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dc.contributor.authorChapman, M. John
dc.contributor.authorGinsberg, Henry N.
dc.contributor.authorAmarenco, Pierre
dc.contributor.authorAndreotti, Felicita
dc.contributor.authorBoren, Jan
dc.contributor.authorCatapano, Alberico L.
dc.contributor.authorDescamps, Olivier S.
dc.contributor.authorFisher, Edward
dc.contributor.authorKovanen, Petri T.
dc.contributor.authorKuivenhoven, Jan Albert
dc.contributor.authorLesnik, Philippe
dc.contributor.authorMasana, Luis
dc.contributor.authorNordestgaard, Borge G.
dc.contributor.authorRay, Kausik K.
dc.contributor.authorReiner, Zeljko
dc.contributor.authorTaskinen, Marja-Riitta
dc.contributor.authorTokgozoglu, Lale
dc.contributor.authorTybjaerg-Hansen, Anne
dc.contributor.authorWatts, Gerald F.
dc.date.accessioned2019-12-10T11:24:12Z
dc.date.available2019-12-10T11:24:12Z
dc.date.issued2011
dc.identifier.issn0195-668X
dc.identifier.urihttps://doi.org/10.1093/eurheartj/ehr112
dc.identifier.urihttp://hdl.handle.net/11655/15629
dc.description.abstractEven at low-density lipoprotein cholesterol (LDL-C) goal, patients with cardiometabolic abnormalities remain at high risk of cardiovascular events. This paper aims (i) to critically appraise evidence for elevated levels of triglyceride-rich lipoproteins (TRLs) and low levels of high-density lipoprotein cholesterol (HDL-C) as cardiovascular risk factors, and (ii) to advise on therapeutic strategies for management. Current evidence supports a causal association between elevated TRL and their remnants, low HDL-C, and cardiovascular risk. This interpretation is based on mechanistic and genetic studies for TRL and remnants, together with the epidemiological data suggestive of the association for circulating triglycerides and cardiovascular disease. For HDL, epidemiological, mechanistic, and clinical intervention data are consistent with the view that low HDL-C contributes to elevated cardiovascular risk; genetic evidence is unclear however, potentially reflecting the complexity of HDL metabolism. The Panel believes that therapeutic targeting of elevated triglycerides (>= 1.7 mmol/L or 150 mg/dL), a marker of TRL and their remnants, and/or low HDL-C (< 1.0 mmol/L or 40 mg/dL) may provide further benefit. The first step should be lifestyle interventions together with consideration of compliance with pharmacotherapy and secondary causes of dyslipidaemia. If inadequately corrected, adding niacin or a fibrate, or intensifying LDL-C lowering therapy may be considered. Treatment decisions regarding statin combination therapy should take into account relevant safety concerns, i. e. the risk of elevation of blood glucose, uric acid or liver enzymes with niacin, and myopathy, increased serum creatinine and cholelithiasis with fibrates. These recommendations will facilitate reduction in the substantial cardiovascular risk that persists in patients with cardiometabolic abnormalities at LDL-C goal.
dc.language.isoen
dc.publisherOxford Univ Press
dc.relation.isversionof10.1093/eurheartj/ehr112
dc.rightsinfo:eu-repo/semantics/openAccess
dc.subjectCardiovascular System & Cardiology
dc.titleTriglyceride-Rich Lipoproteins And High-Density Lipoprotein Cholesterol In Patients At High Risk Of Cardiovascular Disease: Evidence And Guidance For Management
dc.typeinfo:eu-repo/semantics/article
dc.typeinfo:eu-repo/semantics/publishedVersion
dc.relation.journalEuropean Heart Journal
dc.contributor.departmentKardiyoloji
dc.identifier.volume32
dc.identifier.issue11
dc.identifier.startpage1345
dc.identifier.endpage1361
dc.description.indexWoS
dc.description.indexScopus


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