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Apolipoprotein A-I concentrations and risk of coronary artery disease: A Mendelian randomization study

Minna K Karjalainen1, Michael V Holmes2, Qin Wang3

  • 1Computational Medicine, Faculty of Medicine, University of Oulu, Oulu, Finland; Center for Life Course Health Research, Faculty of Medicine, University of Oulu, Oulu, Finland; Biocenter Oulu, University of Oulu, Oulu, Finland.

Atherosclerosis
|March 2, 2020
PubMed

Insights

Genetic studies show apolipoprotein A-I (apoA-I) does not protect against coronary artery disease (CAD). This finding challenges the potential of apoA-I infusions as a novel therapy for CAD prevention.

Area of Science:

  • Cardiovascular Genetics
  • Biochemistry

Background:

  • Apolipoprotein A-I (apoA-I) is being investigated as a potential therapeutic for coronary artery disease (CAD).
  • Observational studies suggest a link between lower apoA-I levels and increased CAD risk, but causality remains unproven.

Purpose of the Study:

  • To investigate the causal role of apoA-I in the development of CAD using human genetic data.
  • To compare genetic findings with observational associations between apoA-I and CAD risk.

Main Methods:

  • A genetic variant (rs12225230) in the APOA1 locus was identified and associated with apoA-I concentrations in a Finnish cohort.
  • Two-sample Mendelian randomization analysis was performed using genetic estimates of CAD from large UK Biobank and CARDIoGRAMplusC4D datasets.
  • Observational associations of apoA-I with incident CAD were analyzed in population-based prospective cohorts.

Main Results:

  • Observational analyses showed an inverse association between apoA-I and CAD risk (HR 0.81 per 1-SD higher apoA-I).
  • The identified genetic variant strongly associated with apoA-I levels but not with confounders.
  • Mendelian randomization analysis revealed no significant relationship between apoA-I and CAD risk (OR 1.13 per 1-SD higher apoA-I), differing from observational findings.

Conclusions:

  • Genetic evidence does not support a cardioprotective role for apoA-I.
  • These findings suggest that HDL-related phenotypes may not offer protection against CAD.
  • The therapeutic potential of apoA-I infusions for CAD prevention requires re-evaluation.
Abstract

Keywords:
ApolipoproteinHeart diseaseLipidsMendelian randomization

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