简介：

简介：

简介：Elevatedheartrateisamajorriskfactorforcardiovasculardiseases.Theinhibitoroffunnycurrent(I(f)),ahyperpolarization-activatedcyclicnucleotide-gatedchannelcurrent,ivabradineisanewagentselectivelyreducingheartratedevoidofothercardiovasculareffects,whichhascomeintothemarketinEuropeformorethan3years.Ithasbeenapprovedthatpureheartratereductionbyivabradinecanimprovemyocardialischemia,endothelialfunctionandmyocardialcontractilefunction.Long-termadministrationwillnotincreaseall-causemortality.Itstherapeuticvalueinstablecoronaryarterydiseasehasbeenverifiedinclinicalpractice,whileinotherfieldsofcardiovasculardiseasesstillneedsmoreevidence-basedmedicalresearch.Thisarticleisareviewaboutitsrecentresearchadvancesinexperimentalandclinicalstudies.

简介：ObjectiveThestudywillexploreeffectsoftheautoantibodiesagainstAT1receptorandangiotensinⅡontherefractoryhypertension.MethodsSeventy-sevenpatients(46menand31women)withessentialhypertensionweredividedintogroupsofrefractoryhypertension(RH)andhypertension(HT)accordingtothe1999WHO-ISHGuidelinesfortheManagementofHypertension.Fortynormotensives(22men)wererecruitedascontrols.Themeanagewas54.3±13yearsoldinRHgroup,53.5±9yearsoldinHTgroupand51.2±11.9yearsoldinnormotensives(NT)group.Themeanbloodpressurewas154.2±9.4/98.4±8.2mmHginRHgroupand130.1±7.6/80.5±6.7mmHginHTgroupaftercombinationdrugtherapyofhypertensionfor4weeks.BloodpressureinNTgroupwas120.8±11.7/76.4±7.2mmHg.Theepitopeofthe2ndextracellularloopsofAT1receptorwassynthesizedandusedasantigenstoscreentheautoantibodiesbyELISA.Plasmaangiotensin(Ang)IIwereexaminedbyaradioimmunoassay.ResultsT

简介：BackgroundFlavonoidsfromfruits,vegetablesandplantshavebeenwidelystudiedontheireffectsofimprovinglipidemia,anti-inflammation,anti-plateletaggregationandanti-oxidativeactivities.However,wedon'tknowifflavonoidsfromrapebeepollenhavethesameeffectsinpatientswithdyslipidemia(DL),type2diabetesmellitus(T2DM),andcerebralinfarction(CI).MethodsThestudyinvolvedwithpatientsselectedanddividedinto4groups,30casesofDL,ofT2DM,ofCIandhealthcontrol(HC)foreach.Fortymgflavonoidsfromrapebeepollenadministratedorallytwiceadayfortwomonths.Bloodsugar(BG),totalcholesterol(TC),triglyceride(TG),highdensitylipoprotein-cholesterol(HDL-C),lowdensitylipoprotein-cholesterol(LDL-C),whiteblood-cellcounts(WBC),plateletcounts(PLT),high-sensitivityC-reactiveprotein(hsCRP)andmalondialdehyde(MDA)wereanalyzedinfourgroupsbeforeandaftertakingflavonoidsfortwomonths.Results(1)BasiclevelsofTC,BG,WBC,PLTandhsCRPingroupsofT2DM,CI,andTGandMDAingroupsofDL,T2DMandCIweresignificantlyhigherthanthoseinHC(P<0.05-0.001).(2)ThelevelsofTG,WBC,PLT,hsCRPandMDAweresignificantlydecreased,whileHDL-Cwasremarkablyincreasedaftertakingflavonoidsfortwomonths(P<0.05-0.001)ingroupofDL,T2MD,andCI.TheseindexeswerenotdifferentinthegroupofHCaftertakingflavonoids(P>0.05).ConclusionsTheresultscouldindicatemetabolicdisturbance,inflammation,andhighoxidativestressinpatientswithdyslipidemisa,type2diabetesmellitus,andcerebralinfarction.Theflavonoidsfromrapebeepollenmayhaveeffectsofantioxidantactivity,improvinglipids,andanti-inflammationonthesepatients.

