简介：Elevatedheartrateisamajorriskfactorforcardiovasculardiseases.Theinhibitoroffunnycurrent(I(f)),ahyperpolarization-activatedcyclicnucleotide-gatedchannelcurrent,ivabradineisanewagentselectivelyreducingheartratedevoidofothercardiovasculareffects,whichhascomeintothemarketinEuropeformorethan3years.Ithasbeenapprovedthatpureheartratereductionbyivabradinecanimprovemyocardialischemia,endothelialfunctionandmyocardialcontractilefunction.Long-termadministrationwillnotincreaseall-causemortality.Itstherapeuticvalueinstablecoronaryarterydiseasehasbeenverifiedinclinicalpractice,whileinotherfieldsofcardiovasculardiseasesstillneedsmoreevidence-basedmedicalresearch.Thisarticleisareviewaboutitsrecentresearchadvancesinexperimentalandclinicalstudies.

简介：Thereisagrowingneedworldwidetotakemedicalcaretodistantlocationsfarfromthemainurbancenters,particularlytoruralareas.Furthermore,thereistheethicalimperativetoprovideequalaccesstomedicalcaretoallpatients,regardlessoftheirplaceofresidence,soastosatisfyanincreasinglydemandingpopulation.Awidespreadproblem,fromwhichcardiologyisnotexcepted,istheinsufficientnumberofspecialistsandtheirunevendistribution.Theupsurgeininformationandcommunicationstechnologyhasmadeavailablealargecollectionoftools,mainlycomputers,smartphones,e-mail,andtheInternet,tonamejustafew,tomeettheneedsofcommunicationbetweenindividualsandorganizations.ThisarticledefinestelemedicineanddescribesitsapplicationinthepracticeofcardiologyanditsimpactinChile.

简介：BackgroundRecentstudieshaveshowedthatperivascularadiposetissue(PVAT)maysecretetheadventitial-derivedrelaxingfactor(ADRF)toaffectvascularfunction.However,thefunctionalchangeofADRFinhypertensivestatusisseldomstudied;andthemechanismsofADRFremainunclear.OurstudyexaminedtheADRFsecretedbyperivascularadiposetissueofcontrolratswithnormalbloodpressure(WistarKyotorats,WKY)anddiscussedthemechanismsofADRF;WeobservedthefunctionalchangeinADRFofperivascularadiposetissueinspontaneouslyhypertensiverats(SHRs).MethodThetwoadjacentthoracicaortaringsofSHRandWKYratsweredividedintonakedvesselsubgroupandPVATsubgroup.Thedifferencesofvascularcontractilitybetweenthetwosubgroupsinducedby10-6mmol/Lphenylephrinewerecompared.TheeffectofPVATculturemediumofWKYonthevasculartensionofFat(-)vesselswasobservedbyliquidtransfermeasure.ThemechanismofADRFwasdeterminedbytooldrugs.ResultsInWKYgroup,vascularcontractilityofFat(+)subgroupwaslowerthanthatoftheFat(-)subgroup(P<0.05);whileinSHRgroup,therewasnodifferencebetweenthetwosubgroups(P>0.05).TransferringtheincubationsolutionofWKYFat(+)subgrouptothematchedFat(-)subgroupinducedrapidvasodilation.WhenincubatingbloodvesselsincalciumfreePSSsolution,therewasnosignificantdifferenceofphenylephrine-inducedvasoconstrictionbetweenFat(-)andFat(+)subgroup.Bothglibenclamide,theblockerofATP-sensitivepotassium(KATP)channelandTetraethy-lammoniumchloride(TEA),theinhibitorofcalcium-dependentpotassium(KCa)channel,effectivelyinhibitedvasodilationfunctionofADRF.ConclusionsPerivascularadiposetissueinWKYreleasesADRFwhichcancausevasodilation,whilethisfunctionwasinhibitedinSHR.ADRFactsthroughtheactivationofKCaandKATPchannelsandcalciumionisinvolved.

