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were excluded.ACE inhibitorswere not administeredin the six monthsfollow-upperiod.Thepolimerasechainreactionmethodwasusedtoanalyzethe l/D polymorphism.Twop had subacuteocclusion(1.7%)and 113hadangiogrephy(A) at 6.2 + 1.7 months.QuantitativecoronaryanalysiswasperformedintwoorthogonalviewsbeforeandafterPTCAandat sixmonthsfollow-up(f-up)(table).(*)Analysisof thevarfance.

Noaignificsntdifferencewasfoundat f-up A amongp withthe D allele,whilethe VIgenotypeseemato preventlateIuminalnarrowingafterCS.

DR

E.Alt,J. Paaquantonio,C. Beilharz,D.Preter,T.Fliedner,W.Erhardl,A. Stembergerl,A. Schbmig.1/. Med.Klinik,Inst.forExp.SurgerxTschnischeUniversitdtMtincherr,GermarrxKlinikumrechtsderlsqTwhniacheUnivemittJtMOnchen,Germany,DeufschesHerzzentmm,TwhniecheUniveKSiti5tM(h?chan,Garmany

Background:Restenosisremainsa”majorconcerflincoronaryarterystefltiflg.Thepurposeof thisstudywaatoexaminetheeffectof thesymmetryofstentstrutsandvascularinjuryon restenosis.

Methods:Thirty-twoPalmez-Schatzslottedtubestentswereimplantedin16healthysheepinboththeIAD andLCX.After30dayshistomorphometricanalysiswaspdormed withstentstrutsintact.Neointimalthickness,injuryindex,andstentsymmetryweremeasuredin segmentsfor eachindividualstrut.Symmetrywasquantifiedby angularburden,a measurementof thesegmentof openvesselwall supportedby eachstrut relatedto the totalcircumference,expressedin degrees.

Results:Histomorphometricresultswereasfollows(mean+ SD):neoin-timalthickness=360+ 160wm;injuryindex= 0.4+ 0.6;angularburden=24.2+ Il.@. Therewassignificantpositivecorrelationbetweenneointimathicknessandangularburden(p < 0.02)andbetwwn neointimathicknessandinjury(p < 0.01).

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Conclusion:Stentsymmetryandvascularinjurybothhavestrongeffectson experimentalrestenosis.This finding impliesthat stentewhichexpandmoreasymmetricallyand distributeforce evenlyalongthe vesselwall willexperienwIesalatelumenarea10ss.

D P

R.Komateu,M.Ueda,M.Kawasaki,N.Monta,Y.Naketeuchi,K.Fujii,M.Nakeo,S.Toyama,A.E.Becker.OsakaCifyUniversityMedicSISchOOl,Osaka,Japan,AcademicMedicalCentecAmsterdam,TheNetherlands

Coronarystentingpresentlyiswidelyacceptedasa methodto preventearlyocclusionafter percutaneoustransluminalcoronaryangioplaety(PTCA)ordirectionalcoronaryatherectomy(DCA).However,complicationsdo occur,suchseacuteor subacutethrombosis,and“late”restenosiscertainlyis notcompletelyabolished.Thusfar, little ia knownwith regardto the pathologyafter stentingin humancoronaryarteries.We investigatedimmunocyto-chemicsllythe cellularcompositionof the neointimaaftercoronarystentingin humans.Six coronaryarteries,obtainedfrom 6 patientswho had died

6 daysto 12 monthsafter stenting,werestudied.Onlyone patientdevel-opedclinicalrestenosis.Monoclinalantibodiesagainstsmoothmusclecells(SMCS),macrophages(M 0) and endotheliaicells were used.At 6 daysafterstenting(n = 1), thrombiwith accumulationof someM @wereseenaroundthe wiresof the stent.At 1 month(n = 1),eartyneointimalprolifera-tioncomposedof actin-negativespindlecells,actin-positiveSMCSand M@wasfound,intermingledwith remnantsof thrombus.Threearterieswithoutrestenoeis(5-12 monthsafter stenting)showeda diatinctneointimapre-dominantlycomposedof SMCS.Thearterywith restenosis(5 monthsafterstenting)revealedalmosttotalocclusiondueto a richlyvascularizedneointi-malproliferation,whichcontainedSMCSandabundantMO.Thesefindingsshowthatcoronarystentingin humansis associatedwithneointimalforma-tion. The strikingneovascularizationin the casewith restenosissuggeststhatongoingorganizationof stent-relatedthrombosismayplaya role.

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M.E.Kleinman,G.D.Cipolla,J. Cui,N.Chronos,S.B.KingIll,K.A.Robinson.Dapt.of Medicine(Cardiology)EmoryUniversitySchoolofMedicine,Atlanta,GA,USA

Stentseliminateacuteand chronicrecoilafter PTCAbut are associatedwithgreaterneointimaformation,whichmaybedueto stimulationof cellularproliferation(CP).We testedwhetherstentscausedgreaterarterialwallCP than balloonangioplasty(AP)by giving3H-thymidine(100 ~Ci/kg IV)to rabbitsat 3, 7, 14,and 28 d afterAP in one iliacarteryand stent in thecontralateralartety,asameasureoftheextentofDNAsynthesia.Thearlerieswereexcised2 hafterinjectionofthenucleicacidradiolabel,solubilized,andradioactivitywasmeasuredby liquidscintillationcounting.

Rasu/ts:Peaksampleradioactivitywasobservedat3d for bothstentandAP,and decreasedthereafter.At 14d (2.52+ 0.47 vs 1.064C0.42 nCi,p< 0.05)and 26 d (2.21+ 0.95 vs 0.53 + 0.14 nCi, p = 0.056),however,radioactivitywashigherin stentthanin AP.

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Conclusions.’Stentimplantationcausedincreasedlate (2 and4 wk)cel-lular proliferationcomparedto ballcenangioplasfyin the iliac arteriesofnormalrabbits.Greaterneointimaformationobsenmdfor stentedhumanarteriesmaybeexplainedin partbycontinuedlatecellularproliferation.

I I l SA

P IH.Yokoi,H.Nosaka,T.Kimure,T.Tamura,Y.Nakagawa,N. Hamaaakl,M.Nobuyoehi.KokursMemorfa/Hospital,Kitakyushu,Japan

Recentreportsshowedthat betterlate outcomeof coronarystentingwasprimarilyrelatedto the minimallumendiameter(MLD)immediatelyaftertheprocedure,andthe useof high-pressurestentdilatation(HPSD)achievedthe biggerMLDby IVUSexaminations.The purposeof.the presentstudywas to investigatethe impactof HPSDon late angiographicand cllnicaloutcomewithPalmsz-Schatz(PS)stentimplantation.Asof December1994,mnsecutive192patients(pts)(212lesions)underwentsuccessfulsinglePSstentimplantationfor new,discrete(< 15mm)lesionsin larger(> 3.0 mm)coronaryarteries,excludingvein graft,total ecclusionand severecalcifiedlesions.Accordingto final balloonpressure,these pts were divided intothreegroups:lowpressure(< 10atm),mediumpressure(lC-14 atm),highpressure(> 14atm).Follow-up(FU)quantitativeangiographywasobtainedfmm1971esions(93%)after6monthsorearlierwhenindicatedbysymptoms.