简介：ObjectivesToinvestigateserumconcentrationofprocollagentypeIcarboxyterminalpeptide(PIP),typeⅢaminopeptide(PⅢP)andtypeIcollagentelopeptide(ICTP)inessentialhypertension(EH).MethodsSerumlevelsofPIP,PⅢPandICTPin42EHpatientsand30healthycontrolweremeasuredbyradioimmunoassays.ResultsInEHpatients,serumconcentrationofPIP,PⅢPwassignificantlyhigherthanthatin30healthycontrol.AlthoughEHpatientsdidtendtoexhibitahigherserumICTPconcentrationthannormalcontrolsubjects,thedifferencewasnotstatisticallysignificant.EHpatientswithleftventricularhypertrophyexhibitedhighervaluesofPIP(P<0.05)andlowervaluesofICTP(P<0.05)thanEHpatientswithoutleftventricularhypertrophy.NosignificantdifferencewasnotedbetweentheserumPⅢPoftheEHpatientswithandwithoutleftventricularhypertrophy(P>0.05).ConclusionsTheresultssuggestthatPIPandPⅢParesensitiveserummarkersofmyocardialcollagensynthesis.Myocardialfibrosismaybeduetotheexcessivesynthesisandinsufficientdegradationofcollagen.PIP,PⅢPandICTPmaybeindirectmarkersofmyocardialfibrosis.

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

简介：Heartfailure(HF)isacomplexclinicalsyndromethatresultsfromanystructuralorfunctionalimpairmentofventricularfillingorejectionofblood.HFisoneofthemostimportantandsevereendstagesofmanycardiovasculardiseases.EpidemiologicalstudiesofHFhavefocusedmainlyontheprevalence,incidence,mortality,fatality,anddistributionandtemporaltrendsoftheseindicatorsamongdifferentpopulations.ThisreviewhighlightsimportantepidemiologicalstudiesofHFinChina.

简介：Congenitalventricularseptaldefect(VSD)spontaneouscloseinducedbytranscathetertreatmentisrareandhasnotyetbeenreported.WereportononecaseofVSDspontaneouscloseinducedbytranscathetertreatmentina10yearsoldgirl.

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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：INTRODUCTIONCurrently,angiographyiswidelyusedforthediagnosisofcoronaryarterydisease,however,itsdiagnosticaccuracyislimitedbecauseitisunabletovisualizethecoronarywall~(1,2).Fortunately,intravascularultrasound(IVUS)andopticalcoherencetomography(OCT)provideuniqueinsightsoncoronarypathology

简介：ObjectivesIschemiainducedarrhythmia(ventriculartachycardia/ventricularfibrillation)isoneofthemajorcausesofdeath.Potassiumchannelschangearelikelytoberesponsiblefortheischemia-relatedarrhythmias.Cardiacpotassiumcurrentisthemajoroutwardcurrentinvolvedincardiacrepolarization.Thepropertiesofpotassiumchannelshavebeenintensivelystudied.Here,weinvestigatedtheassociationbetweenischemiainducedarrhythmiaandpotassiumchannelsgeneticvariations.Methods23patientswithventriculartachycardia/ventricularfibrillationinducedbyischemiawereselectedasobjects.5MLperipheralbloodweretakenfromeachperson,fromwhichDNAwasextractedus-ingastandardenzymaticphenol-chloroformmethod.Candidategenes(HERG、KCNJ2、KCNQ1、Mink、Mirp1、Kir2.1、KV4.3、Kir3.1、KV1.5、Kir6.1、Kir6.2、Kir2.1)Werescreenedforpotassiumchannelsgenemutationswithdirectsequencingmethods.ResultsHere4potassiumchannelsgenemutationshavebeendiscovered.InthegenecodingfortheATP-sensitiveK~+channelssubunitKir6.2,thereisachangefromvalinetoisoleucineatthepositionof326(V326I).Attheposition448,argininesubstitutesproline(P448R)intheKC-NQ1gene.InthegeneKCNJ2twomutationshavebeenfound(P156L,Q193H).ConclusionsThisstudyimplicatedthatthereisahighrelationshipbetweenischemiainducedarrhythmiaandthemutationofpotassiumchannels.Inordertoidentifythepreciselyrelationshipthereisneedfunctionalanalysis.