简介：ObjectivesToevaluatetheeffectofdifferentstylesofcoronaryheartdisease(CHD),differentregionsofacutemyocardialinfarction(AMI),itsriskfactorsandbranchesofcoronarystenosisonleftventricularremodelinganddysfunctionbyapplyingechocardiography.Methods251patientswithCHDand96patientswithoutCHD(NoCHD)wereverifiedbyselectivecoronaryangiography.CHDpatientsweredividedintostableanginapectoris(SAP)26,unstableanginapectoris(UAP)53,acutemyocardialinfarction(AMI)140andoldmyocardialinfarction(OMI)30basedonclinicalsituation,cTnT,cardiacenzymeandEGG.AMIpatientswerefurtherdividedintosubgroupsincludingacuteanteriormyocardialinfarct(Aa,n=53),acuteinferiormyocardialinfarction(Ai,n,=54)andAa+Ai(n=33)basedonECG.Cardiacparameters:end-diastolicinterventricularseptumthickness(IVSd),end-diastolicleftventricularinternaldiameter(LVd),leftventricularmass(LM),end-diastolicleftventricularvolume(EDV),end-systolicleftventricularvolume(ESV)andleftventricularejectionfraction(LVEF)weremeasuredbyACUSON128XP/10echocardiography.MultipleslinearregressionanalyseswereperformedtoteststatisticalassociationsbetweenLVEFandtheinvolvedbranchesofcoronarystenosis,bloodpressure,lipids,glucoseandetcafteronsetofmyocardialinfarction.ResultsEDVandESVwereincreasedandLVEFdecreasedonpatientswithAMI,OMIandUAP(P<0.05-0.0001).LMwasmainlyincreasedinpatientswithOMI(P<0.01)andLVdwasmainlyenlargedinpatientswithAMI.EFwassignificantlydecreasedandEDV,ESV,LMandLVdwereremarkablyincreasedinAMIpatientswithAaandAa+Ai.WiththemultiplelinearregressionanalysesbySPSSsoftware,wefoundthatLVEFwasnegativelycorrelatedtotheinvolvedbranchesofcoronarystenosisaswellastosystolicbloodpressureafteronsetofmyocardialinfarctionwhiletherewasnosignificantcorrelationbetweenLVEFandotherfactors.LVEFwassignificantlydecreased,and

简介：ObjectivesToinvestigatetherelatedpathogenicfactorsofhypertensionaffectingthemiddle-agedinsuburbanareasinMudanjiangCityandfurtherpopularizehealtheducationwithregardtohypertension.MethodsAsurveywasconductedon858middle-agedpeopleof35to59yearsoldfromsuchsuburbanareasasJinglongvillage,BadavillageandFengshouvillagebyadoptingthehypertensivedefinitionandclassifyingstandardofanWHO/ISHhypertensivetreatmentguidancein1999.ResultsPositivecorrelationwasshownbetweenoccurrenceofhypertensionandsuchelementsasdietinexcesssalt,drinking,obesity,smoking.ConclusionsItisofgreatclinicalsignificancetocombatandpreventthehypertensionbyregulatingone'sdietandlifestyle.

简介：BackgroundTheregulationoft-PAgeneistheessenceandcoreofthrombosis.Therefore,thepresentstudyaimedtopreparenanot-PAgenecoatedstentandtoobserveitseffectoncoronarystentthrombosisindogs.MethodsHighlyexpressedt-PAgeneplasmidwasconstructedandalbuminnanot-PAgenecoatingstentwasprepared.Themajorbranchvesselsofdogcoronaryarterywerepre-expandedwitha3.0mm×20balloonwith8-10atmosphericpressure.10dogsofthecontrolgroupwereimplantedwithbaremetalstent;while12dogsoftheexperimentalgroupwereimplantedwithnanot-PAgenecoatingstent.Bothgroupswerenotgivenanti-coagulationtreatments.Bloodsamplesweretakenfort-PAandD-dimerbeforetheoperation,at1,2,4and8weeksafteroperation.Pathologicalanalysisfoundthrombosisinthecavityandthehyperplasiaoftheintima.t-PAexpressionwasdetectedbyimmunohistochemicalindirectly,andthethicknessoftheintimaofthesectioncrosswasdirectlymeasuredbymorphometry.Liver,heart,kidneysandlungweretakenforpathologicalobservation.ResultsAllexperimentalanimalssurvivedatpostoperative8weeks.Vascularstentthrombosiswasseenin10casesofthecontrolgroupwiththethrombosisrateof100%;whilewasseenin2casesamong12casesoftheexperimentalgroupwiththethrombosisratewas16.67%(P=0.00087).Immunohistochemicalstainingshowedthatthepositivet-PAgenetransfectionoftheexperimentalgroupwasmainlydistributedonthesurfaceofhyperplasiaintima,andvascularwallt-PAexpressionofthecontrolgroupwasnegative.Positivet-PAsignalwasnotfoundintheliver,heart,kidneysandlung.ConclusionNanot-PAgenevectorcoatingstentcaneffectivelyexpresst-PAinvascularwallandeffectivelypreventsstentthrombosis.

