1.Thefailureofahigh-profilecholesteroldrughasthrownaspotlightonthecomplicatedmachinerythatregulatescholesterollevels.Butmanyresearchersremainconfidentthatdrugstoboostlevelsof'good'cholesterolarestilloneofthemostpromisingmeanstocombatspirallingheartdisease.
2.DrugcompanyPfizerannouncedon2Decemberthatitwascancellingallclinicaltrialsoftorcetrapib，adrugdesignedtoraiseheart-protectivehigh-densitylipoproteins(HDLs).Inatrialof15000patients，asafetyboardfoundthatmorepeoplediedorsufferedcardiovascularproblemsaftertakingthedrugplusacholesterol-loweringstatinthanthoseinacontrolgroupwhotookthestatinalone.
3.Thenewscameasakickintheteethtomanycardiologistsbecauseearliertestsinanimalsandpeoplesuggesteditwouldlowerratesofcardiovasculardisease."Therehavebeennoredflagstomyknowledge,"saysJohnChapman，aspecialistinlipoproteinsandatherosclerosisattheNationalInstituteforHealthandMedicalResearch(INSERM)inPariswhohasalsostudiedtorcetrapib."Thiscancellationcameasacompleteshock."
4.TorcetrapibisoneofthemostadvancedofanewbreedofdrugsdesignedtoraiselevelsofHDLs，whichferrycholesteroloutofartery-cloggingplaquestotheliverforremovalfromthebody.Specifically，torcetrapibblocksaproteincalledcholesterolestertransferprotein(CETP)，whichnormallytransfersthecholesterolfromhigh-densitylipoproteinstolowdensity，plaque-promotingones.Statins，incontrast，mainlyworkbyloweringthe'bad'low-densitylipoproteins.
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5.Researchersarenowtryingtoworkoutwhyandhowthedrugbackfired，somethingthatwillnotbecomeclearuntiltheclinicaldetailsarereleasedbyPfizer.Onehintliesinevidencefromearliertrialsthatitslightlyraisesbloodpressureinsomepatients.Itwasthoughtthatthismildproblemwouldbeoffsetbytheheartbenefitsofthedrug.Butitispossiblethatitactuallyprovedfatalinsomepatientswhoalreadysufferedhighbloodpressure.Ifbloodpressureistheexplanation，itwouldactuallybegoodnewsfordrugdevelopersbecauseitsuggeststhattheproblemsarespecifictothiscompound.OtherprototypedrugsthatarebeingdevelopedtoblockCETPworkinaslightlydifferentwayandmightnotsufferthesamedownfall.
6.ButitisalsopossiblethatthewholeideaofblockingCETPisflawed，saysMotiKashyap，whodirectsatherosclerosisresearchattheVAMedicalCenterinLongBeach，California.WhenHDLsexcretecholesterolintheliver，theyactuallyrelyonLDLsforpartofthisprocess.SoinhibitingCETP，whichpreventsthetransferofcholesterolfromHDLtoLDL，mightactuallycauseanabnormalandirreversibleaccumulationofcholesterolinthebody."You'reblockingaphysiologicmechanismtoeliminatecholesterolandeffectivelyconstipatingthepathway,"saysKashyap.Goingup
7.Mostresearchersremainconfidentthatelevatinghighdensitylipoproteinslevelsbyonemeansoranotherisoneofthebestroutesforhelpingheartdiseasepatients.ButHDLsarecomplexandnotentirelyunderstood.Oneapproveddrug，calledniacin，isknowntobothraiseHDLandreducecardiovascularriskbutalsocausesanunpleasantsensationofheatandtingling.Researchersareexploringwhethertheycanbypassthissideeffectandwhetherniacincanlowerdiseaseriskmorethanstatinsalone.Scientistsarealsoworkingonseveralothermeanstobumpuphigh-densitylipoproteinsby，forexample，introducingsyntheticHDLs."Theonlythingw
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