简介：

简介：

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：Toinvestigatetheelectricalremodelingandtheeffectsofamiodaroneandlosartanonelectricalremodelinginrapidatrialpacingonrabbitmodel.Methods40normalrabbitswererandomlydividedinto4groups:thesalinegroup(controlgroup),amiodaronegroup,losartangroup,ami+losgroup.Allrabbitswereraiseddrugsinaweek.Theatrialeffectiverefractoryperiod(AERP)wasmeasured.Then,takearapidatrialpacing(600bpm)andtheAERPwasmeasuredafter0.5,1,2,4,6and8hourspacingand30minutesaftertheterminationofrapidpacing.Results①Incontrolgroup,after8hoursrapidpacing,AERP200andAERP150weresignificantlyshortened16.11%±3.1%(P<0.01)and9.99%±4.2%(P<0.01).AndthedegreeofAERPshorteninginducedbyrapidpacingwasgreateratbasiccyclelengthsof200ms(BCL200)thanthatatBCL150.TheAERPofamiodarone,losartangroupandami+losgroupwerenotshortenedduringrapidpacing.②Inthecontrolgroup,aftertheterminationofrapidpacing,theAERPgraduallyincreased.TheAERPatalloftheBCLSexaminedrecoveredtoalmostthe95.78%and96.76%ofbaselinevalueswithinthefirst10minutesandrecoveredtoalmostthe99.07%and99.39%ofbaselinevalueswithinthefirst30minutes.ConclusionsShort-termatrialrapidpacingcaninducetheatrialelectricalremodeling.Amiodaroneandlosartancanpreventtheelectricalremodeling.

简介：ObjectivesToinvestigatetheanti-apoptoticeffectsofmesenchymalstemcells(MSCs)onhypoxicinjuredcardiacmyocytesinvitro.MethodsMSCswereisolatedfrombonemarrowofSprague-Dawley(SD)rats,andcardiacmyocytesfromneonatalrats.Theratcardiacmyocyteswereco-culturedwithMSCsorMSC-conditionedmediainanoxia(95%N2+5%CO2)for72hours.CellapoptosiswasmeasuredbyHoechst33258staining.TheexpressionofBcl-2andBaxincardiacmyocyteswastestedbyWesternBlot.ResultsTheapoptoticratewas51.6%±2.4%whencardiacmyocyteswereculturedincontinuoushypoxiaandwassignificantlydecreasedwhencardiacmyocyteswerecoculturedwithMSCsorMSC-conditionedmedia(15.1%±5.4%and24.0%±4.2%respectively,P<0.001).ThedecreasedexpressionofBaxinthecardiacmyocyteswasgreatlyrelatedtothedecreasingofapoptosis,buttherewasnodifferenceinBcl-2expressionamongthesegroups.ConclusionsCo-culturedMSCsshowedsignificantanti-apoptoticeffectsoncardiacmyocytesincontinuoushypoxia.ThemechanismmaybetheinteractofcelltocellandparacrineofcytokineswhicheffectedtheexpressionofBaxinthecardiacmyocytes.

简介：BackgroundIt'saneffectivetreatmenttoachievepercutaneouscoronaryinterventioninAMIpatients,whichrapidlyimprovesthebloodsupplyofcoronaryartery.StudieshaveshownthatdifferentmodesofPCItherapyhavedifferenteffectsinAMIpatients.TheaimofthisstudywastoexploretheeffectsandclinicalsignificancesofemergencyorlatePCItherapyonleftventricularremodelingandcardiacautonomicfunctioninacutemyocardialinfarction(AMI)patients.MethodsOnehundredandfiftycasesofAMIpatientswererandomlydividedintothreegroups,whichallweregiventheroutinemedicine.ThetwotherapygroupsweretheemergencyPCIgroup(n=60)andthelatePCIgroup(n=50).Thevariationsofheartrateturbulence(HRT)andheartratevariability(HRV)parameterswereobservedafter2weeksoftreatmentby24-hourambulatoryECG.ResultsComparedwiththecontrolgroup,after2weeksoftreatment,thelevelsofTS,SDNNandSDANNoftwoPCI-treatedgroupwassignificantlyhigher(P<0.01),TOwerelower(P<0.01)thanwhichinthecontrolgroup.ThereweresignificantdifferencesinTS,SDNN,SDANNandTObetweenthetwoPCItreatmentgroup(P<0.05).ConclusionEmergencyPCIorlatePCImaygivecoronaryeffectivereperfusion,improveleftventricularfunctionandautonomicnervousfunction,andpreventmalignantarrhythmiastooccur.ThetreatmentofprimaryPCIissuperiortodelayedPCI.

