简介:1临床资料患者女性,46岁,既往有甲亢病史5年,阵发性房颤间歇服用胺碘酮一年.于2002年8月19日因精神悲伤,突然意识丧失,晕倒在地,口唇发绀小便失禁,5min后送入我院急救中心,心电图示:尖端扭转型室速室颤,前、后反复电除颤10次,恢复窦性心律,频发房早,间歇短阵房颤,T波倒置,Q-T间期440~480ms,为防止再次室颤,于2002年9月7日安置单腔起博复律除颤器(ICD),测R波幅度5.7mV,感知灵敏度0.5mV,电极阻抗420Ω,程控诱发室速室颤感知11秒,20J放电一次转复成功,术后半年平稳.于2003年4月~8月间,自感间断4次电击感,ICD程控资料显示:快速房扑,超过设定心率上限频率,误放电(5~10J)4次,均终止.后程控打开,增加QRS宽度识别,减少抗心动过速起博次数,增加放电能量,调整为8、16、20、30、30J能级,同时长期口服β受体阻滞剂(富马酸比索洛尔5mg/d)控制心室率,至今未再放电.
简介:Thepanaxnotoginsengsaponin(PNS)hadbeenclinicallyusedforthetreatmentofcardiovasculardiseasesandstrokeinChina.IthadbeendemonstratedthatPNScouldprotectcardiomyocytesfrominjuryinducedbyischemi-a,buttheunderlyingmolecularmechanismsofthisprotectiveeffectwerestillunclear.ThisstudywasaimedtoinvestigatetheprotectiveeffectandmolecularmechanismsofPNSonapoptosisinH9c2cellsinvitroandratmyocardialischemiainjurymodelinvivo.Annexin-V/PIassayshewthatPNScouldprotectH9c2cellsfromapoptosisinducedbyserum,glucoseandoxygendeprivation(SGOD)inadose-dependentmanner.However,theanti-apoptoticeffectofPNSwasreversedbyLY294002,aspecificPI3Kinhibitor.ThisantiapoptoticeffectofPNSwasconfirmedbyJC-1,aspecificprobeofmitochondrialmembranepotentialstaining.PNScouldsignificantlyincreasephos-AktinH9c2cellsbyWesternblotassaysanditseffectcouldbeinhibitedbyLY294002.Furthermore,PNScouldimproveischemic-inducedleftventricularfunctionasreflectedbyEF,LVDdandLVDs.PNScouldalsoinhibitedcellularapoptosisinmyocardialtissuesinischemicratsbyTUNELassay.PNSadministrationalsoincreasedtheexpressionofphos-Aktinratischemicmyocardialtissues.TheseresultssuggestedthatPNScouldprotectmyocardialcellsfromapoptosisinducedbyischemiainvitromodelandinvivomodelthroughactivating-PI3K/AktsignalpathwaywhichmaybemeaningfulforfurtherunderstandingthemolecularmechanismsofcardiacprotectionofPNS.Andtheresultsmightbeusefulintreatmentofmyocardialischemiainfuture.
简介:目的探讨甲型H1N1流感患者心脏损害的特点。方法回顾性研究分析2009年7月至2010年1月期间确诊为甲型H1N1流感患者172例的临床资料,所有患者根据病情分为轻症组,重症组,危重症组,并收集非甲型H1N1流感患者21例作为对照。大部分患者接受分子生物学检测磷酸肌酸激酶,磷酸肌酸激酶同工酶,高敏C反应蛋白,并接受胸部X线摄片检查,计算心胸比。结果甲型H1N1流感多发生于青壮年患者,轻症患者较重症患者更年轻(P<0.05)。在危重症患者中,磷酸肌酸激酶,磷酸肌酸激酶同工酶,高敏C反应蛋白和心胸比均较其他组高(P<0.05或P<0.01)。1例死于心肌损害。结论与既往研究相符,2009甲型H1N1流感可以导致心肌损害,特别是在危重症患者中心肌损害较显著,从而将导致心脏扩大等损害,导致死亡率升高。
简介:ObjectivesToexploretheprotectiveeffectofirbesartan(Irb)undertheinterferencewithangiotensinⅡ(AngⅡ)onABCA1.MethodsElectronmicroscopywasusedtodetectthemorphousoffoamcells.TheexpressionofABCA1mRNAanditsproteinweredeterminedbyRT-PCRandWesternblotting,respectively.Thevarianceofcellularcholesterolcontentwasmeasuredbyzymochemistryvia-fluorospectrophotometer.ResultsApositivefacilitativeeffectofAngⅡontheformationoffoamcellswasobserved.TotalcholesterolwasincreasedsignificantlybyAngⅡ,theexpressionofABCA1wasdown-regulatedobviouslybyAngⅡ;IrbcouldprotectABCA1againstthelesionofAngⅡ;TotalcellularcholesterolcontentwasreducedsignificantlyinIrb+AngⅡgroup;However,considerablealterationaboutthecholesterolcontentandtheexpressionofABCA1werenotobservedinIrbgroupwithoutincubationwithAngⅡ.ConclusionsIrbcouldprotectABCA1againstthelesionofAngⅡ,whichmaycontributetoitsanti-atheroscleroticproperties.
