简介：Thisstudyinvestigatedtheeffectofcatheter-basedrenalsympatheticdenervation(RD)onleftventricularhypertrophy(LVH)andsystolicanddiastolicfunctioninpatientswithresistanthypertension.LVHanddiastolicdysfunctionareassociatedwithelevatedsympatheticactivityandincreasedmorbidityandmortality.TheeffectofRDonLVHandLVfunctionisunclear.MethodsandResultsForty-sixpatientsunderwentbilateralRD,and18patientsservedascontrols.Transthoracicechocardiographywasperformedatbaseline,andafter1monthand6months.Besidesreductionofsystolicanddiastolicbloodpressure(-22.5/-7.2mmHgat1monthand-27.8/-8.8mmHgat6months,P<0.001ateachtimepoint),RDsignificantlyreducedmeaninterventricularseptumthicknessfrom14.1±1.9mmto13.4±2.1mmand12.5±1.4mm(P=0.007),andLVmassindexfrom53.9±15.6g/m(2.7)(112.4±33.9g/m(2))to47.0±14.2g/m(2.7)(103.6±30.5g/m(2))and44.7±14.9g/m(2.7)(94.9±29.8g/m(2))(P<0.001)at1monthand6months,respectively.ThemitralvalvelateralE/E'decreasedafterRDfrom9.9±4.0to7.9±2.2at1monthand7.4±2.7at6months(P<0.001),indicatingreductionofLVfillingpressures.Isovolumicrelaxationtimeshortened(baseline109.1±21.7msvs.85.6±24.4msat6months,P=0.006),whereasejectionfractionsignificantlyincreasedafterRD(baseline:63.1±8.1%vs.70.1±11.5%at6months,P<0.001).Nosignificantchangeswereobtainedincontrolpatients.ConslusionsBesidestheknowneffectonbloodpressure,ourstudyshowedforthefirsttimethatRDsignificantlyreducesLVmassandimprovesdiastolicfunction,whichmighthaveimportantprognosticimplicationsinpatientswithresistanthypertensionathighcardiovascularrisk.

简介：ObjectivesToexamineeffectofatorvastatinontheexpressionofCOX-2inperipheralbloodmonocytesfrompatientswithearlystageofacutemyocardialinfarction(AMI)invitro,andtheIL-6concentrationinsupernatantwasalsoexamined.MethodsPatientswithAMI(n=40)andwithstablecoronaryheartdisease(CHD)(n=18)wereregistered.Peripheralbloodmonocytesfromallparticipantswereisolatedandculturedfor24hrs,butthosefrompatientswithAMIwererandomlyexposedtovariousconcentrationofatorvastatin(0,0.1,1,10μmol/L)duringthecultivation.COX-2mRNAexpressioninmonocyteswasanalyzedbyreversetranscriptionpolymerasechainreaction(RT-PCR).ConcentrationofIL-6insupernatantwasmeasuredbyenzyme-linkedimmunosorbentassay(ELISA).ResultsCOX-2expressionandIL-6secretionbyperipheralbloodmonocytesfrompatientswithAMI(0.92±0.13,205±46pg/ml)werehigherthanthatfromcontrols(0.19±0.08,41±8pg/ml)(bothP<0.05),andCOX-2expressionwasdramaticallyreducedupto52%byatorvastatin(P<0.05),inaconcentration-dependentmannerrespectively.TheexpressionofCOX-2frompatientswithAMIwasobviouslycorrelatedwiththesecretionofIL-6(r=0.636,P<0.05).COX-2expressioninthemonocytesafterinterventionofatorvastatinwasalsopositivelycorrelatedwithIL-6secretionbythesecells(r=0.783,P<0.05).ConclusionsCOX-2involvesinflammatoryrespondinearly-stageofAMI.AtorvastatinmaydecreaseCOX-2expressioninperipheralbloodmonocytesfrompatientswithAMIandcyclooxygenase-dependentpathwaymightbecorrelatedwiththeanti-inflammationmechanismofstatin.

简介：BackgroundTotheeffectofpercutaneouscoronaryintervention(PCI)onplasmalevelofN-terminalpro-Btypenatriureticpeptide(NT-proBNP)inpatientswithcoronaryheartdisease(CHD)andnormalleftventricularfunction.MethodsOnehundredandfivepatientswithCHDandnormalventricularfunctionwereenrolled.BloodsamplesforassessmentofNT-proBNPandcTn-TwerecollectedbeforeandafterPCI.ResultsThemeanleftventricularejectionfractionwas60.3±5.3%.Afterrevascularization,theleveloflgNT-proBNPwassignificantlyreduced(2.40±0.44vs2.23±0.43,P<0.001).SubgroupanalysisshowedthattheleveloflgNT-proBNPwasconsistentlydecreasedindifferentclinicalclassifications(stableangina45,unstableangina31andacutemyocardialinfarction29)andtarget-vesselrevascularization(leftanteriordescendingartery30,leftcircumflexartery26andrightcoronaryartery49),andin99patientswithoutelevationofpost-proceduralcTnT,butitshowedatrendofnon-significantincreasein6patientswithelevatedcTn-T.ConclusionsOurstudydemonstratesthatsuccessfulPCIreducesplasmaNT-proBNPconcentrationinpatientswithCHDandnormalventricularfunction.ThisimplicatesthattheimpactofPCIshouldbeconsideredintheinterpretationofNT-proBNPchangeinclinicalpractice,andfurtherstudiesarenecessarytoinvestigatethedirectand/orindirecteffectofmyocardialischemiaonBNP/NT-proBNP.

简介：Previousstudiessuggestthatreductionanddysfunctionofcirculatingendothelialprogenitorcells(EPCs),anddysregulationinstromalcellderivedfactor-1/CXC-chemokinereceptor4(SDF-1/CXCR4)axisindiabetescouldbetherapeutictargetsfordiabeticischemicstroke.ThisstudyinvestigatedtheefficacyofCXCR4-primingEPCsoncerebralrepairfollowingischemicstrokeindb/dbdiabeticmice.BonemarrowderivedEPCsfromdb/+controlmiceweretransfectedwithadenovirus(1×10~7IU)carryingCXCR4(Ad-CXCR4-EPCs)ornull(Ad-null-EPCs).Thedb/dbmiceweredividedintothreegroupsforEPCsinjection(2×10~5cells/100μl):Ad-CXCR4-EPCs,Ad-null-EPCsorsaline(vehicle),viatailvein2hrsaftermiddlecerebralarteryocclusion(MCAO)surgery.Cerebralbloodflow(CBF)wasmeasuredwithlaserDopplerflowmeter.Miceweresacrificedat2or7daysthereafter.LevelofcirculatingEPCswasmeasuredbyflowcytometry.Ischemicdamage,cerebralmicrovasculardensity(MVD),angiogenesisandneurogenesisweredeterminedbyhistologicalstainingwithFluoro-J,CD31,CD31+BrdU,NeuN+BrdU,GFAP+BrdU,respectively.Results(table)showed:1)LevelsofCXCR4expressionwerereducedinthebrainandEPCsofdb/dbmiceasmeasuredbyreal-timeRT-PCRandwesternblotanalyses(datanotshown);2)ThelevelofcirculatingEPCswasmoreinthemicetreatedwithAd-CXCR4-EPCs;3)EPCtransfusionimprovedCBF,increasedMVD,angiogenesisandneurogenesisinperi-infarctarea,anddecreasedischemicdamage.TheefficacieswerebetterinAd-CXCR4-EPCsgroup.DatasuggestthattransfusionofAd-CXCR4-EPCscouldbeatherapeuticavenueforischemiastrokeindiabetes.

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