简介:backgroundIn-hospital(IH)mortalityforpatientsunderwentpercutaneouscoronaryintervention(PCI)inourcenterfrom1994to2004was1.01%(33/3252).ThePCIvolumeinourstateincreasedquicklyduringthelastfewyears,sodiditinourcenter.MethodsandResultsWeretrospectivelyscreenedatotalof3274caseswhounderwentPCIin2009,amongwhich24(0.73%,P=0.22vs.1994-2004)IHdeathoccurred.Analysisofthese24casesrevealedthatallofthemwerediagnosedasacutecoronarysyndrome(ACS),andhadtheindicationofPCI.Fifteen(63%)carriedachanceof≥10%todieinhospitalaccordingtoGRACEmodel.Significantleft-main(LM)and/ortriple-vesseldisease(TVD)weredefinedin21(88%)cases.SYNTAXscoreswere≥23in15(63%)and≥33in12(50%)cases.CompleterevascularizationwithPCIwasfulfilledinonly5(21%)cases.Myocardialischemiaorheartfunctioncouldn'timprovebyPCIwasthemostfrequentcauseofdeath,whichcontributedtothatof11(46%)cases.Cardiacruptureoccurredinallofthe4patientswithSTelevatedacutemyocardialinfarction(STE-AMI)involvinginferiorventricularwallbut'reserved'anteriorwall,andcontributedmainlytotheirmortality.ConclusionsPost-PCIIHmortalityhasmaintainedlowinourcenter.ItmostlikelyoccursinpatientswithACS.Themajorcauseofdeathisthatmyocardialischemiacouldn'timprovebyPCI,exceptforpatientswithinferiorbutnoanteriormyocardialinfarction,whosufferfromcardiacruptureinstead.
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.
简介:IntroductionMyocardialischemiaandanginapectoriscanbecausedbyvariousmechanismssuchascoronaryatherosclerosis,vasospasmorcoronarymicrovasculardysfunction[1].Weherereportacaseofa56-year-oldfemalepatientwithahistoryofpreviouspercutaneouscoronaryinterventions(PCI)whoreportedrepetitiveattacksofrestingangina.Coronaryriskfactorsincludedhypertension,hypercholesterolemia(LDL=97mg/dLonatorvastatin),ex-smoker(ceased2013),andapositivefamilyhistory(fatalmyocardialinfarctioninfatheraged52yearsandbrother59years).
简介:目的:探讨元素与血脂间的关系以及元素、血脂对老年人高血压病的关系。方法:本文测定了39名老年高血压病患者和30名健康老年人的血清微量及宏量元素锌(Zn)、铜(Cu)、铁(Fe)、钙(Ca)、镁(Mg)、钠(Na)、及血脂甘油三脂(TG)、胆固醇(Tc)、高密度脂蛋白胆固醇(HDL-C)、低密度脂蛋胆固醇(LDL-C),并进行了均数t检验,简单相关性分析及胆固醇多因素逐步回归分析。结果:本文所测定的老年高血压病组的血清HDL-C水平下降,同时血清Zn含量也低于对照组,且多元逐步回归分析显示血脂与血清Zn、Cu、Mg均呈显著正相关,本文结果还显示HDL-C和TC与Cu,Cu/zn值及Mg都存在着一定相关关系。结论:老年高血压病患者血清中各元素之间,元索与血脂问都具有一定的内在联系。高血压病特别是老年高血压病,在预防及治疗上可以通过饮食调整来影响血清微量及宏量元素的总体水平及其之间的关系,从而影响血清脂质含量,以达到防治目的。