简介：BackgroundMicroRNAshaverecentlybeenconsideredasbiomarkersinseveraldifferentcardiovasculardiseases,however,sofartherearenocirculatingmiRNAsdataabouthypertension.Therefore,theaimofthepresentpilotstudywastoidentifycirculatingmiRNAsforhypertensionbiomarkers.MethodsUsinganAgilentmicroarray,plasmamiRNAswereprofiledfromplasmasamplesof10patientswithuntreatedessentialhypertensionand10healthycontrols.CandidatebiomarkersidentifiedintheprofilesweresubjectedtovalidationbyusingquantitativePCRinanindependentsamplesetof20patientswithuntreatedessentialhypertensionand20healthycontrols.Then,weassessedtheselectedmiRNAsforthedetectionanddiagnosisofhypertensionfromplasmasamplesof70patientswithuntreatedessentialhypertensionand20healthycontrols.TheSpearmancorrelationcoefficientwasusedtoassessedtheselectedmiRNAscorrelationswithbloodpressure.Theareaunderthereceiveroperatingcharacteristiccurve(AUC)wasusedtoevaluatediagnosticaccuracy.ResultsTheexpressionsofselected8miRNAswereinvestigatedindependentlyinplasmasamplesfrom10hypertensionpatientsand10healthysubjects.ThelevelsofcirculatingmiR-30c-5p,miR-133b,miR-29b-3p,miR-29a-3p,miR-29c-3p,miR-30a-3p,miR-let7b-3pexpressionweresignificantlydownregulatedinhypertensiongroupcomparedwithhealthygroupandthelevelofhsa-miR-92b-3pwassignificantlyunregulatedbetweenthegroups.WeusedqRT-PCRassaytoconfirmtheexpressionof8candidatemiRNAs,miR-30c-5p(P<0.001),miR-29b-3p(P<0.001),miR-29a-3p(P=0.027),miR-29c-3p(P<0.001),miR-92b-3p(P=0.003),miR-30a-3p(P=0.704),miR-133b(P=0.346),andmiR-let7b(P=0.161).ThediagnosticaccuracyofmiR-30c-5p,miR-29b-3p,miR-29a-3p,miR-29c-3pandmiR-92b-3p,asmeasuredbyAUC,were0.897,0.90,0.829,0.825and0.832,respectively,withallP<0.001.ConclusionsTheplasmalevelsofmiR-30c-5p,miR-29b-3p,miR-29a-3p,miR-29c-3pandmiR-92b-3passociatedwithhypertensionwhichprovideanimp

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简介：ObjectivesToevaluatethechangesoftheplasmaendothelinlevelinpatientswithdilatedcardiomyopathy,andtoinvestigatetherelationshipbetweentheplasmaendothelinlevelandtheseverityofheartfailure,heartsize,leftventricularfunctionandwithornotwithpulmonaryarterialhypertension;thechangesoftheplasmaendothelinlevelbeforeandaftertreatment.MethodsTheplasmaendothelinlevelof30patientswithDCM,30healthycontrolsubjects,andtheirLVEF,PAP,heartsize,plasmaendothelinlevelbeforeandaftertreatmentweredetermined.ResultsTheplasmaendothelinlevelinDCMgroupwassignificantlyhigherthanthatincontrolgroup(135.93±70.65pg/mL)vs(43.65±12.07pg/mL),P<0.05;therewasacorrelationbetweenETlevelandheartsize(r=0.4580,P=0.0109);therewasasignificantnegativecorrelationbetweenLVEFofDCMandETlevel(r=-0.6922,P=0.0021);anditwasasignificantpositivecorrelationbetweenETlevelandpulmonaryarterialhypertension(r=0.8974,P<0.0005).Aftertreatment,theETleveldecreasedsignificantlythanbeforeinDCMgroup(129.15±43.93pg/mL)vs(63.12±22.20pg/mL),P<0.05.ConclusionsPlasmaETlevelmaybeanewparameterofevaluatingseverityofheartfailure,efficacyoftherapyandprognosis.

简介：INTRODUCTIONPulmonaryarteriovenousfistula(PAVF)isararecongenitalpulmonaryvascularmalformationwiththeincidenceof2-3/100,000.Itistheabnormalcommunicationbetweenthepulmonaryarteryandpulmonaryvein.Theclinicalmanifestationsofthisdiseasearevarioussothatitiseasytobemisdiagnosed1.Atpresent,DSAisthegoldstandardforthediagnosisof

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简介：Acuteaorticsyndromeincludesclassicaorticdissection,aorticintramuralhematoma,andpenetratingatheroscleroticulcer–agroupofconditionsthataredefinedbytheirdynamicevolutionandsimilarclinicalmanifestation.Accuratediagnosisandprompttreatmentareessentialasalltheaforementionedconditionsareasignificantthreattoapatient’slife.However,acuteaorticsyndromeandespeciallyaorticintramuralhematomamaybechallengingdiagnosticproblems.Intravascularultrasoundimagingisadiagnosticmethodthatcanbeusefulformorethoroughevaluationoftheaorticlesionandcanparticularlyaidindiscerningthedifferentformsofacuteaorticsyndrome.Wepresentacaseofapatientwithaorticintramuralhematomathatwasmissedbyconventionalimagingstudiesbutwassuccessfullyvisualizedwithintravascularultrasoundimaging.

