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：BackgroundNowadays,thestudiesmainlyfocusonthefunctionofdecreasingtheinflammatoryfactorandimprovingthefunctionsofendothelium,buttheeffectsofstatinsonventricularremodelingarerarelystudied.MethodsThe2-kindey,1-cliphypertensiverats(2K1C,Goldblatt)werepreparedwithSprague-Dawley(SD)rat.SDratswererandomlydividedintothreegroups:controlrats,hypertensiveratsandhypertensiveratstreatedwithatorvastatin(2mg·kg-1·d-1).After6weeks,systolicbloodpressure(SBP)wasmeasuredusingthetail-cuffmethod.TheplasmaconcentrationofangiotensinⅡandreninactivityweredeterminedbyradioimmunoassay.Theheartweight,theratioofleftventricularweightandbodyweightwascalculated.ResultsTheplasmaconcentrationofangiotensinⅡ(106.4±7.8)ng/Landreninactivity(20.6±2.4)ng/Lweresignificantlyincreaedinhypertensiveratscomparedwithnormalrats[(72.3±5.4)ng/Land(12.5±3.7)ng/L](P<0.01).Theheartweight(1.46±0.09)g,theratio3.54±0.19(×10-3)ofleftventricularweightandbodyweightinhypertensiveratswereobviouslyhigherthanthatinnormalrats[(0.98±0.07)gand(2.28±0.06)×10-3](P<0.01).Aftertreatmentwithatorvastatin,theplasmaconcentrationofangiotensinⅡ(68.3±6.9)ng/Landreninactivity(8.7±2.3)ng/L,heartweight(1.05±0.04)g,theratio2.36±0.07(×10-3)aboveweredecreasedsignificantly,therewerenodifferencebetweenthegroupofhypertensiveratsandthenormal.ConclusionsAtorvastatincandecreasetheratioofleftventricularweightandbodyweightandhastheeffectsoncardiovascularremodelinginhypertensiverats.

简介：ObjectivesToexamineinvivointeractionsbetweenangiotensinⅡ(AngⅡ)AT1areceptor(AT1aR),angiotensin-convertingenzymes(ACE)andACE2usingsmallhairpinRNA(shRNA)gene-silencingmethodsinmicebrainstemnucleustractussolitarius(NTS).MethodsC57BLmice(n=8)wereusedasanimalmodel.MethodofmicroinjectioninthenucleusofNTSwasadopted.Aftertendays,micewerekilledandtheirbraintissuewerefixedandsectioned.TheexpressionlevelsofAT1aR,ACEandACE2mRNAatbothsidesofNTSwereexaminedbyinsituhybridization.Basedoncomparedt-test,thechangingformRNAexpressionwasexamined.ResultsAftertheexpressionofAT1aRmRNAwassignificantlyinhibited(61.6%±6.8%)byAT1aR-shRNA,itwasassociatedwithdecreasesinACE2mRNAexpressionfrom(1.05±0.12)μCi/mgto(0.74±0.09)μCi/mg(29.0%±14.5%,P<0.01)onthesamesideofthebrainstem.ACEmRNAexpressionwasconsistentatbothsides(0.50μCi/mg±0.09μCi/mgand0.53μCi/mg±0.08μCi/mg),withinsignificantdifference(P>0.05).ConclusionsThegenesilencingresultshowedthattherewereinteractionsbetweenbrainstemAT1aRandACE2.ACEmRNAexpressionwasnotalteredbyRNAinterferencetreatmentatAT1aR.

简介：患者男性,79岁.因"全身软困乏力1W"门诊以"冠心病"收入心内科.体检:T36.0℃,R20次/min,P50次/min,BP142/62mmHg,神志清楚,精神欠佳,双肺呼吸音清,双肺未闻及干湿罗音,叩诊心界不大,心率50次/min,律齐,心尖部可闻及2/6级收缩期吹风样杂音.

