusedtoassessmyocardialviabilitybythedeterminationofMBF.MethodsandResultsMCEwasperformedat4hoursafterligationofproximalleftanteriordescendingcoronaryarteryin7dogswithconstantvenousinfusionsofmicrobubbles.Thevideointensityversuspulsingintervalplotsderivedfromeachmyocardialpixelwerefittedtoanexponentialfunction:y=A(1-e-βt),whereyisⅥatpulsingintervalt,Areflectsmicrovascularcross-sectionalarea(ormyocardialbloodvolume),and(3reflectsmeanmyocardialmicrobubblevelocity.TheproductofA·β　representsMBF.MBFwasalsoobtainedbyra-diolabeledmicrospheremethodserveredasreference.MBFderivedbyradiolabeledmicrosphere-methodinthere

简介：BackgroundMyocardialfibrosisisoneprocessofthevariousheartdiseases,whichleadstocommonpathologicalchangeswhenitdevelopstoacertainstage.Itisthemaincauseofventricularremodelingwhicheventuallyleadstodifferentdegreesofcardiacdysfunction,malignantarrhythmiasandsuddencardiacdeath.Manystudieshaveshownthatvariouscytokinesplayaveryimportantroleinthedevelopmentofmyocardialfibrosis.Thispaperreviewsthelatestresearchesontheroleofcytokinesinmyocardialfibrosis.

简介：AbstractThe regeneration capacity of cardiomyocytes (CMs) is retained in neonatal mouse hearts but is limited in adult mouse hearts. Myocardial infarction (MI) in adult hearts usually leads to the loss of large amounts of cardiac tissue, and then accelerates the process of cardiac remodeling and heart failure. Therefore, it is necessary to explore the potential mechanisms of CM regeneration in the neonates and develop potential therapies aimed at promoting CM regeneration and cardiac repair in adults. Currently, studies indicate that a number of mechanisms are involved in neonatal endogenous myocardial regeneration, including cell cycle regulators, transcription factors, non-coding RNA, signaling pathways, acute inflammation, hypoxia, protein kinases, and others. Understanding the mechanisms of regeneration in neonatal CMs after MI provides theoretical support for the studies related to the promotion of heart repair after MI in adult mammals. However, several difficulties in the study of CM regeneration still need to be overcome. This article reviews the potential mechanisms of endogenous CM regeneration in neonatal mouse hearts and discusses possible therapeutic targets and future research directions.

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：ObjectivesToinvestigatetheprotectiveeffectofthrombopoietin(TPO)onmyocardialcellsinvitro.MethodsH9C2celllinewasmaintainedinIscove’smodifiedDulbecco’smedium(IMDM)supplementedwith10%calfserum.Beatingcellsfromheartventriclesofneonatalheartwereculturedataninvitrosystem.Apoptosisofthecelllineabovewasinducedbytreatmentofdoxorubicin(DOX)andwasblockedbyTPO.CellsurvivalrateofH9C2cellwasmeasuredbytheMTTassay.Changesofbeatingrateofneonatalmyocardialcellswerecapturedbydigitalcameraandbeatingratewascalculated.Flowcytometrywasemployedtostudyanti-apoptoticeffectofTPObystainingJC-1proteintoH9C2cell.ResultsMTTassaydemonstratedthatdoxorubicinreducedcellsurvivalrateby73.8%±1.1%,50ng·mL-1and100ng·mL-1TPOincreasedcellsurvivalrateby84.6%±3.6%(P<0.05),86%±4%(P<0.01)atadose-dependentmanner.Beatingrateofprimaryneonatalmyocardialcellsalsodecreasedto15%±8%at48h,100ng·mL-1TPOimprovedbeatingrateto48%±11%(P<0.01).TPOdecreasedapoptoticratefrom19%±9%to11%±6%(P<0.05).ConclusionsTPOhasprotectiveeffectonmyocardialcellsinvitro.Anti-apoptosisisoneofthemechanismsbywhichTPOprotectsinjuredheart.