简介:目的:观察热应激诱导心肌热休克蛋白(HSP)70表达上调,对兔快速心房起搏致房颤心肌钙激活钾通道(KCa)3.1表达的影响。方法:将24只新西兰大白兔随机分为假手术组(n=8,仅植入电极而不起博)、起搏组(n=8,以600次/min快速起搏右心房6h)和热应激起搏组(热应激组,n=8,先行热应激预处理,再行与起搏组一样的快速起搏)。结果:与假手术组和起搏组比较,热应激组心脏各部位HSP70mRNA和蛋白表达显著上调[HSP70蛋白,左房:(39.00±3.21)比(39.75±2.82)比(69.75±3.45),右房:(38.38±2.92)比(39.50±3.89)比(69.00±2.93),左心耳:(37.75±3.28)比(39.00±3.89)比(68.63±3.23),右心耳:(37.00±3.85)比(38.38±3.74)比(68.75±2.82)],P均〈0.01,而起搏组和假手术组间无显著性差异(P〉0.05);与起搏组KCa3.1mRNA和蛋白表达量显著下调比较,热应激组心脏各部位KCa3.1mRNA和蛋白表达量显著上调[KCa3.1蛋白,左房:(21.25±1.67)比(24.00±2.62),右房:(21.13±1.96)比(23.75±1.83),左心耳:(21.00±2.07)比(23.75±1.67),右心耳:(20.88±2.03)比(23.50±2.45)],P均〈0.05,且热应激组与假手术组间无显著差异(P〉0.05)。结论:热应激可诱导心房起搏心肌热休克蛋白(HSP)70表达上调,抑制KCa3.1mRNA和蛋白表达量显著下降。
简介:T1mappingusingcardiovascularmagneticresonance(CMR)introducesnoveltechniquesformyocardialtissuecharacterizationtodetectandquantifydiseaseprocessesoccurringatthemicroscopiclevel.EventhoughT1mappinghaslimitedspatialresolution,cellularandmolecularchangesoccurringwithineachvoxelcanaffecttheaggregateT1signalrenderingthemquantifiable.TheestimatedT1-basedparametersquantifiedona“map”demonstratethespatiallocalizationofthesechangeswherebyeachpixelexpressesthequantitativevalueofthatparameter.Thisquantificationpermitsdetectionofdiffusediseaseevenifitisnotdirectlyvisible.Ratherthanrelyingonnonspecificfunctionalmeasures,T1mappingfocusesonintrinsicchangesofmyocardialcompositionthatadvancesunderstandingaboutspecificdiseasepathways.Thesechangesinmyocardialtissuecompositioninformdiagnosisandprognosis.T1mappingencompassestwokeyparameters:native(i.e.,precontrast)T1andextracellularvolumefraction(ECV)derivedfromadditionalpostcontrastT1andbloodT1measurements.Theseadvancesintroducenewtoolstodetectfocalanddiffusemyocardialderangementsoccurringincardiacdiseasethatcanbeotherwisedifficulttodetect.T1andECVmappingfosterprecisionmedicineandpersonalizedcare,promisingtoimprovepatientoutcomesthroughtargetedtherapy.CapitalizingontheopportunitiesintroducedbyT1mappingandECVrequiresfurtherinvestigation.
