简介：Inrecentyears,intravascularultrasound(IVUS)follow-upisalwaysusedintheevaluationofthedevelopmentofatherosclerosis,anditcanalsobeusedastheendpointofdrugtherapyinclinicalobservation.Since1994,thefirststatinlipid-lowering4Sexperimentresultswasreported,thefollowingstatinforlipid-loweringtestsrepresentedbyREVERSALPROVE-IT,TNT,IDEAL,ASTEROIDandJUPITERstronglyconfirmedthatfurtherreducetheefficacyoflow-densitylipoproteincholesterol(LDL-C)(toenhancethelipid-loweringtreatment)accesstoincreaseeffectofthecardiovascularprotectionandalsoreversetheplaques'progress.Butscholars'opinionsonthemeritsanddemeritsofenhancestatincholesterol-loweringtherapyhasbeenindebate.Wereviewtherecentworkonstatinsandreversalofarterialplaquesforanumberofclinicalstudies.

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简介：Objective:Toobservetheeffectofstatinsonpreventingparoxysmalatrialfibrillation(PAF)afterpacemakerimlantationinpatientswithsicksinussyndrome.MaterialsandMethods:68patientswereselectedinwhichthepacemakershadbeenimplantedduetosicksinussyndrome,andwererandomlydividedintoastatintreatmentgroupandacontrolgroup.Afterthepacemakerimplantation,onlythepatientsintreatmentgroupweregiven20mgatorvastatinoncepernight,withotherconditionsbasicallysimilartothoseinthecontrolgroup.Atthe3rd,9th,15th,and21stmonthsaftertheimplantation,thepacemakerswereprogrammed,andthePAF-relatedinformationstoredinthepacemakerwererecalledandanalyzedstatistically.Results:Aftertheadministrationofstatinsfor9monthssincetheimlantation,theoccurrenceratesofPAFinthetreatmentgroupwasrelativelylowerthanthoseinthecontrolgroup.Afterfurtheradministrationofstatinsfor15months,boththeoccurrencerateofPAFandtheburdenofatrialfibrillationinthetreatmentgrouphadsignificantlydeclined.Aftercontinuousadministrationofstatinsfor21months,boththeoccurrencerateofPAFandtheburdenofatrialfibrillationinthetreatmentgroupweresignificantlylowerthanthoseinthecontrolgroup.Conclusion:Long-termadministrationofstatinscanreducetheriskofPAFaftertheimplantationofapacemakerinpatientswithsicksinussyndrome.

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简介：TheannualmeetingoftheHeartFailureAssociationofESCinLisbon,inJune2005,wasexceptionallysuccessful.Thereweremanyveryinterestingpresentationsandworkshopswiththeuniquetitle:StatinsinheartfailureCholesterol-loweringisnottheonlygoalHeartfailure(HF)isaprogressivediseasewithcoronaryarterydisease(CAD)asthemostoftenunderlyingetiology.TreatmenttopreventprogressionofheartfailurehasbeentargetedtoreversetheconsequencesofHFandtoalessextentthecause-theatheroscleroticplaqueitself.Ontheaverage50%ofpatientswithheartfailurearetreatedwithlipidintervention.Lipid-loweringtreatmentwithstatinsclearlyreducesmorbidityandmortalityofpatientswithdocumentedCAD.SincetheprevalentetiologyofheartfailureisCAD,itspreventionmayreduceheartfailureprogression.However,recentstudiessuggestthatpleiotropiceffectsofstatinsaremoreimportantthantheinfluencerelatedtotheircholesterolloweringmechanism.Furthermoreitissuggestedthatlowlevelsofcirculatinglipoproteinsandcholesterolmaybeindependentpredictorsofimpairedoutcomeinpatientswithheartfailure.Therearesomepossibleexplanationsforthisfinding.Highlevelsofcholesterolcanbebeneficialtoheartfailurepatients;cholesterol-richserumlipoproteinsareabletomodulateinflammatoryimmunefunctionbecausetheybindanddetoxifybacteriallipopolysaccharide,averystrongstimulatorofthereleaseofproinflammatorycytokinesthatpromoteheartfailureprogressionanddeath.SocurrentrecommendationsstronglyemphasizethattheaimoftreatmentofHFisnottolowercholesterol.