简介：Earlyrepolarizationisawell-described,commonelectrocardiographicvariant.Itwasinitiallyfelttobebenign,butinthelasttwentyyearsasuggestedalinkbetweenspecifictypesofearlyrepolarizationandsuddencardiacdeathhasemerged.ThisassociationwashasbeentermedtheJwavesyndromeandincludesboththehighriskearlyrepolarizationandBrugadaECGpatterns.Theoddsofearlyrepolarizationchangebeingassociatedwithpooroutcomesarestillexceedinglysmall.Nevertheless,theassociationofafairlyubiquitousECGfindingwithfatalornearfatalclinicaloutcomeshasraisedconcern.Howcanweidentifythetrulyhigh-riskpatients?IfapatienthasasignificantclinicaleventwithaconcerningECGrepolarizationpattern,whatshouldbedonenext?TheauthorsofthisreviewpresentcurrentinformationregardingtheEarlyRepolarizationandBrugadaSyndromesandhowtoproceedwithdiagnosis,management,andriskstratificationwhenearlyrepolarizationchangeisobservedonECG.

简介：Heartratevariaty(HRV)of85caseswithAMIwasobservedintheearlyphaseafteronsetandrehabilitationphaseatfirstmonthandsixthmonth,andwascontrastedwithsixtimethresholdindicesof111caseswithcoronaryheartdiseaseandthatof35normalcontrol.WefoundtheHRVofAMIwasapperantlylowerintheacutephasethanthatofcoronaryheartdiseaseandnormalcontrols.HRVrecoveredgraduallywithincliningtobestableafterhalfayear,butitwasstilllowerthanthatofcontrols.LowHRVinearlyphaseofAMIsuggestedthepoorprognosis.

简介：ObjectivesItisnotfullyclarifiedhowdiabetesmellitusinducedcardiacdysfunctionandmyocardialultrastructuralchangesintheearlystate.Inthepresentstudy,weprovidedanintegratedapproachtoinvestigateearlychangesinmyocardialfunctionofdiabeticrabbitsandassessedthestructuralalteration.MethodsandResultsDiabeteswasinducedbyalloxaninjection.After30days,echocardio-graphyandleftventricularcannulationwereperformedindia-betic(D,n=8)andcontrolrabbits(C,n=10).Aftercatheterization,animalswerekilledforhistologicalstudies.Hema-toxylin-eosinandMasson’sTrichromestainingoftheheartwereanalyzed.Theultrastructureofleftventriclewasalsoexaminedwithelectronmicroscopy.EchocardiographyrevealedthatearlydiabeticcardiomyopathyhadimpairedLVdiastolicfunctionexpressedbydiminishedE-waves,increasedAwaves,E/AratioreversionandincreasedE-wavedecelerationtime(EDT).Concurrently,LVend-diastolicpressure(LVEDP)anddiastolictimeconstant(T)wereincreased,minimumdP/dt(LV-dp/dt)wasreduced,obtainedthroughcardiaccatheterization.TherewerenosignificantdifferencesinLVejectionfraction(EF),LVpeaksystolicpressure(LVSP),ormaximumdP/dt(LV+dp/dt).Qualitativelightmicroscopyrevealednohistologicchangesinmyocardiumfromdiabeticrabbits.Themostevidentultrastructuralchangewasspottedmyofibrillardamage,whileinterstitialfibrosiswasslight.ConclusionsTheseresultssuggestthatearlydiabeticcardiomyopathyinanimalmodelischaracterizedbyleftventriculardiastolicdysfunction,bothimpairedactiverelaxationandincreasedpassivechamberstiffness.Whereas,leftventricularsystolicfunctioncanremainnormal.Itmightpartlycontributetomyofibrillardamage,butnotmyocardialfibrosis.

