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：ObjectivesTheeffectsofcarvediloloncalciumcurrent(ICa)wereinvestigatedinisolatedadultratventricularmyocytes.MethodsICawasrecordedbyusingwhole-cellpatch-clamprecordingtechnique.ResultsCarvedilolreversiblyinhibitedICainaconcentration-dependentmanner,carvedilolat0.1,0.3,1and10μmol/LintheextracellularsolutiondecreasedpeakICaby1.52%,18.04%,37.34%and72.18%,respectively.Thesteady-stateinactivationcurveofICawasshiftedtomorenegativepotentials,whiletheactivationcurvewasnotaltered.Therecoveryfrominactivationwasshiftedtorightdirection,itcouldnotberecoveredcompletely.Inaddition,Pretreatmentofventricularmyocyteswithprazosinandpropranololcouldn'tblockthecarvedilol-inducedreductionofICa.ConclusionsCarvedilolinhibitsICainadultratventricularmyocytesbymechanismsinvolvingpreferentialinteractionwiththeinactivatedstateofcalciumchannel.

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简介：ObjectivesToevaluateantihypertensiveefficiencyandsafetyofanewdomesticofL-&N-typeCa^2+antagonist-eilnidipinewithimidaprilasapositivecontrol.MethodsAfter2weeks'placebowashingout,22patientsweretreatedwitheilnidipine5mgdailyand27patientsweretreatedwithimidapril5mgdaily.4weekslater,ifpatient'ssittingdiastolicbloodpressureisover90mmHg,his/herdosagewasdoubledforanother4weeks,theothersmeasuringupremainedtheirdosageunchangedforanother4weeks.Bloodpressure,heartrate,bloodandurineroutineexamination,serumglucose,serumchemicalexaminationincludingtotalcholesterol,triglyceride,HDL,LDL,transaminase,creatineetcandsidereactionswererecordedbeforeandafterthetrial.Datawereanalyzedstatistically.ResultsAfter8weeks'treatment,bloodpressurewassignificantlydecreased(P<0.05)inbothgroups,andthetwomedicineshadsimilarantihypertensiveeffects.Furthermore,thereducingofheartratewasstatisticallysignificantcomparedwithbaseline(P<0.01)inthecilnidipinegroup,butnotintheimidaprilgroup.Thenegativechronotropiceffectofcilnidipinehadlittleeffectoncontinuingthetherapy.Therewerenochangesonbloodandurineroutineexaminationandserumlipid,serumglucose,creatine,transaminaseandetcinbothgroups.Theirsidereactionsweremildandwell-tolerated.ConclusionsCilnidipinehasacon-vincingantihypertensiveeffectsimilartothatofimi-dapril.Especiallycilnidipinemaybeadministeredtopatientswithrelativelymildtachycardia.

简介：患者女,66岁。1年前无明显原因出现发作性心前区不适,无心悸、胸闷、头昏、黑蒙等。无高血压、冠心病(冠状动脉造影阴性)及糖尿病等病史。常规心电图(图略),P波顺序出现,P—R间期0.28s,P—P间期0.85s,心率72次/min,一度房室阻滞。发病时心电图(图1)示,P_(1-9)为窦性P波,P—P间

简介：目的探讨L－精氨酸治疗心肌缺血患者的次极量运动试验结果的改善作用。方法用药前后行次极量运动试验观察心肌缺血情况。结果L-精氨酸治疗后运动应激对冠脉血流明显好转。结论L－精氨酸具有缓冲缺血性心脏病在次极量运动负荷时交感神经张力过度增高而导致的心肌缺血的作用。

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

简介：目的观察扩张型心肌病（DCM）24h12导联动态心电图改变。方法58例均经心脏超声检查诊断为DCM，再行24h12导联动态心电图监测。结果所有病例动态心电图均有异常改变，以心律失常最为常见。其中室性心律失常56例（96．6％），房性心律失常43例（74．1％），ST—T改变32例（55．2％）、室性心动过速29例（50．0％）。心功能越差，复合性心律失常越多见。传导阻滞25例（43．1％），房室肥大27例（46．6％），Q—T间期延长24例（41．4％），异常Q波8例（13．8％）等。结论DCM有多种心电图表现，其多发、多样性心律失常对DCM早期诊断有重要意义。有复合心律失常的患者有必要进行心脏超声心动图检查。

简介：患者男，74岁，临床诊断：冠心病。心电图(图1)示窦性P波在同一导联形态相同，在V3导联呈双峰，峰距0.04s，PP间距不等，在Ⅱ导联上相差最大0.12s，每隔2个P波后跟……

简介：目的评价L-精氨酸对急性冠脉综合征患者血管内皮功能的影响.方法97例急性冠脉综合征患者被随机分到对照组、维生素C治疗组和L-精氨酸治疗组.所有患者分别于入院时及用药3周后取静脉血,测定血浆一氧化氮(NO)、内皮素-1(ET-1)、C-反应蛋白(CRP)和脂蛋白(a)[Lp(a)]的浓度.结果治疗3周后,L-精氨酸治疗组N0高于对照组(P＜0.05),ET-1、CRP、Lp(a)低于对照组(P＜0.01).结论L-精氨酸能够改善急性冠脉综合征患者血管内皮功能.

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：电交替是1种心电现象,复合性电交替者较少见,现报告1例.

简介：患者男,35岁.临床诊断心肌炎.图为Ⅱ导联记录.可见P波顺序出现,正向传导,P-R间期0.16s,窦性P-P间期较规则为:0.80s.图中可见数组P波已经脱离了生理不应期,但是仍然出现传导迟延(上行P13P-R间期为0.36s;中行P5p-R间期为0.32s,下行P9P-R间期为0.32s)和传导中断(中行图R5、R6之后,下行Rt之后).

简介：患者男性，79岁。4年前出现活动后胸闷、气短，经休息或口服利尿剂缓解，无典型心绞痛症状，未经系统治疗。于2004年12月气短加重，不能平卧。心电图（ECG）（图1A）示：P波顺序出现，Ⅰ、Ⅱ、Ⅲ、aVF、V6导联直立，aVR导联倒置，其振幅、时间均正常，ST—T改变（ST1、aVL、V4-V6呈下斜型下移达0．3mV，TI、aVL、V4-V6倒置0．2～0．5mV）。

简介：正常成年人12导联心电图的V1导联呈rS型。当V1导联以R波为主或R/S〉1时,临床可见于完全性右束支阻滞、后壁心肌梗死、右心室肥大、肥厚型心肌病、右位心、A型心室预激及正常变异等多种情况。本文结合心电图与心电向量图,对V1导联R/S〉1的几种表现进行分析总结。

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：患者女性，45岁，主因“发作性心悸10年，加重9h”于2015年4月3日入院。既往白塞病史20年，间断出现口腔溃疡，反复外阴溃疡，针刺试验（+）。9:30出现心悸，持续无缓解，伴头晕、头痛，无胸痛、气短，就诊于当地医院，测血压60/45mmHg（1mmHg=0.133kPa），给予药物处理后（具体用药不详）急诊转入我院。

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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.