简介：患者男,25岁.因反复阵发性心悸、头晕就诊.T36.8℃,P92次/min,BP110/70mmHg.心肺体征(-).临床诊断:阵发性室上性心动过速.阵发性心悸发作时,心动过速呈突发突止特点.图为V1导联:P波直立,为异位P波.p-P及R-R间期呈长短交替,分别为0.42s及0.35s,互差0.07s,平均0.385s,频率156次/min.R-P间期固定.为起源于交接区心动过速.QRS波呈rsr'型.P及R形态一致.上述现象为交接区异位起搏点分别经快、慢2条径路同步、传导速度比例恒定(R-P间期恒定)的顺传、逆传所致(见梯形图).P-及R波形态一致,系2条径路分别到达心室及心房前,均经共同通道到达心室及心房之故.

简介：患者男性,73岁。因反复咳嗽、咯痰30余年,加重伴双下肢水肿3天入院,查体：体温36.4℃、呼吸19次/分、心率56次/分、血压130/80mmhg。神志清楚,唇舌发绀,桶状胸,叩诊过轻音,双肺呼吸音粗,

简介：自从开展孕妇产前常规心电图检查以来,笔者观察到孕妇尤其是晚期妊娠的孕妇中P-R间期缩短者明显多于其他患者.现就2000年10月～2001年10月的所有病例分析报告如下.

简介：Objectives:Apoptosisisrecognizedasanimportantmechanismincontrast-inducednephropathy(CIN).Cordycepssinensis(CS),atime-honoredtonicfoodandherbalmedicineinChina,canimprovethemicrocirculation,increasethetolerancetoischemiainpatientswithmicrocirculatorydisorders.AsCShasbeenfoundtoberenoprotectiveandanti-apoptoticinmultiplekidneyinjuries,wehypothesizedthatCSwouldpreventCIN.TheobjectiveofthisresearchistostudythemechanismofCSontubularepithelialcellapoptosisindiabeticCINrats.

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：目的研究妊娠中晚期心电图短P—R间期产生机制以及对胎儿的影响。方法对32例妊娠中晚期发现短P—R间期者（观察组）和30例P—R间期正常的中晚期孕妇（对照组）进行24h动态心电图（DCG）及胎儿心电图（FECG）检查；对观察组进行输氧一周后复查常规心电图（ECG）、FECG、及产后3个月复查ECG。结果观察组心率变异（HRV）较正常对照组明显降低，有显著性差异（P〈0．001、P〈0．005及P〈0．01）；观察组输氧后短P—R间期恢复正常，FECG前后变化不大。结论妊娠中晚期的P—R间期缩短与需氧量增加、自主神经功能失调、交感神经占优势相关．可作为中晚期妊娠者自主神经功能失衡的客观指标；对胎儿影响不大。

简介：P波异常改变在常规心电图检查中较为常见。P波为心房除极波，正常P波是窦房结发出的激动，右心房除极构成P波的前半部，左心房除极构成P波的后半部。心房肌较薄，又存在三条结间束和房间束，心房除极所产生的电位差并不大，整个除极过程也较短，平均0．10s完成。P波改变是指P波形态、时限、电压的改变，反映心房除极异常、房内传导或激动源的变化。

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：BackgroundInthisstudy,weaimedtoevaluatetheimpactofabnormalglucose,lipidandCystatin-ConthevirtualPvectorcharacteristics,whichhaven’tbeenreportedinpreviousstudies.Methods204ofnon-diabetesmellitus(NDM),130ofDM(type2)and39ofimpairedglucosetolerance(IGT)patientswereconsecutivelyandretrospectivelyrecruited.Weselectedaone-minutelengthofelectrocardiogramat4AMforanalysis.Afteraseriesofcalculatingalgorisms,weobtainedthevirtualplanarPvectorparameters.ResultsTherewerenosignificantdifferencesinFPV,FPA,RSPV,RSPA,HPVandHPAgroups.Afteradjustingconfoundingfactors,theregressioncoefficients(RC)wereestimatedasfollow:forFPV,femalegender(RC-0.21,P=0.02),triglyceride(RC-0.09,P<0.01),RVOT(RC0.03,P=0.02);forRSPV,femalegender(RC-0.21,P<0.01),triglyceride(RC-0.10,P<0.01),averageheartrate(RC0.01,P=0.02);forHPV,triglyceride(RC-0.08,P<0.001),LDL(RC-0.19,P<0.01),ApoB(RC0.67,P<0.01);forRSPA,Btypeofblood(RC-22.06,P=0.02),Cystatin-C(RC-72.79,P=0.02),thicknessofinterventricularseptum(RC3.70,P=0.01).Cystatin-CwassuggestedasacurerelatedtoRSPA,andthecut-offpointwas1.6mg/L.TherewerenosignificantriskfactorsassociatedwithFPAandHPA.TherewasnodifferenceinvirtualPvectoramongDM,IGTandNDMgroups.ConclusionIncreasedlevelsoflipidandCystatin-CsignificantlyimpactthecharacteristicsofvirtualPvector,whereasglucosedoesnot.Thesechangesmaycomefromahigherlowvoltageatrialareaandabnormalorientationofatrialdepolarization.

简介：患者男性，80岁。因气急、胸闷2月，加重1周就诊。既往有冠心病、高血压。查体：BP160／80mmHg，心界向左下扩大，心律不齐，各瓣膜听诊区可闻及Ⅲ级病理性杂音。X线胸片示：双肺纹理增深。心脏彩超示：左心房轻度扩大，主动脉瓣轻度返流，左室顺应性降低。临床诊断：心律失常。

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；观察高脂蛋白血症患者血浆P－选择素表达及普伐他汀的作用。方法：应用酶联免疫吸附法检测31例高脂蛋白血症患者服用普伐他汀前后血浆P－选择素水平，并与35例血脂正常者对照。结果；高脂蛋白血症组血清总胆固醇，低密度脂蛋白胆固醇及血浆P－选择素水平均显著高于正常对照组（P＜0．01），普伐他汀治疗后血浆P－选择素水平显著下降（P＜0．01）。结论：高脂蛋白血症患者血浆P－选择素表达异常可能参与高脂蛋白血症的致动脉粥样硬化作用。

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：目的探讨慢性肺心病合并冠心病P波离散度（Pd）的临床价值。方法观察26例阵发性心房颤动者（A组）及26例健康者（B组）12导联同步体表心电图P波最大时间及离散度。结果A组P波最大时间及离散度均较B组增大（P〈0.01）,P波最大时间〉110ms、Pd〉40ms以及两者相结合对阵发性心房颤动预测的敏感性分别为89%、86%、76%,特异性分别为80%、85%、89%。结论Pd是预测心房颤动的一个体表心电图新指标。

简介：患者男性,20岁.临床诊断:病毒性心肌炎.心电图检查(图1A)可见:窦性心律,频率为68次/min,Ⅰ、aVL、aVR、V4～V6导联P波呈三峰型,除aVL导联外均呈高-低梯形排列,而aVL导联三峰电压高低互有参差,1～2峰间距0.04s,2～3峰间距0.04s,P波时限0.14s,1、2、3峰各占时0.06s、0.04s、0.04s.

简介：近年来,许多分析和研究认为P-R间期缩短可以是变异型James束传导异常引起,也可以是一种非传导异常所致.本院从门诊、住院孕妇中随机抽取970例进行分析,发现在孕妇中P-R间期缩短的现象远较其他年龄相仿的非孕女性比例要高得多(P＜0.001);同时对其在分娩6个月后进行追踪随访,绝大部分人P-R间期恢复正常.