简介：Coronaryarterycalcification(CAC)isasanindependentriskpredictorofcardiovasculardiseaseandcanclassifyanindividual’sriskofatheroscleroticcardiovasculardisease,particularlyinintermediate-riskindividuals.Also,CACprogressionisassociatedwithgreaterratesofcardiovascularevents.ThisarticleprovidesavailabledataandexpertrecommendationsforCACbasedoncurrentpublications.WefocusontheutilityofCACforstratificationofindividualsanddescribeitsdiagnosticvalueinidentifyingpatientsatrisk.WealsodescribetheimportantabilityofCACtoderiskapatientwithascoreofzero.

简介：BackgroundAtrialfibrillation(AF)isthemostcommonsustainedcardiacarrhythmiawithouteffectivetreatment.AFisassociatedwithatrialconductiondisturbancescausedbyelectricaland/orstructuralremodel-ing.Buttheroleofconnexin(Cx)43intheregulationofLtypecalciumchannel(LCC)remainsunclear.WehypothesizedthatCx43mightco-localizeandregulatetheLtypecalciumchannelcurrent(ICa,L).MethodsReal-timePCRandwhole-cellpatchclampwereusedtodetecttheexpressionofLCC1csubunitandthecurrentdensityofICa,L,beforeandafterCx43knockingdownrespectively.Theco-localizationofCx43withLCCwasinvestigatedbyco-immunoprecipitationandconfocalmicroscopy.ResultsKnockingdownofCx43significantlyinhibitedthecurrentdensityofICa,LthroughdecreasingthegeneexpressionofLCCα1cinculturedatrium-derivedmyocytes(HL-1cells).Cx43co-localizedwithLCCα1csubunitinatrialmyocytes.ConclusionsCx43regulatestheICa,LinatrialmyoctyesthroughLCC,representingapotentialpathogenicmechanisminatrialarrhythmias.

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简介：ObjectivesToinvestigatethegeneexpressionofcalcium-handlingproteinsinpatientswithrheumaticheartdisease(RHD)andatrialfibrillation(AF).MethodsAtotalof50patientswithrheumaticmitralvalvediseasewereincluded.AccordingtocardiacrhythmanddurationofepisodeofAF,patientsweredividedintofourgroups:sinusrhythmgroup,oaroxvsmalAFre'our,persistentAFforlessthan6monthsgroupandpersistentAFformorethan6monthsgroup.Atrialtissuewasobtainedfromtherightatrialappendage,therightatrialfreewallandtheleftatrialappendagerespectivelyduringopenheartsurgery.TotalRNAwasisolatedandreverslytran-scribedintocDNA.Inasemi-quantitativepolymerasechainreactionthecDNAofinterestandofglyceralde-hyde3-phosphatedehydrogenase(GAPDH)weream-plifiedandseparatedbyethidiumbromide-stainedgelelectrophoresis.MultiplelinerregresswasusedforcorrelationbetweenthemRNAamountandage,sex,rightatrialdiameter(RAd)andleftatrialdiameter(LAd)ResultsThemRNAofL-typecalciumchannelα1osubunit,ofCa^2+-ATPaseandofryanodinereceptorinpatientswithpersistentAFformorethan6monthsweresignificantlydecreased(Pall<0.01)ButnoalterationsofthemRNAlevelsforSRphos-pholambanandcalsequestrinwereobservedinpatientswithpersistentAFformorethan6monthscomparedwithpatientswithsinusrhythm,paroxysmalAFandpersistentAFforlessthan6months(Pall>0.05)Therewasnodifferenceofthegeneexpressionamongthethreeatrialtissuesamplingsites(Pall>0.05).Age,gender,RAdandLAdhadnosignificanteffectsonthegeneexpressionofcalcium-handlingproteins(Pall>0.05).ConclusionsThemRNAexpressionofcalcium-handlingproteinsisdown-regulatedonlyinpatientswithRHDandlong-termpersistentAF.Suchabnormalitiesmayberelatedtotheinitiationand/orperpetuationofAFinthepatientswithRHD.

简介：ObjectivesToinvestigateeffectofAngll,captoprilonsingleguineamyocytesonL-typecalciumcurrentandsodiumcurrent.MethodsMembranepatchclampwholecellrecordingtechniquewasusedtoinvestigateeffectofangll,captoprilonL-Camaximumcurrentdensityandsodiummaximumcurrentdensity.ResutlsAngllincreasedthemaximumcurrentdensitycomparedwithcontrolafterperfused5min,357.7±219.7Vs279.5±240.5PA/PF,increaserateis27.9%,theshapeofcurrent-voltagerelationshipcurvewasunchanged,peakedat+10mv,indicatedthatangllincreasedL-Cacurrentdensityinvoltage-dependent.Afterperfusedwithcaptopril,captopril+angll3,5min,L-Cacurrentwasrecorded,resultssuggestL-Camaximumcurrentdensitydecreasedsignificantlycomparedwithcontrol,incaptoprilgroup,128.4±92.6Vs286.2±89.7,66.7±68.3Vs286.2±89.7,respectively,rateofinhibitionis55.1%,76.6%,respectively.L-Cacurrentfurtherdecreasedincaptoprilpe