简介:APeruviannative,Dr.VelardeearnedhermedicaldegreefromtheNewYorkUniversitySchoolofMedicineinNewYorkandwentontocompleteherresidencytraininginInternalMedicineatColumbiaPresbyterianMedicalCenterandCardiovascularDiseasefellowshiptrainingatMountSinaiHospitalinNewYorkandBostonUniversity.Dr.GladysP.VelardeisAssociateProfessorofMedicine/CardiologyatTheUniversityofFlorida,JacksonvillewhereshedirectstheWomen’sCardiovascularHealthProgramandisDirectoroftheCardiovascularDiseaseFellowshiptrainingprogram.
简介:波士顿科学国际有限公司是一家全球性的医疗技术产品研发、生产、营销公司,现有17,500名雇员,2005年的销售收入为63亿美金。在过去的二十五年中,公司为广泛的医疗技术领域提供了具有深度和广度的众多创新产品,从而推动了微创介入产品的实践和发展。通过提供传统外科手术的替代产品,波士顿科学公司致力于帮助医生和其它医疗行业工作者改善病人的生命质量。
简介:StandardTherapyforHeartFailureUntilnowtheprincipalfocusofheartfailuretherapyhasbeenonthesympatheticnervoussystemandtherenin-angiotensinsystem.Betablockadecounterstheunwantedeffectsofcatecholaminesonthemyocardiumaswellasmoderatelyreducingafterload.Sinceangiotensinisavasoconstrictorandhassometoxiceffectonthemyocardium,bothcontributingtoheartfailure,inhibitionoftherenin–angiotensinsystemhasbeenlogicaltherapyforheartfailure.However,useofangiotensinconvertingenzyme(ACE)inhibitorsmayincreasebradykininlevels,whichareresponsibleforthecoughthatmaybeassociatedwiththeiruseaswellasangioedemathatmayresultfromthesamemedications.
简介:目的探讨广谱氯离子通道阻滞剂4,4’-二异硫氰基芪-2,2’-二磺酸(DIDS)对大鼠缺血再灌注损伤心肌细胞凋亡的影响及其机制。方法雄性SD大鼠36只随机分为3组:缺血再灌注组(A组)、DIDS处理组(B组)和LY294002预处理组(C组)。伊文兰和TTC染色测定心肌梗死范围,TUNEL方法定性和定量检测心肌细胞凋亡指数,Westernblot测定蛋白激酶B(Akt)的表达。结果与A组比较,B组心肌梗死范围和心肌细胞凋亡指数明显降低[(38.8±7.7)%”(54.2±10.8)%,(8.9±1.8)%”(17.6±3.5)%.P〈0.01];磷酸化Akt表达水平明显增加(P〈0.01)。与A组比较,C组梗死面积、凋亡指数无明显减小,磷酸化Akt水平无明显变化(P〉0.05)。结论DIDS能够抑制大鼠缺血再灌注所致的心肌细胞损伤,可能是通过信号分子磷脂酰肌酶三羟基激酶/Akt的调节。
简介:患者女性,64岁,因活动后心慌。心前区不适3年.加重伴心前区疼痛1天就诊。查体:患者痛苦面容.皮肤湿冷;体温35.50℃;心率160次/分;呼吸28次/分;血压80/60mmHg。立即检查心电图示房室折返性心动过速。随即在心电监测下做左侧颈脉窦按摩,按摩约3s后,即出现1.34s的窦性停搏,又在一次P—R间期缩短的室上性激动后出现-12.38s的窦性停搏.当停搏8.86s时,患者出现两眼上翻,面色苍白.肌张力增强,立即心前区叩击一次并胸外心脏按压,3.5s后相继出现2.4s的室性心动过速,6s的室性自主心律,频率为27次/分的窦性心动过缓,以及3~6s的窦性停搏,持续心脏按压.吸氧约2min后.患者意识恢复,心电图转为窦性心律,呈窦性心动过缓.LGL预激综合症,缺血性ST段压低,继续观察心电图变化,可见ST段压低有所缓解,遂送入病房,给予抗凝。抗血小板凝集,J3受体阻滞剂等治疗,7天后临床治愈出院。
简介:BackgroundAldosteroneblockerscouldreducetheincidenceofventriculararrhythmiasinmyocardialinfarction(MI)patientsbyregulatinghyperpolarization-activatedcyclicnucleotide-gatedchannel(HCN)expression.ButthemechanismunderlingHCNexpressionisunclear.MethodsEighteenratssurviving24hourspostMIwererandomlydividedinto3groups:MI,spironolactone,andspironolactone+antagomir-133(miRNA-133suppression).Shamgroupratshadasuturelooselytiedaroundtheleftcoronaryartery,withoutligation.HCN2andHCN4proteinandmRNAlevel,andmiRNA-133levelintheborderzoneofpost-MI1weekmyocardiumweremeasured.ResultsSpironolactonesignificantlyincreasedmiRNA-133levelsanddown-regulatedHCN2andHCN4atbothmRNAandproteinlevelsinpost-MIborderzonemyocardium.Antagomir-133reducedtheeffectsofspironolactoneonHCN2andHCN4proteinlevels.ConclusionsTheresultssuggestthatmiRNA-133isinvolvedinspironolactoneinducedHCNexpression,andpartiallycontributedtopost-MIventriculararrhythmias.