简介：例1患者女,51岁,有频发室早史,因近来反复发作胸闷、心悸、头晕就诊.查心电图(图1)示:P波在宽大QRS波前的位置不固定,即PR间期不等,QRS波起始部无粗钝,与相邻正常波PP间期不等于两者的JJ间期,为典型舒张晚期室早.

简介：BackgroundAngiotensinⅡtype1receptor(ATR1)/AngiotensinⅡtype2receptor(ATR2)usuallyinteractwitheachotherintheirexpressionandphysiologicalfunctions,andnitricoxide(NO)isalwaysinvolvedinATR1/ATR2regulationinvivo.Endothelialcellsplayacrucialroleinthemaintenanceofvascularfunctionandinthepreventionofcardiovasculardiseases.ObjectivesToinvestigatetheeffectsofangiotensinⅡ(AngⅡ)andATR1blockervalsartanonATR1,ATR2expressionandtheirrelationwithendothelialnitricoxidesynthase(eNOS)expression,andNOproductioninculturedvascularendothelialcells.MethodsHumanumbilicalveinendothelialcellline(HUVEC)andbovineaorticendothelialcell(BAEC)wereused.BAECwereisolatedfromaortaofnewborncalfbyenzymedigestionandcellsof3-5passageswereused.Cellswereincubatedwithvehicle,AngⅡ,valsartan,orAngⅡplusvalsartanrespectivelyforvariousperiods.ATR1,ATR2,eNOSexpressionandNOproductionweredetected.ResultsIncubationwithAngⅡorvalsartanapparentlydownregulatedATR1mRNAandproteinexpressioninvascularendothelialcells,andthecombinationeffectofthetwodrugsweremoreapparent.AngⅡshowedatransientslightlypromotiveeffectoneNOSandNOgenerationinBAECandanapparentlyinhibitoryeffectwithprolongedincubation,whilevalsartancanapparentlyreversethoseeffects.ConclusionsBothAngⅡandvalsartandownregulatedtheexpressionofATR1invascularendothelialcells.Thesynergisticeffectofthetwodrugswasmoreapparent.ProlongedincubationwithAngⅡcanapparentlyinhibiteNOSexpressionandNOproductioninendothelialcells,whilevalsartancanapparentlyreversethatinhibitoryeffect.

简介：目的探讨急性冠脉综合征（ACS）患者血清肌细胞增强因子2A（MEF2A）与纤溶酶原激活抑制剂-1（PAI-1）、单核细胞趋化蛋白-1（MCP-1）水平及冠状动脉病变程度之间的关系,分析变化产生的可能机制.方法采用ELISA法检测75例ACS患者及健康对照组35例血清MEF2A、PAI-1、MCP-1水平的变化.结果①ACS组患者血清MEF2A水平明显低于对照组[（88.70±4.38）ng/L比640.42±46.66）ng/L]（P＜0.05）;②ACS组患者血清PAI-1、MCP-1水平明显高于对照组[12.85±2.60）U/L比（7.61±5.23）U/L,（842.2±20.86）μg/L比（408.88±29.56）.μg/L]（P＜0.05）;③ACS组患者MEF2A水平与PAI-1、MCP-1水平变化呈负相关（r=-0.739,P＜0.01;r=-0.544,P＜0.01）.结论血清MEF2A水平与PAI-1、MCP-1水平变化呈负相关;MEF2A、PAI-1、MCP-1水平变化对评价ACS血管炎症反应和斑块的稳定程度具有重要的临床意义.