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：ObjectivesToobservetheeffectsoftelmisartanandrosiglitazoneandexplorethemechanismonearlyatherogenesisinmaleratswithtype2diabetesmellitus.MethodsFortymaleSDratswererandomlyandequallydividedintofourgroups:controlgroup,type2diabetesmellitusgroup,telmisartangroupandrosiglitazonegroup.HighlipidandhighglucosewereusedforinducingDMinSDrats.Theratswereraisedforsixteenweeks.TC,TG,LDL-CandBG,PGIweremeasured.Theaortaewerecollectedforhistopathlogicalandimmunohistochemicalstudies.Immunohisto-chemistrywasusedtoanalyzetheexpressionofPPAR-γ,VCAM-1andICAM-1inthearterialvesselwall.ResultsComparedwiththecontrolgroup,thelevelofTC,TG,LDL-C,andBGinbloodwereincreasedsignificantly(P<0.01)intype2Diabeticgroup.ThetelmisartanandrosiglitazonetreatmentdecreasedbloodTC,TG,LDL-CandBG.TheexpressionofPPAR-γintype2diabeticgroup,telmisartanandrosiglitazonegroupshadsignificantdifferencescomparedwiththecontrolgroup,buttherewasn'tanysignificantdifferences(P>0.05)amongthosethreegroups.ExpressionofVCAM-1,ICAM-1andthemonocytesinfilitratingintotheintimaoftheaortastelmisartanandrosiglitazoregroupwassignificantlylowerthanthoseindiabeticgroup(P<0.01).Theendothelialdamageoftheaortaeintehnisartanandrosiglitazonegroupwaslessseverethanthatindiabetesmellitusgroup.ConclusionTelmisartanandrosiglitazonecanpreventearlyatherogenesisthroughalleviatingthedamagetothearterialwallbyincreasingtheactivationofPPAR-γandinhibitingtheVCAM-1,ICAM-1expressionandthemonocytesinfilitratingintothearterialwall.

简介：BackgroundMyocardialdamageoftenoccursafterburns.Previously,cardiacenzymeprofilewasoftenmeasuredtodeterminemyocardialinjury,butwashardlyspecific.Inthisstudy,weinvestigatedearlychangesofplasmaN-terminalpro-brainnatriureticpeptide(NT-proBNP)overtimeanditsdiagnosticvalueinburnedpatients.Methods39patientswithheatburnedwereassignedtoheartfailuregroup(n=9),controlgroup(n=30).PlasmaNT-ProBNPandtroponinI(cTnT)weremeasuredat1st,3rd,5thdaysand7thday,andpatientsweresubdividedinto2groupsaccordingtotheircardiacfunction.ResultsNinepatientshadheartfailure(27.7%)andtheirNT-proBNPwas1676.03±2190.41pg/L.Significantdifferencewasfoundbetweentheheartfailuregroupandcontrolgroup(P<0.01).ConclusionNT-proBNPisrelatedtotheseverityofburningandcanwellreflectthestatusofmyocardialinjuryinpatientswithsevereburn,andcanbeusedasanidealmarkerformyocardialinjuryinburnedpatients.

简介：ObjectiveThecoronaryanatomicfeatureanddevelopmentafterthrombolysisinacutemyocardialinfarction(AMI)werestudied.Mehtods100patientswithAMIreceivedurokinaseandstrepokinase.Coronaryangiography(CAG)wasperformedat90minutsandagainat3to4weeks.ResultsSuccessfulthrombolysisoccurredin60cases,butfailedin40.Theratioofreperfusionwas60%.CAGshowedtherewereresidualthrombiin84patients(84%)andcompletecoronaryocclusionin40(40%).Angiographyat3to4weeksafterthrombolysisshowedthestenosisworsenedin8patientsandimprovedin10.ConclusionAMIiscausedbysuddencoronarythromboticocclusionandcanbereperfusedbyusingthrombolyticagentormechanicalmethods.Throm-bolyticagentsusuallycannotresolvethrombicompletely.Sopercutaneoustransluminalcoronaryangiography(PTCA)isrecommendedasanimportantmethodtoimproveseriousresidualstenosis.

