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:ObjectivesToevaluatetheeffectsofn-3fattyacidsonthecoronaryheartdiseasepatients.MethodsFromSeptember2007toMarch2008,60patientswithcoronaryheartdiseasewererandomlyassignedton-3fattyacidsgroup(groupN)andcontrolgroup(groupC).BothgroupsreceivedstandardcoronaryarterydiseasesecondarypreventiontreatmentandgroupNalsoreceivedeicosapentaenoicacid(EPA)1.8gplusdocosahexaenoicacid(DHA)1.2gperdayfor12weeks.Plasmatriacylglycerols,totalcholesterol,low-densitylipoproteincholesterol(LDL-C),high-densitylipoproteincholesterol(HDL-C)andbloodpressureweremeasuredbeforeandafterthestudy.ResultsPlasmatriacylglycerols,bloodpressureandLDL-ClevelwereloweringroupNaftern-3fattyacidstreatmentwhilenochangewasfoundingroupC(P<0.05).HDL-Clevelslightlyincreasedandtotalcholesterollevelslightlydecreasedaftern-3fattyacidsbutbothchangewerenotsignificant(P>0.05).ConclusionsN-3fattyacidshavebeneficialeffectsonthecoronaryarterydiseasepatients.
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.
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: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:BackgroundAcuterespiratorydistresssyndrome(ARDS)causedbyH7N9influenzainpregnantwomanisalife-threateningeventwithanincreasedriskformaternalandbaby'sdeath.Theaimofthisstudywastoevaluatetheimpactofpoint-of-careultrasonography(POCUS)onthemanagementandprognosisofthesepatients.MethodsAcaseof31-yr-oldpregnantwomaninourhospital,whowasunderwentPOCUSforevaluatingcardiopulmonaryfunctions,volumestate,fluidresponsivenessandultrasound-guidedprocedureswasadmittedtoIntensiveCareUnit(ICU).Weperformedultrasonographydailyformonitoringorganfunctions.Reviewofrelatedliteratureswasalsoconducted.ResultsWiththehelpofPOCUS,wemadequicklydiagnosisofseverepneumoniaandARDScausedbyH7N9influenza.ThetherapieshadalsobeenchangedafterPOCUSexaminations,suchasrestrictfluidadministrationrelyingontheassessmentsoftheinferiorvenacava(IVC)toestimatepreloadandlungultrasoundmonitoringtoidentifytheearlypresenceofextravascularlungwater(EVLW)andavoidfluidoverresuscitation,ultrasound-guidedrecruitmentmaneuvertoimprovedrespiratorydistresssyndrome,andsoon.ConclusionsPOCUShasasignificantimpactondecision-makingandtherapeuticmanagementandshouldbecomeaclinicalroutineinthemanagementofARDSpatientscausedbyH7N9influenzainpregnancy.
简介:目的:探讨慢性心力衰竭(心衰,CHF)患者N端脑钠肽前体(NT-proBNP)、内皮素(ET)水平与心功能的关系。方法入选56例CHF患者作为研究对象,29例心功能正常者作为对照组。心衰患者按照NYHA分级分为心功能Ⅱ级、Ⅲ级、Ⅳ级3个亚组,分别测定患者NT-proBNP、ET水平,同时用心脏彩色多普勒超声心动仪测定左室射血分数(LVEF)和左室舒张末期内径(LVDD)并进行组间比较及相关性分析。结果对照组及CHF心功能Ⅱ级、Ⅲ级、Ⅳ级亚组的患者NT-proBNP水平分别为(336.24±41.25)ng/ml、(1761.35±21.43)ng/ml、(2693.45±41.54)ng/ml、(3161.26±67.56)ng/ml,ET水平分别为(19.89±11.35)ng/L、(48.60〈21.25)ng/L、(61.56±31.68)ng/L、(161.67±46.56)ng/L。对照组患者及CHF心功能Ⅱ级组、Ⅲ级组、Ⅳ级组患者血浆NT-proBNP、ET水平呈逐渐增高趋势,差异具有显著统计学意义(P<0.01)。除心功能Ⅱ级组与心功能Ⅲ级组间ET与LVEF水平比较无统计学差异(P>0.051),其余各组间NT-proBNP、ET水平及LVEF、LVDD水平比较,均有显著统计学差异(P均<0.01)。NT-proBNP与心功能分级呈正相关(r=0.769,P<0.05),与LVDD呈正相关(r=0.606,P<0.05),与LVEF呈负相关(r=-0.656,P<0.05)。ET水平与心功能分级呈正相关(r=0.357,P<0.05),与LVDD呈正相关(r=0.265,P<0.05),与LVEF呈负相关(r=-0.274,P<0.05)。结论CHF患者NT-proBNP与ET水平随心力衰竭程度的加重而相应升高,与心功能分级有良好的相关性,对心力衰竭患者心力衰竭严重程度及预后的评价有意义。
简介:目的通过磁共振氢谱(1Hmagneticresonancespectroscopy,1HMRS)检查,了解猫脑缺血后不同受累脑区N-乙酰天冬氨酸(N-aeetylaspartate,NAA)的动态变化.方法在猫持续性局灶脑缺血模型基础上,以磁共振弥散加权成像(diffusionweightedimaging,DWI)异常区作为1HMRS检查体域的定位标准,在缺血前后不同时间进行1HMRS检查,动态观察缺血中心区、半暗带区及其对侧镜相区城NAA的变化特点.结果脑缺血后NAA很快减少,在中心区,缺血后6h减至对侧的50%左右,缺血后12h减至对侧的20%左右,2d后完全消失;而在半暗带区,NAA减少速度较慢,缺血后12h减至正常的60%左右,随后维持在正常的50%左右,差异无显著性意义.结论在缺血中心区,缺血后6h内,NAA的变化最为剧烈;而在半暗带区,以缺血后12h内变化明显.因此,挽救缺血半暗带和缺血中心区应有不同的治疗时间窗.
