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van Capelleveen, Julian C.; Bochem, Andrea E.; Boekholdt, S. Matthijs; Mora, Samia; Hoogeveen, Ron C.; Ballantyne, Christie M.; Ridker, Paul M; Sun, Wensheng; Barter, Philip J.; Tall, Alan R.; Zwinderman, Aeilko H.; Kastelein, John J. P.; Wareham, Nick J.; Khaw, Kay‐Tee; Hovingh, G. Kees

Association of High‐Density Lipoprotein‐Cholesterol Versus Apolipoprotein A‐I With Risk of Coronary Heart Disease: The European Prospective Investigation Into Cancer‐Norfolk Prospective Population Study, the Atherosclerosis Risk in Communities Study, and the Women's Health Study

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  • Media type: E-Article
  • Title: Association of High‐Density Lipoprotein‐Cholesterol Versus Apolipoprotein A‐I With Risk of Coronary Heart Disease: The European Prospective Investigation Into Cancer‐Norfolk Prospective Population Study, the Atherosclerosis Risk in Communities Study, and the Women's Health Study
  • Contributor: van Capelleveen, Julian C.; Bochem, Andrea E.; Boekholdt, S. Matthijs; Mora, Samia; Hoogeveen, Ron C.; Ballantyne, Christie M.; Ridker, Paul M; Sun, Wensheng; Barter, Philip J.; Tall, Alan R.; Zwinderman, Aeilko H.; Kastelein, John J. P.; Wareham, Nick J.; Khaw, Kay‐Tee; Hovingh, G. Kees
  • imprint: Ovid Technologies (Wolters Kluwer Health), 2017
  • Published in: Journal of the American Heart Association
  • Language: English
  • DOI: 10.1161/jaha.117.006636
  • ISSN: 2047-9980
  • Keywords: Cardiology and Cardiovascular Medicine
  • Origination:
  • Footnote:
  • Description: <jats:sec xml:lang="en"> <jats:title>Background</jats:title> <jats:p xml:lang="en"> The contribution of apolipoprotein A‐I (apoA‐I) to coronary heart disease ( <jats:styled-content style="fixed-case">CHD</jats:styled-content> ) risk stratification over and above high‐density lipoprotein cholesterol ( <jats:styled-content style="fixed-case">HDL</jats:styled-content> ‐C) is unclear. We studied the associations between plasma levels of <jats:styled-content style="fixed-case">HDL</jats:styled-content> ‐C and apoA‐I, either alone or combined, with risk of <jats:styled-content style="fixed-case">CHD</jats:styled-content> events and cardiovascular risk factors among apparently healthy men and women. </jats:p> </jats:sec> <jats:sec xml:lang="en"> <jats:title>Methods and Results</jats:title> <jats:p xml:lang="en"> <jats:styled-content style="fixed-case">HDL</jats:styled-content> ‐C and apoA‐I levels were measured among 17 661 participants of the <jats:styled-content style="fixed-case">EPIC</jats:styled-content> (European Prospective Investigation into Cancer)‐Norfolk prospective population study. Hazard ratios for <jats:styled-content style="fixed-case">CHD</jats:styled-content> events and distributions of risk factors were calculated by quartiles of <jats:styled-content style="fixed-case">HDL</jats:styled-content> ‐C and apoA‐I. Results were validated using data from the <jats:styled-content style="fixed-case">ARIC</jats:styled-content> (Atherosclerosis Risk in Communities) and <jats:styled-content style="fixed-case">WHS</jats:styled-content> (Women's Health Study) cohorts, comprising 15 494 and 27 552 individuals, respectively. In <jats:styled-content style="fixed-case">EPIC</jats:styled-content> ‐Norfolk, both <jats:styled-content style="fixed-case">HDL</jats:styled-content> ‐C and apoA‐I quartiles were strongly and inversely associated with <jats:styled-content style="fixed-case">CHD</jats:styled-content> risk. Within <jats:styled-content style="fixed-case">HDL</jats:styled-content> ‐C quartiles, higher apoA‐I levels were not associated with lower <jats:styled-content style="fixed-case">CHD</jats:styled-content> risk; in fact, <jats:styled-content style="fixed-case">CHD</jats:styled-content> risk was higher within some <jats:styled-content style="fixed-case">HDL</jats:styled-content> ‐C quartiles. ApoA‐I levels were associated with higher levels of <jats:styled-content style="fixed-case">CHD</jats:styled-content> risk factors: higher body mass index, HbA1c, non‐ <jats:styled-content style="fixed-case">HDL</jats:styled-content> ‐C, triglycerides, apolipoprotein B, systolic blood pressure, and C‐reactive protein, within fixed <jats:styled-content style="fixed-case">HDL</jats:styled-content> ‐C quartiles. In contrast, <jats:styled-content style="fixed-case">HDL</jats:styled-content> ‐C levels were consistently inversely associated with overall <jats:styled-content style="fixed-case">CHD</jats:styled-content> risk and <jats:styled-content style="fixed-case">CHD</jats:styled-content> risk factors within apoA‐I quartiles ( <jats:italic>P</jats:italic> &lt;0.001). These findings were validated in the <jats:styled-content style="fixed-case">ARIC</jats:styled-content> and <jats:styled-content style="fixed-case">WHS</jats:styled-content> cohorts. </jats:p> </jats:sec> <jats:sec xml:lang="en"> <jats:title>Conclusions</jats:title> <jats:p xml:lang="en"> Our findings demonstrate that apoA‐I levels do not offer predictive information over and above <jats:styled-content style="fixed-case">HDL</jats:styled-content> ‐C. In fact, within some <jats:styled-content style="fixed-case">HDL</jats:styled-content> ‐C quartiles, higher apoA‐I levels were associated with higher risk of <jats:styled-content style="fixed-case">CHD</jats:styled-content> events, possibly because of the unexpected higher prevalence of cardiovascular risk factors in association with higher apoA‐I levels. </jats:p> </jats:sec> <jats:sec xml:lang="en"> <jats:title>Clinical Trial Registration</jats:title> <jats:p xml:lang="en"> <jats:styled-content style="fixed-case">URL</jats:styled-content> : <jats:ext-link xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="uri" xlink:href="https://www.clinicaltrials.gov">https://www.clinicaltrials.gov</jats:ext-link> . Unique identifier: <jats:styled-content style="fixed-case">NCT</jats:styled-content> 00000479. </jats:p> </jats:sec>
  • Access State: Open Access