简介:BackgroundCoronarymicroembolization(CME)ischaracterizedbydistalmicrovascularocclusion.However,theinflammatorymechanismsandtherapeutictargetsofCMEarelargelyunknown.MethodsAtotalof11GuangxiBamaminiatureswinesweredividedintotwogroups:sham(n=5)andCME(n=6).MicrosphereswereinjectedintotheleftanteriordescendingarteryoftheCMEgrouptomakeananimalmodelofCME.TheexpressionsofmicroRNA-146a(miR-146a)andIRAK1,TRAF6,andAUF1inthemyocardiumweredetectedbyqPCR.ResultsIntheCMEgroup,microspheres,microinfarction,andinflammatorycellinfiltrationwerefoundunderanopticalmicroscope.TheexpressionlevelsofmiR-146awerelowinbothgroups.AfterCME,theexpressionlevelsofIRAK1,TRAF6,andAUF1intheCMEgroupwereupregulatedcomparedwiththoseintheshamgroup(P<0.01;P<0.05;P<0.05,respectively).ConclusionsAUF1,IRAK1andTRAF6,butnotmiR-146a,couldbeinvolved,inmyocardiuminflammationfollowingCME.
简介:BackgroundEssentialhypertension(EH)hasbecomethemostcommonchronicnon-infectiousepidemicandisoneofthemostcommonriskfactorsforthedamagetoheart,brain,kidneyandotherorgans.TheserumlevelsofICAM-1,IGF-1andIL-8playimportantrolesinthepathogenesisofEH.MethodsInthemedicalcheck-upcenteroftheAffiliatedHospitalofQingdaoUniversityMedicalCollege,sixtynormaloffspringwithafamilyhistoryofEHwererandomlyrecruitedintotwogroups:30offspringwithafatherormothersufferingfromEHassingle-parentgroup,and30offspringwithbothparentssufferingfromEHasdouble-parentgroup,andanother30normaloffspringwhoseparentsdidnotsufferfromEHascontrolgroup.TheserumlevelsofICAM-1,IGF-1andIL-8weredeterminedbyenzyme-linkedimmunosorbentassay(ELISA).ResultTheserumlevelsofICAM-1,IGF-1andIL-8weresignificantlyhigherinbothsingle-parentgroupanddouble-parentgroupthaninthecontrolgroup(P<0.05),andtheserumlevelsofICAM-1,IGF-1andIL-8werehigherinthedouble-parentgroupthaninthesingle-parentgroup(P<0.05).TheserumlevelsofICAM-1,IGF-1andIL-8werepositivelycorrelatedwiththeseverityofbloodpressureelevation(r=0.375,r=0.465,r=0.326,P<0.05,P<0.01,P<0.05respectively).ConclusionsDuetotheinfluenceofheredity,theseruminflammatoryfactorcontentsinnormaloffspringwithEHfamilyhistorymayincreasebeforebloodpressurerise.DetectionofseruminflammatoryfactorsinhealthyoffspringwithafamilyhistoryofEHcouldpredictoccurrenceofhypertension,andprovideamorereliablebasisfortheprimarypreventionofhypertension.
简介:目的探讨在起搏器类的手术后,患者囊袋中出现积血症状的护理。方法2012年5月16日到2013年5月16日,我院对32例心脏有跳动故障的人员装置了起搏器,其中有2例囊袋中出现积血症状的患者。在这2例囊袋中出现积血症状的患者中,有1例男性患者囊袋中出现积血症状,有1例女性患者囊袋中出现积血症状,都上了一定的年纪,在68岁到86岁之间,他们囊袋中出现的积血的数量最少的有4.9毫升,囊袋中出现的积血的数量最多的有9.9毫升。在囊袋中有积压血液的现象的患者中,有1例心脏中发生病态窦房类的综合性病症,有1例的二度房室在心脏传导之中出现阻滞性的情形,此外,三度房室在心脏传导之中出现阻滞性的情形。这2例囊袋中出现积血症状的患者,凝血所用时间都很正常。在准备做装设起搏器类的手术时,一些类似波立维以及抗血小板的药物都已经停止使用。之后,用无菌注射器将囊袋之中所积压的血液抽到外部。最后,又针对囊袋之中积压有血液的现象制定了一套专用的护理方案,来辅助治疗囊袋中出现积血现象的患者。结果通过用穿刺的形式将患者囊袋中所积压的血液抽出,再结合对囊袋中积压有血液的患者采用专用的护理方案,这2例囊袋中已无积血现象,积血得到全部性的抽出。结论对于囊袋中有积血现象的患者,采用适当的穿刺抽血方法和专用的护理方案,可使囊袋中的积血消失。