简介：

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：BackgroundStudieshaveshownthattheapo(a)gene(LPA)rs3798220polymorphismisassociatedwiththelevelsoflipidsandthecurativeeffectofstatintherapyforcarotidatherosclerosis(CAS).Whethercarriersofanapo(a)variantbenefitmorefromstatinremainsunclear.MethodsOnehundredandthreepatientswithCASwererecruitedfromApril2012toApril2013intheShundeFirstPeoplesHospitalAffiliatedtoSouthernMedicalUniversityinFoshan.Allpatientswereadministeredatorvastatin20mg/dandwerefollowed-upfor2years.withthelevelsofplasmaLp(a),totalcholesterol(TC),triglyceride(TG),highdensitylipoprotein(HDL),lowdensitylipoprotein(LDL).LPArs3798220genotypesofallpatientswereanalyzed.ResultsStatintreatmentsignificantlyreducedthelevelsofIMT,TC,TG,LDLandincreasedthelevelofHDL,butstatintreatmentdidnotreducethelevelofLp(a).AccordingtothecurativeeffectofstatintherapyinpatientswithCAS,rs3798220polymorphismhadacertaininfluenceonLDLandTClevels,butnotontheimprovementoftheIMT,TG,HDLandLp(a).ConclusionRs3798220polymorphismhasacertainimpactonthecurativeeffectsofstatin,onLDLandTClevels.

简介：Thestudyaimedtoinvestigatetheeffectsofivabradineonthelevelsofhypoxia-induciblefactor-1alpha(HIF-1α)andVEGFinserumofrabbitwithacutemyocardialinfarction(AMI).MethodsAMImodelwasestablishedbyligatingtheleftanteriordescendingbranchofthecoronaryarteryinNewZealandwhiterabbits.Twentyfiverabbitswererandomlydividedinto4groups:sham-operated(S),myocardial-infarction(M)withbisoprololtreatment(M+B)andivabradine-treated(I+M).Themedicaltreatmentbeganimmediatelyafterinfarctionandcontinuedfor3weeks.Serumofeachrabbitwasobtainedatthefollowingtimepoints(24hbeforetheoperation,24h,3d,1week,2weeksand3weeksaftertheoperation).ELISAwasusedtomeasurethelevelsofHIF-1αandVEGFofeachsample.ECGandheartrates(beforeandaftertreatment)wereanalyzed.ResultsBaselineheartrateshowednosignificantdifferencesbetweenthe3infarctedgroups(M,M+B,M+I).ThreeweekslatertheheartratesweresignificantlyloweringroupM+BandgroupM+IthaningroupM.However,therewasnostatisticdifferencebetweenthetwodrug-treatedgroups(P=0.848).ThelevelsofHIF-1αandVEGFingroupsM,M+BandM+I)increasedsignificantlycomparedwithgroupS(P<0.01).TheproductionsofHIF-1αandVEGFwereloweringroupM+BandgroupM+IcomparedwithgroupM(P<0.01).TherewasnostatisticaldifferencebetweenthegroupM+BandgroupM+I(P>0.05),andthecorrelativeanalysisrevealedthattheproductionofHIF-1αwaspositivelycorrelatedwiththatofVEGF(r=0.732,P<0.01).ConclusionIvabradinecanreduceheartrateandmeanwhiledecreasetheserumlevelsofHIF-1αandVEGFafterAMI.

简介：ObjectivesNitroglycerine(NTG)enhancescoronarybloodflowtocompromisedmyocardiumisimportantinrelievingischemia.However,themechanismforthisincreaseinmyocardialbloodflow(MBF)isnotwelldefined.Insmallvesselsandcapillaries,relativebloodviscosityplaysaveryimportantroleindeterminingmyocardialvascularresistance(MVR).MVRreduceisduepartlytotheincreaseinnegativechargeoferythrocytesurface.WethereforehypothesizedthattheenhancementofnutrientbloodflowtozonesofmyocardialischemiaduringNTGispartlysecondarytoreducedMVRandbloodflowviscosity.Thelatterisaffectedbythenegativechargeoferythrocytesurface.Methods6dogswithLADflow-limitingstenosis(group1)and6dogswithLADflow-limitingstenosisandLCxoccmusion(group2)werestudied.AtbaselineandduringintracoronaryinfusionsofNTG(0.3-0.6μg·kg-1·min-1),hemodynamics,MBF(mL·min-1·g-1),wholebloodviscosity(WBη,mPa.S),elongationindex(EI),eletrophoreticmobilityoferythocytes(EME,[μ.s-1)/(V.cm-1)])andpercentwallthickening(%WT)weredetermined.MVRwascalculatedusingdrivingpressure/MBF.ResultsAscomparedtobaseline,nochangesinhemodynamicswereseenduringNTG.MBFincreasedandMVRdecreasedsignificantlyinnormalbed,thecentral25%andtheentireofstenosedbed(P<0.05),withadecreaseinWBηinbothgroup1andgroup2dogs(18.6±9.7%and19.2±14.5%,respectively).However,the%decreaseinWBηwasproportionedtothe%increaseinMBForthe%decreaseinMVRonlyinthecentral25%ofstenosedbed(r=0.87,P<0.001),butnotintheentirestenosedbedandnormalbed.EIdidnotshowstatisticallysignificantdifferencesbetweenduringNTGandatbaseline,butEMEdidincrease.Andthe%decreaseinWBηduringNTGwasrelatedtothe%increaseinEME(r=0.83,P=0.01).ConclusionsNTGreducedmyocardialvascularresistanceandbloodviscosityduetothechangeofnegativechargeoferythrocytesurfacemay,inpart,bethe