简介：T1mappingusingcardiovascularmagneticresonance(CMR)introducesnoveltechniquesformyocardialtissuecharacterizationtodetectandquantifydiseaseprocessesoccurringatthemicroscopiclevel.EventhoughT1mappinghaslimitedspatialresolution,cellularandmolecularchangesoccurringwithineachvoxelcanaffecttheaggregateT1signalrenderingthemquantifiable.TheestimatedT1-basedparametersquantifiedona“map”demonstratethespatiallocalizationofthesechangeswherebyeachpixelexpressesthequantitativevalueofthatparameter.Thisquantificationpermitsdetectionofdiffusediseaseevenifitisnotdirectlyvisible.Ratherthanrelyingonnonspecificfunctionalmeasures,T1mappingfocusesonintrinsicchangesofmyocardialcompositionthatadvancesunderstandingaboutspecificdiseasepathways.Thesechangesinmyocardialtissuecompositioninformdiagnosisandprognosis.T1mappingencompassestwokeyparameters:native(i.e.,precontrast)T1andextracellularvolumefraction(ECV)derivedfromadditionalpostcontrastT1andbloodT1measurements.Theseadvancesintroducenewtoolstodetectfocalanddiffusemyocardialderangementsoccurringincardiacdiseasethatcanbeotherwisedifficulttodetect.T1andECVmappingfosterprecisionmedicineandpersonalizedcare,promisingtoimprovepatientoutcomesthroughtargetedtherapy.CapitalizingontheopportunitiesintroducedbyT1mappingandECVrequiresfurtherinvestigation.

简介：BackgroundMyocardialfibrosisplaysacriticalroleintheprocessofdiabeticcardiacremolding.MicroRNAs(miRNAs)areendogenous,smallnon-codingRNAsthatnegativelyregulategeneexpressionindiversebiologicalandpathologicalprocesses.However,therolesofmiRNAsinmyocardialfibrosishavenotbeenwellelucidated.Inthepresentstudy,miRNAsprofilesinthefibroticmyocardiumofdb/dbmiceandmiRNAsexpressioninTGF-β1-stimulatedmousecardiacmyofibroblastswasexamined.MethodsHeartfunctionof18-week-olddb/dbmiceanddb/mcontrolmicewasdetectedbyechocardiography.miRNAexpressionprofileindiabeticmyocardiumwasdetectedbymiRNAmicroarray.Quantitativereal-timePCRwasusedtodeterminetheexpressionoffibrosis-relatedgenesandmiRNAprecursorsofinterest.Westernblotwasusedtodetectthelevelsoffibrosis-relatedproteins,activatedSmad3andtotalSmad3.ResultsTheresultofechocardiographyshowedthatleftventricularsystolicanddiastolicfunctionwasimpairedin18-week-olddb/dbmicewithoutsignificantchangeofejectionfraction(EF)andfractionalshortening(FS).Fibrosis-relatedgenesexpressionwasupregulatedandtheamountofphosphorylatedSmad3wasincreasedsignificantlyinthediabeticmyocardium.miRNAsdysregulationwasshownindiabeticmyocardium,sixty-eightmiRNAs,includingmiR-208b,miR-29b,miR-26bandmiR-30e,wereincreasedovertwo-fold,meanwhile,sixty-twomiRNAsweredecreasedmorethantwo-foldinthemyocardiumofdb/dbmicecomparedtodb/mcontrols.InparallelwithasignificantupregulationofCol1a1,Col3a1andCTGFmiRNAexpression,miR-208b,miR-29b,miR-26bandmiR-30eprecursorswerealsoshowntobeupregulatedinTGF-β1-inducedC57bl/6mousecardiacmyofibroblasts.ConclusionsmicroRNAsweredysregulatedindiabeticmyocardium,withtheactivationofTGF-β/smad3pathway,contributingtodiabeticmyocardialfibrosis.

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.

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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：摘要ObjectiveTo investigate a 5-generation Chinese Han family with PRKAG2 cardiac syndrome resulting from mutations in the PRKAG2 gene encoding the AMP-activated protein kinase (AMPK) gamma 2 subunit and the treatment of myocardial hypertrophy in patients with PRKAG2 cardiac syndrome.MethodIn this study, a 5-generation Chinese Han family (n = 40) with complete atrioventricular block and asymmetric interventricular septal hypertrophy was taken as the research object, and the DNA were obtained from 30 of them (6 patients and 24 normal persons). Objective gene capture combined with high-throughput sequencing technique was used to detect the genes of family members. After the gene diagnosis was confirmed, the cardiac data of patients taking beta-blockers in this family were analyzed retrospectively with the average annual increase in thickness of interventricular septum (expressed in mm/year) as an index.ResultsA total of 6 family members were associated with PRKAG2 (c.905G>A; pR302Q) heterozygous variation. The phenotype of pedigree patients is characterized by complete atrioventricular block and asymmetric interventricular septal hypertrophy, which has high homogeneity. No syncope occurs after implantation of permanent pacemaker, but atrial flutter and atrial fibrillation occur. The 5 patients with PRKAG2 cardiac syndrome in the family took beta-blockers for a long time, and the progress of cardiac hypertrophy was significantly delayed.ConclusionsOur results suggest that the possibility of PRKAG2 mutations should be considered in patients with complete atrioventricular block and asymmetric interventricular septal hypertrophy, and that prompt implantation of pacemakers and long-term use of beta blockers may improve the prognosis of PRKAG2 cardiac syndrome patients.

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.