简介：Leftbundlebranchblock(LBBB),traditionallyviewedasanelectrophysiologicabnormality,isincreasinglyrecognizedforitseffectsonhemodynamicsandpatient’sprognosis[1].Exercisenuclearstudiesfrequentlyshowreversibleperfusiondefectsintheabsenceofobstructivecoronaryarterydisease[2]andsomepatientswithintermittentLBBBdevelopanginacoincidentwiththeonsetofLBBB[3].WereportacaseofintermittentLBBBwithabnormalstresstechnetium99mTcsingle-photonemissioncomputedtomography(SPECT)studyandnormalcoronaryarteryangiography.

简介：BackgroundClinicalapplicationofimplantablecardioverterdefibrillator(ICD)cansignificantlyreducetheincidenceofsuddencardiacdeath(SCD).However,ICDcannotpreventventriculartachycardia(VT)orventricularfibrillation(VF).PreviousstudiesindicatedthatICDcombinedwithreasonableanti-arrhythmicdrugtherapycanimproveanti-arrhythmiceffect.EMIAT,CAMIAandOPTICtrialsreportedthatcombinedtreatmentofAmiodaroneandβreceptorblockerswassuperiortotheirtreatmentalone.Therefore,itisnecessarytogiveanti-arrhythmictreatmentafterICDimplantation.MethodsTotally180ICDimplantationrecipientsenrolledinourhospitalfromJan2011toMarch2014.Amongthem,39recipientsweretreatedwithAmiodarone(GroupA),89recipientsweretreatedwithβblocker(GroupB),and52recipientsweretreatedwithAmiodaronecombinedwithβblocker(GroupC)afterICDimplantation.Patientswerefollowedupfor3to40monthsbymonitoringtheheartrate,LVEFValueandrapidventriculararrhythmiasevents.ResultsTherewerenosignificantdifferencesonheartratebeforeandafterICDimplantationamongthethreegroups(P=1.28,P=0.85),butthechangeofheartratewasstatisticallyhigher(P=0.04)inGroupBcomparedwithGroupAandGroupC.TherewerenostatisticalsignificanceinLVEFvaluebeforeICDimplantationandafterICDimplantationandthechangeofLVEFvalue(P=0.56,P=0.50,P=0.99).TheoccurrencerateofrapidventriculararrhythmiasinGroupA(10.26%)andGroupB(10.11%)wassignificantlyhigher(P=0.04)thaninGroupC(1.92%).whichwaeslightlyincreasedbyAmiodaroneinGroupAandGroupC.Therewere2casesofthyroiddysfunctioninGroupA,1caseinGroupCandnocaseinGroupB.Nopulmonaryinterstitialfibrosiscaseswerefoundinthisstudy.ConclusionsCombinedtreatmentwithAmiodaroneandβreceptorblockerscouldsignificantlyreducerapidventriculararrhythmiaswhencomparedwithtreatmentofAmiodaroneorβblockeralone.

简介：ObjectivesToinvestigatetheanti-apoptoticeffectsofmesenchymalstemcells(MSCs)onhypoxicinjuredcardiacmyocytesinvitro.MethodsMSCswereisolatedfrombonemarrowofSprague-Dawley(SD)rats,andcardiacmyocytesfromneonatalrats.Theratcardiacmyocyteswereco-culturedwithMSCsorMSC-conditionedmediainanoxia(95%N2+5%CO2)for72hours.CellapoptosiswasmeasuredbyHoechst33258staining.TheexpressionofBcl-2andBaxincardiacmyocyteswastestedbyWesternBlot.ResultsTheapoptoticratewas51.6%±2.4%whencardiacmyocyteswereculturedincontinuoushypoxiaandwassignificantlydecreasedwhencardiacmyocyteswerecoculturedwithMSCsorMSC-conditionedmedia(15.1%±5.4%and24.0%±4.2%respectively,P<0.001).ThedecreasedexpressionofBaxinthecardiacmyocyteswasgreatlyrelatedtothedecreasingofapoptosis,buttherewasnodifferenceinBcl-2expressionamongthesegroups.ConclusionsCo-culturedMSCsshowedsignificantanti-apoptoticeffectsoncardiacmyocytesincontinuoushypoxia.ThemechanismmaybetheinteractofcelltocellandparacrineofcytokineswhicheffectedtheexpressionofBaxinthecardiacmyocytes.