简介：Themyocardialprotectionaffordedbyischemicpreconditioning(IPC)canalleviateischemia-reperfusioninjuryinnormalratheart.However,thismyocardialprotectionisseldomstudiedinthetype2diabeticratwithmyocardialischemiadisease.Inthisstudy,weaimedtoevaluatetheeffectsofATP-sensitivepotassiumchannels(KATPchannels)onIPCintheisolatedtype2diabeticratheartandtheroleofthesulfonylureagliclazide.MethodsStreptozotocin(STZ)-inducedtype2diabeticmaleWistarratswithorwithoutgliclazide(64mg/kgbodyweight,orally)andage-matchednon-diabeticcontrolratswereusedforallstudies.TheisolatedheartswereperfusedwithLangendorff'ssystemundertheconstantflow,pressureandtemperatureconditionswithKreb's-Henseleitsolution(K-H).After5minutesofbalanceperfusion,theseratswererandomlydividedintosixgroups:non-diabeticcontrolratswithoutIPC(CIR);non-diabeticcontrolratswithIPC(CIP);diabeticratswithoutIPC(DIR);diabeticratswithIPC(DIP);gliclazide-treateddiabeticratswithoutIPC(GIR);andgliclazide-treateddiabeticratswithIPC(GIP).GroupsCIR,DIR,andGIRweresubjectedto30-minglobalischemiaand60-minreperfusionforinductionofischemia/reperfusioninjury.GroupsCIP,DIP,andGIPweregiventhreecyclesof5-minischemiaand5-minreperfusionasIPC,andthenischemia/reperfusioninjuryprogramwasimplemented.Extentofischemia/reperfusioninjurywasmeasuredintermsofthereleaseoflactatedehydrogenase(LDH),creatinekinase(CK),andcreatinkinase-MB(CKMB)incoronaryeffluent.Afterperfusion,Kir6.2andSUR2AmRNAexpressionsinthemyocardialtissuewerecharacterizedbyfluorescentquantitativereal-timePCRmethod,andKir6.2andSUR2Aproteinexpressionswereassessedbyimmunohistochemistry.ResultInnon-diabeticcontrolrats,thereleaseofLDH,CK,andCK-MBincoronaryeffluentmarkedlydecreasedwithIPCcomparedwithNo-IPC(P<0.05),butnotindiabeticrats.However,ingliclazide-treateddiabeticrats,IPC-induceddecreaseintherele

简介：Toinvestigatetheeffectsofsimvastatinonmembraneioniccurrentsinleftventricularmyocytesofrabbitheartsufferingfromacutemyocardialinfarction(AMI),soastoexploretheionicmechanismofstatintreatmentforantiarrhythmia.MethodsForty-fiveNewZealandrabbitswererandomlydividedintothreegroups:AMIgroup,simvastatininterventiongroup(Statingroup)andsham-operatedcontrolgroup(CON).Rabbitswereinfarctedbyligationoftheleftanteriordescendingcoronaryarteryafteradministrationoforalsimvastatin5mg·kg-1·d-1(Statingroup)orplacebo(AMIgroup)for3days.Singleventricularmyocyteswereisolatedenzymaticallyfromtheepicardialzoneoftheinfractedregion72hlater.Wholecellpatchclamptechniquewasusedtorecordmembraneioniccurrents,includingsodiumcurrent(INa),L-typecalciumcurrent(ICa-L)andtransientoutwardpotassiumcurrent(Ito).Results①Therewasnotsignificantdifferenceinserumcholesterolconcentrationamongthreegroups.②ThepeakINacurrentdensity(at-30mV)wassignificantlydecreasedinAMIgroup(-25.26±5.28,n=13),comparingwithCON(-42.78±5.48,n=16),P<0.05,whileitwassignificantlyincreasedinStatingroup(-39.83±5.65pA/pF,n=12)comparingwithAMIgroup,P<0.01;ThepeakICa-Lcurrentdensity(at0mV)wassignificantlydecreasedinAMIgroup(-3.43±0.92pA/pF,n=13)comparingwithCON(-4.56±1.01pA/pF,n=15),P<0.05,whileitwassignificantlyincreasedinStatingroup(-4.18±0.96pA/pF,n=12)comparingwithAMIgroup,P<0.05;TheItocurrentdensity(at+60mV)wassignificantlydecreasedinAMIgroup(11.41±1.94pA/pF,n=13)comparingwithCON(17.41±3.13pA/pF,n=15),P<0.01,whileitwassignificantlyincreasedinStatingroup(16.11±2.43pA/pF,n=14)comparingwithAMIgroup,P<0.01.ConclusionsAMIinducessignificantdown-regulationofINa,ICa-LandIto.Pretreatmentwithsimvastatincouldattenuatethischangewithoutloweringtheserumcholesterollevel,suggestingthatsimvastatincouldrev