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简介：ObjectivesEndothelialdysfunctionistheearliestmarkerforatherosclerosisandplayskeyroleinthepathogenesisofcardiovasculardiseases.Thepresentstudywasperformedtoevaluateeffectofagingonarterialelasticitybyusingpulsewaveformanalysisandinvestigatewhetherthechangesinarterialelasticitycanbeusedasanon-invasivemeasureforearlydetectionofendothelialdysfunction.MethodsUsingmodifiedWindkesselmodelofthecirculationandpulsewaveformanalysis,C1largearteryandC2smallarteryelasticityindicesof204normalhealthysubjects(age15-80years)weremeasured.Amongthemtwenty-fourmalehealthysubjectsweredividedintoboththeyoung(age20-30years,n=12)andelderly(age60-70years,n=12)groups.Wedeliveredacethycholine(Ach),anendotheliumdependentvasodilator,andsodiumnitroprusside(SNP),anendothelium-independentvasodilator,todermalvesselsoftheforearmusingiontophoresis,respectively,andmeasuredbasalandpeakbloodflowusinglaserdopplerfluximetry.ResultsC1largearteryandC2smallarteryelasticityindiceswerereducedwithadvancingage.C1largearteryandC2smallarteryelasticityindiceswerenegativelycorrelatedwithage(r=-0.628,p＜0.001;r=-0.595,p＜0.001).Basalbloodflowwassimilarbetweentheyoungandelderlygroups(14.58±3.4vs13.52±3.41PU,p=NS).PeakbloodflowinducedbyAchwassignificantlyreducedintheelderlygroupcomparedwiththeyounggroup(83.4±11.9vs93.75±10.87PU,p＜0.05).However,peakbloodflowinducedbySNPwassimilarinthetwogroups(119.17±16.76vs128.33±21.29PU,p=NS).Ach-inducedpeakbloodflowcorrelatedpositivelywithC1largearteryandC2smallarteryelasticityindices(r=0.56,p＜0.01;r=0.53,p＜0.01).ConclusionsAdvancingageleadstoimpairedarteryelasticityandendothelialdysfunction.Reducedarterialelasticityis,inparallel,associatedwithdiminishedendothelium-dependentvasodilation.Itisconcludedthata

简介：BackgroundCurrentlyusedheartvalveprosthesesareassociatedwithanticoagulationcomplicationsorlimiteddurability.Theadvancementofstemcellstudyandtissue-engineeredheartvalveresearchmayofferarelativelyidealsolutiontotheseproblems.MethodsBonemarrowwasaspiratedfromsternumoflambgoatstoisolateBMCs.Cellswereidentifiedbyflowcytometryanditscapacityofdifferentiation.CellularviabilitywasassessedwithRhdomine123staining.1×107cellswereseededonapatchofPGAsheet.Aftertwo-dayinvitroculture,theautologouscell/scaffoldsheetswereusedtoreplacetherightposteriorpulmonaryvalveleafletsundercardiopulmonarybypass.Theleafletswereexplantedat2days,2,6,8and10weeksafterimplantation.Thesampleswereexaminedmacroscopically,histologically,immunohistochemically,andbyScanningElectronMicroscope(SEM).Twogoatswereimplantedwithacellularsheetsandestablishedasacontrolgroup.ResultsBMCsexhibitedfibroblastoidmorphologywithgoodviability.FlowcytometryshowednegativeCD14andCD45expression.InvitroculturedBMCsdemonstratedthepotentialtodifferentiateintoadipocytes.Theexplantedleafletsresembledthecharacteristicsofnativeleafletsmacroscopicallyinthecellulargroup.Histologyshowedextracellularmatrixwassynthesizedandcellsweredistributedinthesingle-layeredleaflets.ImmunohistochemistryrevealedpositivestainingforvonWillebrandfactor,α-SMA,vimentin.AconfluentcellsurfacewasformedontheexplantedTEHLs.Nocalciumdepositedontheleaflets.Incontrolgroup,theacellularscaffoldswerecompletelydegraded,withoutleafletremainedat8weeks.ConclusionsItispossibletocreatetissue-engineeredheartvalvesinvivousingautologousbonemarrow-derivedcells.