简介：目的探讨血清nesfatin-1水平在2型糖尿病（T2DM）合并冠心病（CHD）患者中的变化及其临床意义。方法选取T2DM合并CHD患者62例（T2DM合并CHD组），单纯T2DM患者60例（单纯T2DM组），单纯CHD患者59例（单纯CHD组），门诊健康体检者55例（对照组），用酶联免疫吸附法检测血清nesfatin-1水平，并测定空腹血糖（FBG）、总胆固醇（TC）、甘油三酯（TG）、低密度脂蛋白胆固醇（LDL-C）、高密度脂蛋白胆固醇（HDL-C）水平，HbA1c和空腹血清胰岛素（FINS），计算体质指数（BMI），并作相关分析。结果T2DM合并CHD组血清nesfatin-1水平均显著高于单纯T2DM组、单纯CHD组和对照组，差异有统计学意义（P＜0.05）；T2DM合并CHD组nesfatin-1水平均与TG和HOMA-IR呈正相关（r＝0.58、0.43，均P＜0.05）；T2DM与nesfatin-1和HOMA-IR密切相关（B＝2.84、2.37，均P＜0.05）；T2DM合并CHD与nesfatin-1和TG密切相关（B＝3.16、2.69，均P＜0.05）。结论血清nesfatin-1与T2DM合并CHD的发病有一定联系。

简介：心肌缺血再灌注损伤（myocardialischemiareperfusioninjury,MIRI）是指心肌组织缺血后再恢复灌注,缺血心肌的损害不仅没有好转反而出现反常增加的现象[1].MIRI是临床医生面临的一大难题[2-4].由于心外科手术需要无血、相对静止的环境,在体外循环、心脏停跳下进行,而体外循环心脏停跳下手术则需要阻断心脏供血,注入停跳液促使心脏停跳,心脏上操作完成后再恢复心脏血供,促使心脏复跳,因此体外循环下心脏停跳过程就是一个缺血再灌注损伤的过程.在经历体外循环后的心脏病患者术后恢复过程及远期疗效很大程度与缺血再灌注损伤相关,所以MIRI的研究具有重要的意义.但MIRI损伤的病理生理机制是复杂的,到目前为止都还不完全清楚,亦缺乏有效的治疗策略[5].

简介：

简介：急性心肌梗塞是一种严重危害人们健康的危重疾病，其并发症严重，死亡率高。心电图检查对于急性心肌梗塞的早期诊断减少梗塞面积至关重要。我们对10例正后壁急性心肌梗死的V1、V2导联心电图进行了观察，分析报告如下。

简介：BackgroundH9c2celllineismononucleatedmyoblastderivedfromembryonicrathearttissue.ActivitiesofTGF-β1,MMP-2andMMP-9increaseinH9c2cellsaftertreatmentwithfibrosisstimuli.MicroRNA(miRNA),akindofendogenoussmallnon-codingRNA,participatesincardiacfibrosis.Inthepresentstudy,expressionsoffibrosis-relatedgenesandmicroRNAsinTGF-β1treatedH9c2cellswereinvestigated.MethodsExpressionsoffibrosis-associatedgenes,includingCol3a1,α-SMA,FN1,CTGFandTSP-1,weremeasuredinTGF-β1treatedH9c2cellsbyquantitativereversetranscriptionandPCR(qRTPCR).Levelofα-SMAinH9c2cellswasdemonstratedbyfluorescenceimmunohistochemistry(FIHC)assay.ExpressionsofmaturemiR-16,-21a,-29binH9c2cellsweredeterminedbyqRT-PCRassay.ActivationsofSmad3andNF-kBsignalinginTGF-β1-treatedH9c2cellswerestudiedbydualluciferaseassay.ExpressionsofCol3a1,α-SMA,FN1,CTGFandTSP-1weredetectedinH9c2cellswithadenovirus-mediatedoverexpressionofmiR-21a.ResultsqRT-PCRassayshowedthatα-SMA,FN1,CTGF,TSP-1,butnotCol3a1,wereup-regulatedinTGF-β1treatedH9c2cells.FIHCresultalsorevealedthatα-SMAwasincreasedinTGF-β1-treatedH9c2cells.Consistently,dualluciferaseassayshowedthatSmad3andNF-kBsignalingproteinswereactivatedinTGF-β1-treatedH9c2cells.miR-21a,butnotmiR-16and-29b,wassignificantlyup-regulated.Additionally,over-expressionofmiR-21asignificantlyincreasesmRNAexpressionsofα-SMA,FN1,CTGFandTSP-1inH9c2cells.ConclusionsMiR-21aisup-regulatedinTGF-β1treatedH9c2cells,andmaycontributetoup-regulationsoffibrosis-associatedgenes.