简介：BackgroundThevideo-assistedthoracoscopicsurgicaltechniquesarewidelyusedinthetreatmentofpatientswithcongenitalheartdiseaseswithgoodoutcomes.However,thefeasibilityandsignificanceofnursebasedearlycardiacrehabilitationincardiacintensivecareunit(ICU)forpatientswithtotallythoracoscopiccardiacoperationhasbeenseldomstudied.MethodsThirty-sixpatientswithtotallythoracoscopiccardiacoperationundertheconditionofthecardiacICUinGuangdongGeneralHospitalwererandomallocatedtotheinterventiongroupandthecontrolgroupbetweenJanuary2012toDecember2014.Thecontrolgroupreceivedstandardnursingcare,andtheinterventiongroupreceivedearlycardiacrehabilitationnursingcareinadditiontostandardcare.Theoutcomemeasuresincludedtheoxygensaturation(SpO2%),vitalcapacity,forcedexpiratoryvolumein1second(FEV1),andpaininthethoracicwound(visualanaloguescale,VAS),whichweremeasuredatthebaselineandwithin2-dayafter4-weeknursingcare.Forsafetyreason,wealsomonitoredtherateofperceivedexertion(RPE),heartrate,systemicbloodpressure.ResultsTherewerenon-significantdifferencesbetweenthegroupsinage,sex,totalnumberofcomorbidconditions,totalnumberofmedications,surgicaltime,andanesthetictime(P>0.05).Following4weekstreatment,thecardiopulmonaryfunctionsandVASscorewereimproved(P<0.05)inallgroups.Inaddition,theimprovementsweremoreintheearlycardiacrehabilitationnursecaregroupthaninthecontrolgroup(P<0.05).ConclusionTheearlycardiacrehabilitationnursingcareincardiacICUissafe,feasibleandbeneficialforpatientswithtotallythoracoscopiccardiacoperation.

简介：BackgroundThiazolidinediones(TZDs)notonlyimproveinsulinresistance,loweringbloodsugar,alsohasanti-atheroscleroticeffect.However,whethertheprotectiveeffectoncardiovascularpioglitazoneisstillcontroversial.MethodsTotally98patientswithcoronarydiseaseanddiabetesmellituswererandomlydividedintopioglitazonegroup(n=48)receivingconventionaltherapyandpioglitazone(15mg/day),andcontrolgroup(n=50)merelyreceivingconventionaltherapy.Thepatientswerefollowedupfor12months.TheplasmalevelofPlasminogenactivatorInhibitor1(PAI-1)andP-selectinweredetectedatbaselineandaftertreatmentfor12monthsbyELISA,andmajoradversecardiacevents(MACE)werestudied.ResultsPioglitazonetherapyfor12monthswasassociatedwithasignificantdecreaseofPAI-1[(7.9±1.4vs4.2±0.5)ng/mL,P<0.05]andP-selectin[(16.6±6.8vs12.4±3.6)ng/mL,P<0.05],MACEwassignificantlylowerinthepioglitazonegroupthaninthecontrolgroup[acutecoronarysyndrome(ACS):32.0%vs10.4%,P<0.05;targetvesselrevascularization:22.0%vs6.3%,P<0.05].ConclusionsPioglitazonecaneffectivelyreducetheplasmalevelofPAI-1,P-selectinandtheoccurrenceofMACEinpatientswithcoronaryheartdiseaseanddiabetesmellitus.