简介:BackgroundThemyocytedysfunctionmaybepresentinaorticstenosis(AS)patientswithpreservedleftventricularejectionfraction(LVEF).Earlyaorticvalvereplacement(AVR)canreversetheLVhypertrophyandimproveLVsystolicperformanceandclinicaloutcome.StrainimaginghasdemonstratedtobethemostappropriatemethodtoevaluateLVmyocardialcontractility.However,4D-strainimagingechocardiographyforthedetectionofsubclinicalleftventriculardysfunctioninASpatientswithpreservedLVEFisseldomstudied.MethodsWeprospectivelyenrolled30consecutivemoderatetosevereASpatientswithpreservedLVEF,and30healthycontrols.Conventionalechocardiographyand4D-strainimagingechocardiographywereundergoneintwogroups.The4Dstrainechocardiographicanalyseswereundertakenbyusing4DAutoLVQsoftware.ResultsComparedwiththehealthycontrols,themoderatetosevereASpatientswithpreservedLVEFhadsignificantlydecreasedglobalradialstrain(GRS),globallongitudinalstrain(GLS),globalareastrain(GAS)and4Dstrain(P<0.05),hadsignificantlyincreasedleftventricularend-diastolicvolumeindex(LVEDVI)andleftventricularmassindex(LVMI)(P<0.05),andhadlowerglobalcircumferentialstrain(GCS)(P>0.05).ConclusionsImpairedLVmyocardialcontractilityexistsinmoderatetosevereASpatients,althoughLVEFispreserved.4D-strainimagingechocardiographycandetectearlyleftventriculardysfunctioninASpatientswithpreservedLVEF.
简介:目的江西地区先心病发病率相对较高,危害百姓健康。江西省政府已从2010年始,将先心病儿童免费救治工作作为一项重要为民工程。虽然先心病病因尚不完全清楚,但近年研究发现某些基因突变与先心病发生密切相关。本课题组对局部地区(江西地区)的先心病患者进行已知致病基因(EVC,TLL1,TBX5和PTPN11)筛查,以发现与疾病密切相关和显性率高的致病基因,为将来个体化治疗提供理论基础,必将有助于局部地区乃至中国先心病出生缺陷的控制。方法从先心病DNA样本库,按照编号随机按序抽取患者DNA标本46份和100个遗传背景匹配的健康对照。根据PubMed文献报道,选择已知的4个致病基因EVC,TLL1,TBX5和PTPN11,并设计相关引物,利用DNA直接测序法四个基因的外显子及外显子-内含子进行双向测序。若核苷酸变异未在100个正常人群中发现,则定为基因突变。结果散发先心病室缺,房缺,动脉导管未闭、复杂先心分别为24例,12例,5例和5例。基因筛查发现EVC基因突变4个,分别是位于3号染色体的L115V突变,6号染色体的Y258H突变,10号染色体的K445Q突变,15号染色体的R760CQ突变,其中Y258H突变出现在房缺患者,其它3个突变见于室缺患者。发现TLL1基因多态性2个,分别是位于7号染色体的E719E,19号染色体的1991A,在房缺、室缺和PDA中均有存在。在房缺和室缺患者中发现PTPN11多态性1个,位于3号染色体的F19L。46个筛查对象中未发现TBX5基因突变和多态性。基因突变患者的临床表型与非基因突变者比,症状和体征的严重程度、发病年龄均无明显差异。结论EVC基因是江西地区间隔缺损患者的常见致病基因。突变患者的临床症状严重程度与非突变者相比无差异。由于是基因筛查工作中的前期结果,还需要后期工作中进一步增大样本量,以便对先心病患者基因型和表型的关联研究加以客观分析。