简介：摘要目的探讨Graves眼病患者Th1／Th2细胞因子及自身抗体水平的相关机制研究。

简介：目的探讨常规体表静息心电图Tv1(Tv2)＞Tv5(Tv6)在冠心病诊断中的价值.方法110例住院行冠脉造影的患者,按造影结果分为冠心病组和非冠心病组,两组均多次记录常规十二导心电图,比较Tv1(Tv2)＞Tv5(Tv6)综合征在两组间检出率的差异,并与心电图ST段压低指标相比,分析Tv1(Tv2)＞Tv5(Tv6)综合征诊断冠心病的价值.结果Tv1(Tv2)＞Tv5(Tv6)综合征的检出率在冠心病组和非冠心病组有显著差异.Tv1(Tv2)＞Tv5(Tv6)诊断冠心病的敏感度为70.3%、特异度为66.6%,与ST段压低相比敏感性较高,但后者特异度高于Tv1(Tv2)＞Tv5(Tv6).结论Tv1(Tv2)＞Tv5(Tv6)综合征对诊断冠心病有一定价值,但特异性不高,应结合临床及其他心电图指标综合进行判断.

简介：BackgroundTaxifolin(Tax)isanessentialnaturalantioxidant.MultiplestudieshaveshownthatTaxcanprotectcardiomyocytesfromischemia-reperfusioninjury.However,theunderlyingmechanismisstillunclear.MethodsH9C2cellswererandomlydividedintocontrol,H_2O_2group,Taxpretreatmentgroup(Tax+H_2O_2);Taxeffectgroup.CellactivitywasdetectedbyCCK-8andtheintracellularstructurewasobservedbytransmissionelectronmicroscopy.AutophagywasdeterminebyWesternblottinganalysisofBeclin-1,Bcl-2andPKC.ResultsTaxpretreatmentsignificantlyincreasedanti-apoptoticproteinBcl-2andautophagyproteinBeclin-1.ExpressionofPKCwasinhibitedbyTax.ConclusionsTaxpretreatmentcouldprotectH9C2cellsagainstH_2O_2-induceddamagethroughtheBcl-2andautophagypathways.

简介：目的：比较胰高血糖素样肽1（GLP-1）受体激动剂与二肽基肽酶4（DPP-4）抑制剂治疗2型糖尿病（T2DM）的临床效果。方法：选择2015年1月~2016年1月我院收治的T2DM患者96例。根据随机数字表法,患者被随机均分为GLP-1受体激动剂组（GLP-1组,接受GLP-1受体激动剂利拉鲁肽治疗）和DPP-4抑制剂组（DPP-4组,接受DPP-4抑制剂西格列汀治疗）,两组均治疗18周。测量比较两组治疗前后空腹血糖（FBG）、餐后2h血糖（2hPG）水平,以及不良反应发生情况。结果：与治疗前比较,治疗18周后两组FBG、2hPG水平均有显著降低（P〈0.05或〈0.01）;与DPP-4组比较,GLP-1组治疗后FBG[（7.48±0.45）mmol/L比（6.64±0.28）mmol/L]和2hPG[（11.15±1.01）mmol/L比（9.26±1.82）mmol/L]水平降低更显著,P均〈0.05。GLP-1组与DPP-4组的总不良反应发生率（29.2%比33.3%）无显著差异,P=0.078。结论：与DPP-4抑制剂比较,GLP-1受体激动剂治疗2型糖尿病在控制血糖和减轻体重方面效果更好,值得推广。