简介:目的:探讨N-末端脑利肭肽前体(NT.proBNP)水平与心衰合并房颤患者复律及脑梗死的关系。方法:150例心衰合并房颤患者接受静脉滴注胺碘酮复律治疗,根据复律结果分为复律组(100例)和未复律组(50例),观察两组复律前后NT-proBNP水平的变化。根据是否发生脑梗死,患者被分为脑梗死组(20例)和无脑梗死组(130例),比较两组发病前后的NT-proBNP水平。结果:服药后48h内100例(66.67%)患者转复为窦性心律。与复律前比较,复律组复律后NT—proBNP水平显著降低[(967.04±366.16)pg/ml比(496.21±142.54)pg/m1],且显著低于未复律组(996.76±351.28)pg/ml,P均〈0.01]。脑梗死组中,与小面积脑梗死组比较,中,大面积梗死组NT—proBNP水平[(784.21±231.26)pg/ml比(1983.24±32.96)pg/ml,(3562.19±1468.32)pg/m1]显著升高,P均〈0.05或〈0.01。结论:入院时NT—proBNP水平对心衰合并房颤患者药物复律效果具有预测价值。NT-proBNP水平与脑梗死的发生有关。急性脑梗死后NT-proBNP水平越高,梗死面积越大,预后越差。
简介:目的探讨急性冠状动脉综合征(ACS)患者血浆N-末端脑钠肽原(Nt-proBNP)和C-反应蛋白(CRP)水平与临床预后的关系。方法选择ACS患者86例(ACS组)、稳定性心绞痛(SAP)患者42例(SAP组),检测24小时(第一次)、5天(第二次)血浆Nt-proBNP和CRP水平,并与正常健康体检者50例(对照组)作对照。所有患者每3个月随访一次,平均随访6个月,以心血管事件为观察终点,观察ACS组、SAP组和ACS患者心血管死亡(死亡组)、心血管事件发生(事件组)与心血管事件未发生(无事件组)患者的两次血浆Nt-proBNP、CRP浓度差异。结果①ACS组两次Nt-proBNP、CRP测值均显著高于SAP组与对照组(P〈0.01);SAP组Nt-proBNP、CRP测值高于对照组(P〈0.05)。②死亡组、事件组第二次Nt-proBNP、CRP测值显著高于第一次测值(P〈0.01)。结论ACS急性期Nt-proBNP、CRP浓度显著升高,且与患者病变严重程度有关,可作为预测和判断预后的参考指标之一。
简介:目的评价ST段抬高急性心肌梗死(STEMI)患者行直接经皮冠状动脉介入治疗(PCI),冠脉侧支循环对N端脑钠肽前体(NT-proBNP)水平及心功能的影响.方法纳入2014年12月至2015年12月在徐州医学院附属医院心内科行直接PCI的STEMI患者60例并成功开通靶血管.根据冠状动脉造影结果按Rentrop方法评价侧支循环情况,有侧支循环组16例,无侧支循环组44例.患者分别于术后24h、7d抽取静脉血行NT-proBNP检查,术后7d、30d应用心脏彩超评价心功能情况.结果STEMI患者急诊PCI后有侧支循环组24h和7d的NT-proBNP水平明显高于无侧支循环组[988.0(628.2~1658.0)pg/ml比3023.0(1947.5~4935.5)pg/ml,832.0(501.7~1062.0)pg/ml比2219.0(1149.0~3445.8)pg/ml],差异均有统计学意义(P<0.05).两组患者入院Killip分级≥2级的比例为6.2%比34.1%,差异有统计学意义(P<0.05).心脏彩超结果比较,PCI术后7d有侧支循环组的左心室射血分数(LVEF)高于无侧支循环组[(53.4±7.1)%比(47.1±8.4)%,P<0.05];术后30d门诊随访心脏彩超结果有侧支循环组LVEF依然高于无侧支循环组[(56.3±6.9)%比(49.5±8.9)%,P<0.05].结论早期开放的侧支循环可降低STEMI患者急诊PCI术后NT-ProBNP水平并且对心功能有保护作用.
简介:目的:探讨老年冠心病患者N端脑钠肽前体(NT-proBNP)、脂蛋白(a)[LP(a)]水平与冠状动脉病变程度之间的关系。方法入选2011年1月~2012年12月在北京老年医院心内科住院并行冠状动脉造影检查的老年患者213例,根据冠状动脉造影结果分为非冠心病组(n=60),冠状动脉单支病变组(n=42),双支病变组(n=48),三支病变组(n=63)。测定四组患者空腹血清NT-proBNP、LP(a)水平并进行比较,分析NT-proBNP、LP(a)水平与冠心病患者冠状动脉病变严重程度的关系。结果随着病变支数的增多,血浆NT-proBNP及LP(a)水平有逐渐增高的趋势。冠状动脉单支病变组、双支病变组和三支病变组患者血浆NT-proBNP及LP(a)水平均高于非冠心病组,差异有统计学意义(P<0.05)。冠状动脉单支病变组与三支病变组NT-proBNP及LP(a)水平有统计学差异(P<0.05),而单支病变组与双支病变组,双支病变组与三支病变组间NT-proBNP及LP(a)水平比较无统计学差异(P>0.05)。Gensini评分与NT-proBNP、LP(a)均呈明显正相关,相关系数分别为0.580、0.406,有显著统计学意义(P<0.01)。结论NT-proBNP、Lp(a)水平与冠状动脉病变的严重程度密切相关,对高NT-proBNP、LP(a)的患者应给予高度重视,尽早予以强化治疗。