简介：ObjectivesToconstructarecombinantplasmidcarryingenhancedgreenfluorescentprotein(EGFP)andhumanvascularendothelialgrowthfactor(VEGF)121geneanddetectitsexpressioninratmesenchymalstemcells(MSCs).MethodsHumanVEGF121cDNAwasamplifiedwithpolymerasechainreaction(PCR)frompCD/hVEGF121andwasinsertedintotheeukaryoticexpressionvectorpEGFPC1.AfterbeingidentifiedwithPCR,doubleenzymedigestionandDNAsequencing.TherecombinantplasmidpEGFP/hVEGF121wastransferredintoratMSCswithlipofectamine.TheexpressionofEGFP/VEGF121fusionproteinweredetectedwithfluorescencemicroscopeandimmunocytochemicalstainingrespectively.ResultsTherecombinantplasmidwasconfirmedwithPCR,doubleenzymedigestionandDNAsequencing.ThefluorescencemicroscopeandimmunocytochemicalstainingresultsshowedthattheEGFPandVEGF121proteinwereexpressedinMSCs48haftertransfection.ConclusionsTherecombinantplasmidcarryingEGFPandhumanVEGFwassuccessfullyconstructedandexpressedpositivelyinratMSCs.ItoffersapromisetoolforfurtherresearchondifferentiationofMSCsandVEGFgenetherapyforischemialcardiovasculardisease.

简介：ObjectivesTocomparethedifferenteffectsoflatesuccessfulreperfusionwithPCIonleftventricularfunctionanditsrelationshipwithviablemyocardiumafteracuteanteriorwallmyocardialinfarctioninpatientswithorwithoutdiabetes.MethodsAtotalof125consecutivesubjectswithacuteanteriorwallmyocardialinfarctionwereselected,anddividedintodiabetesmellitus(DM)group(n=43)andNon-DMgroup(n=82)accordingtoWHOdiabetesdiagnosiscriteria.AllpatientsreceivedsuccessfulPCIat12±8daysfromonset.Ischemicviablemyocardiumwasdetectedwithlow-dosedobutamineechocardiography,andleftventricularfunctionandwallmotionabnormalitywerealsoassessedwithechocardiographybeforePCI.ThedataofclinicalmanifestationsandangiogramsbeforeandafterPCIwereanalyzed.Levelsofcreatininekinase-MB(CK-MB),andtroponinT(TnT)beforePCI,6hoursand24hoursafterPCIwereassessed.Allpatientsreceivedclinicandechocardiographyfollow-upfor6months.ResultsHigherrateofTIMI2flow,andlowerrateofTIMI3flowinDMgroupweredemonstratedimmediatelyafterPCI,andtherateofserumCK-MBand/orTnTlevelswerehigherinDMgroup,comparedwithNon-DMgroup(P<0.05).63%ofDMpatientsand56%ofnon-DMpatientshadviablemyocardiumbeforePCI(P>0.05).Therewerenosignificantdifferencesofleftventricularejectionfraction(LVEF),leftventricularenddiastolicvolumeindex(LVEDVI),leftventricularendsystolicvolumeindex(LVESVI),andwallmotionscore(WMS)betweentwogroupsatbaselinebeforePCI(P>0.05).Aftersixmonths,WMSwasdecreasedandLVEFwasincreasedinNon-DMgroup,buttheWMSandtheLVEFdidnotchanged,andtheLVEDVIwasincreasedinDMgroupcomparedwithbaseline;theLVEDVI,LVESVI,LVEF,andWMSweresignificantlydifferentbetweentwogroups(P<0.05orP<0.01).ConclusionsComparedwithnon-diabetics,delayedsuccessfulrevascularizationwithPCIindiabeticspatientwithacutemyocardialinfarctionhaslessbenefitialeffectontheimprovementoflatephasel