简介：目的评价CHADS22及CHA2DS2-VASc评分系统在冠心病外科治疗中的意义.方法选择2006年1月至2010年1月行不停跳冠状动脉旁路移植术的768例患者,术后新发房颤患者97例.回顾患者的围术期及随访资料,应用CHADS2及CHA2DS2-VASc评分系统进行分析.结果768例患者术后新发房颤发生率12.6％,分为术后新发房颤组与非房颤组.新发房颤组与非房颤组平均年龄分别为（70.74±8.21）岁和（65.90±9.83）岁,围术期脑卒中分别为8例和9例,CHADS2评分值分别为3.20±1.26和2.13±0.94,CHA2DS2-VASc评分值分别为4.20±1.50和3.23±1.07.CHADS2和CHA2DS2-VASc评分是术后新发房颤的预测因素,与围术期脑卒中显著相关（P＜0.01）.结论冠心病外科治疗中应用CHADS2及CHA2DS2-VASc评分系统可预测术后新发房颤及围术期脑卒中,对冠心病术后新发房颤的抗凝及抗血小板治疗决策提供了依据,对卒中风险及预后有一定的评估价值.

简介：Inspiteofrecentadvancesintreatmentandcontrol,theprevalenceofCVDandpulmonaryhypertension(PH)aroundtheworldhasincreasedsignificantly.Webelievethataconceptualbreakthroughisneededandnoveldrugtargetsmustbediscoveredinanattempttocontrolandtreatthem.ACE2,thenewestmemberoftherenin-angiotensinsystem(RAS),appearstoholdthispotential.Ourstudieshaveestablishedanovelconcept:abalancebetweenthevasodeleteriousaxis(ACE/AngⅡ/ATlR)andthevasoprotectiveaxis(ACE2/Ang-1-7/Mas)oftheRASiscriticalinmaintainingnormalCVfunctionsandanyimbalanceinitiatesvasculardysfunctionsleadingtocardiopulmonarydiseases.ThuswehypothesizethatACE2,whichisakeyenzymeindecreasingAngⅡandincreasingAng-1-7,wouldbeanidealforconsiderationasatherapeutictarget.Theobjectiveofmypresentationwillbetopresentevidenceinsupportofthisconcept.ThedatapresentedwilldemonstratethatoverexpressionofACE2bygeneticmeansoritsactivationbenovelACE2activatorsproteststheheartfromhypertension-andMi-inducedcardiacdamage.Also,thisstrategyisextremelyeffectiveinpreventionandreversalofPHandpulmonaryfibrosis.Astructure-baseddrugdiscoveryapproachwillbepresentedtoidentifysmallmoleculeACE2acti-vatorsandtheirpotentialinproducingbeneficialoutcomesonCVDandpulmonaryhypertensionwillbediscussed.

简介：目的探讨橙皮素（HES）对H2O2诱导的H9c2心肌细胞凋亡的影响.方法采用H2O2建立H9c2心肌细胞氧化应激损伤模型.实验分为4组：正常对照组（Control组）、H2O2损伤组（H2O2组）、单纯橙皮素处理组（HES组）、橙皮素预处理＋H2O2组（HES＋H2O2组）.H2O2（400μM）处理2h建立心肌细胞氧化应激损伤模型,HES＋H2O2组于建模前1h加入40μM橙皮素.采用CCK-8法确定H9c2细胞活性,DCFH-DA探针检测细胞活性氧簇（ROS）水平,流式细胞术检测心肌细胞凋亡,分光光度计检测Caspase-3活性.结果橙皮素预处理可明显改善H2O2诱导的H9c2心肌细胞活性降低,且浓度为40μM时保护作用最明显;给予40μM橙皮素预处理后ROS的产生明显减少,Caspase-3活性显著下降,心肌细胞凋亡率为（28.32±2.12）%,明显低于H2O2组（50.33±2.56）%（P〈0.05）.结论橙皮素对氧化应激诱导的心肌细胞凋亡具有抑制效应.

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。