<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Cahill LE</submitter><funding>NHLBI NIH HHS</funding><funding>Foundation for the National Institutes of Health</funding><funding>NCI NIH HHS</funding><pagination>1457-1464</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC6672045</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>60(8)</volume><pubmed_abstract>The capacity of HDLs to accept cholesterol effluxing from macrophages has been proposed as a new biomarker of HDLs' anti-atherogenic function. Whether cholesterol efflux capacity (CEC) is independent of HDL cholesterol (HDL-C) as a biomarker for coronary heart disease (CHD) risk in a generally healthy primary-prevention population remains unanswered. Therefore, in this nested case-control study, we simultaneously assessed CEC (using J774 cells) and plasma HDL-C levels as predictors of CHD in healthy middle-aged and older men not receiving treatment affecting blood lipid concentrations. We used risk-set sampling of participants free of disease at baseline from the Health Professionals Follow-Up Study, and matched cases (n = 701) to controls 1:1 for age, smoking, and blood sampling date. We applied conditional logistic regression models to calculate the multivariable relative risk and 95% CIs of CHD over 16 years of follow-up. CEC and HDL-C were correlated (&lt;i>r&lt;/i> = 0.50, &lt;i>P&lt;/i> &lt; 0.0001). The risk (95% CI) of CHD per one SD higher CEC was 0.82 (0.71-0.96), but completely attenuated to 1.08 (0.85-1.37) with HDL-C in the model. The association per one SD between HDL-C and CHD (0.66; 0.58-0.76) was essentially unchanged (0.68; 0.53-0.88) after adjustment for CEC. These findings indicate that CEC's ability to predict CHD may not be independent of HDL-C in a cohort of generally healthy men.</pubmed_abstract><journal>Journal of lipid research</journal><pubmed_title>Cholesterol efflux capacity, HDL cholesterol, and risk of coronary heart disease: a nested case-control study in men.</pubmed_title><pmcid>PMC6672045</pmcid><funding_grant_id>R01 HL035464</funding_grant_id><funding_grant_id>R01 HL35464</funding_grant_id><funding_grant_id>UM1 CA167552</funding_grant_id><pubmed_authors>Cahill LE</pubmed_authors><pubmed_authors>Rimm EB</pubmed_authors><pubmed_authors>Sacks FM</pubmed_authors><pubmed_authors>Jensen MK</pubmed_authors></additional><is_claimable>false</is_claimable><name>Cholesterol efflux capacity, HDL cholesterol, and risk of coronary heart disease: a nested case-control study in men.</name><description>The capacity of HDLs to accept cholesterol effluxing from macrophages has been proposed as a new biomarker of HDLs' anti-atherogenic function. Whether cholesterol efflux capacity (CEC) is independent of HDL cholesterol (HDL-C) as a biomarker for coronary heart disease (CHD) risk in a generally healthy primary-prevention population remains unanswered. Therefore, in this nested case-control study, we simultaneously assessed CEC (using J774 cells) and plasma HDL-C levels as predictors of CHD in healthy middle-aged and older men not receiving treatment affecting blood lipid concentrations. We used risk-set sampling of participants free of disease at baseline from the Health Professionals Follow-Up Study, and matched cases (n = 701) to controls 1:1 for age, smoking, and blood sampling date. We applied conditional logistic regression models to calculate the multivariable relative risk and 95% CIs of CHD over 16 years of follow-up. CEC and HDL-C were correlated (&lt;i>r&lt;/i> = 0.50, &lt;i>P&lt;/i> &lt; 0.0001). The risk (95% CI) of CHD per one SD higher CEC was 0.82 (0.71-0.96), but completely attenuated to 1.08 (0.85-1.37) with HDL-C in the model. The association per one SD between HDL-C and CHD (0.66; 0.58-0.76) was essentially unchanged (0.68; 0.53-0.88) after adjustment for CEC. These findings indicate that CEC's ability to predict CHD may not be independent of HDL-C in a cohort of generally healthy men.</description><dates><release>2019-01-01T00:00:00Z</release><publication>2019 Aug</publication><modification>2025-04-29T10:31:29.934Z</modification><creation>2025-04-06T19:29:59.537Z</creation></dates><accession>S-EPMC6672045</accession><cross_references><pubmed>31142574</pubmed><doi>10.1194/jlr.p093823</doi><doi>10.1194/jlr.P093823</doi></cross_references></HashMap>