简介：BackgroundAnomalousoriginoftheleftcoronaryarteryfromthepulmonaryarteryisararecongenitalcardiaclesionresultinginmyocardialischemiaeveninfarction,morphologicalimpairmentanddysfunctionofleftventricle,togetherwithmitralregurgitation.Herewewillintroduceourexperienceinthesurgicalrepairofthiskindofcongenitallesionandtheretrospectiveanalysisabouttheimprovementofleftventriculardimensionandmitralregurgitationinearlypostoperativeterm.MethodFromMay1998toJuly2012,38consecutivepatientswithanomalouscoronaryarteryfromthepulmonaryarteryunderwentsurgicalcorrection(33receivedleftcoronaryarteryre-implantation,4leftcoronaryarteryligationorprimaryclosure,1Takeuchiprocedure,and10simultaneousmitralvalveplasty).Leftventriculardimension,mitralregurgitation,andejectionfraction,weremeasuredbycolorDopplerechocardiographypreoperatively,and1monthafterdischarge.ResultsHospitalsurvivalwas94.7%(2in-hospitaldeaths).Tenpaptientswithmorethanmoderatemitralregurgitationreceivedsimultaneousmitralplasty,oneofwhomwasconvertedtomechanicalprostheticvalvereplacement.Mitralvalveannuloplastywasappliedin9casesofcoronaryre-implantationcorrection,3ofwhomalsoreceivedadditionalmitralleafletcleftrepair.Meanwhile8patientsunderwentotherdifferentconcomitantoperations.Echocardiographicresultsforthesurvivals1monthafterdischargeshowedthatleftventricularend-diastolic,endsystolicdimensiondecreasedfrom40.05±5.56mmand28.94±6.21mmto33.07±6.82mm(P<0.01)and23.04±5.87mm(P<0.01)respectively.Theaveragemitralregurgitationgradewasalsoreducedfrom2.36±1.08to1.64±93(P<0.05)inthegroup.AllsurvivalpatientsimprovedclinicallyandNYHAfunctionalclassdecreasedsignificantlyfrom2.37±1.08to2.10±0.54(P<0.05).ConclusionsThesurgicalrepairofanomalousoriginoftheleftcoronaryarteryfromthepulmonaryarteryissafeandeffective,andcange

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简介：BackgroundTheearlyendothelialdysfunctionofcarotidarteryinpatientswithtype2diabetesmellitus(T2DM)hasbeenrecognized.However,thefeasibilityandsignificanceofcarotidarteryendothelialdysfunctiondetectedbyultrasoundradio-frequencytechnologyhasbeenseldomstudied.MethodsThe2Dultrasoundimagesofthebilateralcommoncarotidarteriesfrom112casesofT2DMpatientsand50casesofnormalsubjectsinourhospitalwerecollectedtomeasureintima-mediathicknessmeans(IMTm),end-systolicinnerdiameter(Ds),end-diastolicinnerdiameter(Dd),resistanceindex(RI),pulseindex(PI),andthesystole/diastoleratio(S/D).Wealsoobservedthevariationoftheintima-mediathickness(IMT)aswellastheelasticityindexesofthecommoncarotidartery,suchasthecompliancecoefficient(CC),elasticitycoefficient(β),pulsewavevelocity(PWV)andaugmentationindex(AIx)throughinstrumentswithbuilt-inultrasoundradio-frequencytechniques,includingquantitativeintima-mediathickness(QIMT)andquantitativeanalysisofarterialstiffness(QAS).Thedifferencesoftheabove-mentionedparametersbetweenthetwogroupswereanalyzed.ResultsTherewerenostatisticallysignificantdifferencesinIMTm,Ds,Dd,RI,PIandS/DraitoofthecommoncarotidarteriesbetweengroupT2DMandthenormalgroup(P>0.01).Theβ,PWVandAIxingroupT2DMwereremarkablyhigherthanthoseinthecontrolgroup,withCCvaluebeingsignificantlylowerthanthelater(P<0.01or0.05).ConclusionUltrasoundradio-frequencytechniqueoffersearlierandmoreeffectiveevaluationofcarotidarteryendothelialdysfunctioninT2DMpatientswhencomparedwithconventional2Dultrasound,establishingimagingfoundationfortheearlypreventionandtreatmentofcardio-cerebrovascularcomplicationsinT2DMpatients.