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dc.contributor.authorJensen, Majken Karoline
dc.contributor.authorRimm, Eric B.
dc.contributor.authorFurtado, Jeremy Daniel
dc.contributor.authorSacks, Frank Martin
dc.date.accessioned2013-04-22T19:01:28Z
dc.date.issued2012
dc.identifier.citationJensen, Majken K., Eric B. Rimm, Jeremy D. Furtado, and Frank M. Sacks. 2012. Apolipoprotein C-III as a potential modulator of the association between HDL-cholesterol and incident coronary heart disease. Journal of the American Heart Association 1:jah3-e000232.en_US
dc.identifier.issn2047-9980en_US
dc.identifier.urihttp://nrs.harvard.edu/urn-3:HUL.InstRepos:10579240
dc.description.abstractBackground: High-density lipoproteins (HDL) are structurally and metabolically heterogeneous and subclasses with differential effects on coronary heart disease (CHD) might exist. Apolipoprotein (apo) C-III, a small proinflammatory protein that resides on the surface of lipoproteins, enhances the atherogenicity of VLDL and LDL particles, but little is known about the role apoC-III on HDL. We investigated whether the presence or absence of apoC-III differentiates HDL into subtypes with nonprotective or protective associations with risk of future CHD. Methods and Results: High-density lipoprotein cholesterol (HDL-C) levels were measured in plasma separated according to apoC-III (by immunoaffinity chromatography) in two prospective case-control studies nested within the Nurses’ Health and the Health Professionals Follow-Up Studies. Baseline was in 1990 and 1994, and 634 incident CHD cases were documented through 10 to 14 years of follow-up. The relative risk of CHD per each standard deviation of total HDL-C was 0.78 (95% confidence intervals, 0.63–0.96). The HDL-C subtypes were differentially associated with risk of CHD, HDL-C without apoC-III inversely and HDL-C with apoC-III directly (P=0.02 for a difference between the HDL types). The relative risk per standard deviation of HDL-C without apoC-III was 0.66 (0.53 to 0.93) and 1.18 (1.03 to 1.34) for HDL-C with apoC-III. HDL-C with apoC-III comprised ∼13% of the total HDL-C. Adjustment for triglycerides and apoB attenuated the risks; however, the two HDL-C subgroups remained differentially associated with risk of CHD (P=0.05). Conclusion: Separating HDL-C according to apoC-III identified two types of HDL with opposing associations with risk of CHD. The proatherogenic effects of apoC-III, as a component of VLDL and LDL, may extend to HDL. (J Am Heart Assoc. 2012;1:jah3-e000232 doi: 10.1161/JAHA.111.000232.)en_US
dc.language.isoen_USen_US
dc.publisherBlackwell Publishing Ltden_US
dc.relation.isversionofdoi:10.1161/JAHA.111.000232en_US
dc.relation.hasversionhttp://www.ncbi.nlm.nih.gov/pmc/articles/PMC3487368/pdf/en_US
dash.licenseLAA
dc.subjectCoronary Heart Diseaseen_US
dc.subjectapolipoproteinsen_US
dc.subjectcardiovascular diseaseen_US
dc.subjectepidemiologyen_US
dc.subjectlipidsen_US
dc.titleApolipoprotein C-III as a Potential Modulator of the Association Between HDL-Cholesterol and Incident Coronary Heart Diseaseen_US
dc.typeJournal Articleen_US
dc.description.versionVersion of Recorden_US
dc.relation.journalJournal of the American Heart Associationen_US
dash.depositing.authorJensen, Majken Karoline
dc.date.available2013-04-22T19:01:28Z
dc.identifier.doi10.1161/JAHA.111.000232*
dash.contributor.affiliatedFurtado, Jeremy
dash.contributor.affiliatedJensen, Majken
dash.contributor.affiliatedSacks, Frank
dash.contributor.affiliatedRimm, Eric


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