简介:目的探讨氟伐他汀对冠心病患者白细胞介互素-6(IL-6)、白细胞介素-10(IL-10)和基质金属蛋白酶-1(MMP-1)水平的影响。方法冠心病患者51例:急性心肌梗死(AMI)13例、不稳定型心绞痛(UAP)18例、稳定型心绞痛(SAP)20例;健康对照者20名。所有试验对象当天采集空腹静脉血5ml。冠心病患者随机分为2组:氟伐他汀40mg治疗组(26例)和80mg治疗组(25例),30d时再次采血5ml,测定IL-6、IL-10和MMP-1浓度。结果治疗前AMI、UAP组IL-6和MMP-1显著升高(P〈0.01);两组治疗后IL-6和MMP-1均有明显下降(P〈0.01),但80mg组下降更甚(P〈0.01)。血清IL-6水平与血清MMP-1水平呈显著正相关(r=0.847,P〈0.01)。IL-10在治疗前、后均无明显变化。结论IL-6、MMP-1在ACS患者中血清水平明显升高,可能与炎症反应、斑块不稳定相关,从而促进了冠心病患者发展为临床上的ACS;IL-10在冠心病患者血清水平中无明显变化;IL-6、MMP-1和IL-10与冠脉病变支数无关;氟伐他汀可能通过抑制IL-6、MMP-1的水平而发挥抗炎作用,其效用与药物浓度相关。
简介:心电图改变一般不能提示疾病的病因,但有一些心电图改变具有一定的病因诊断价值,另有一些心电图改变可提供诊断线索.然而,心电图对左侧气胸的诊断意义尚未引起临床关注.本文分析10例左侧气胸病例,发现其有左室面导联(I、aVL、V4、V5、V6导联)R波低电压、位置性Q波、QRS振幅变化及R波逆向递增等较为明显的心电变化,其中左室面导联R波电压于坐位时描记心电图又发生了成倍增加,其增加率107%~780%(376.50±225.99),与正常组-22%~73%(-42.33±37.76)及肺气肿组-28%~40%(-31.28±27.64)比较,P<0.01,有显著统计学意义.
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: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.