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Apolipoprotein(a) Kinetics in Statin-Treated Patients With Elevated Plasma Lipoprotein(a) Concentration

Louis Ma1,2, Dick C Chan1,2, Esther M M Ooi1

  • 1School of Biomedical Sciences, Faculty of Health and Medicine, University of Western Australia, Perth, Western Australia, Australia.

The Journal of Clinical Endocrinology and Metabolism
|August 9, 2019
PubMed

Insights

Elevated Lipoprotein(a) [Lp(a)] in statin-treated patients is due to increased production, not reduced clearance. This highlights the need for therapies targeting apolipoprotein(a) [apo(a)] synthesis to manage cardiovascular risk.

Area of Science:

  • Cardiovascular Medicine
  • Metabolic Disorders
  • Pharmacology

Background:

  • Lipoprotein(a) [Lp(a)] is a key cardiovascular risk factor, even in patients on statin therapy.
  • Elevated Lp(a) levels are associated with increased cardiovascular disease risk.
  • The kinetic basis for elevated Lp(a) in statin-treated patients requires elucidation.

Purpose of the Study:

  • To compare the production rate (PR) and fractional catabolic rate (FCR) of apolipoprotein(a) [apo(a)] between statin-treated patients with and without elevated Lp(a).
  • To investigate the kinetic factors contributing to high Lp(a) levels.
  • To provide a rationale for targeted therapies.

Main Methods:

  • Stable isotope techniques and compartmental modeling were used to study apo(a) kinetics.
  • 14 patients with elevated Lp(a) and 15 with normal Lp(a) were included, all on statin treatment.
  • Plasma apo(a) concentration was measured using liquid chromatography-mass spectrometry.

Main Results:

  • Patients with elevated Lp(a) exhibited significantly higher plasma apo(a) concentration and PR compared to controls (P < 0.01).
  • No significant difference in apo(a) FCR was observed between the groups.
  • Plasma apo(a) concentration strongly correlated with apo(a) PR (r = 0.699 to 0.949), but not FCR.

Conclusions:

  • Increased hepatic production of Lp(a) particles is the primary driver of elevated plasma Lp(a) in these patients.
  • These findings support therapies aimed at reducing apo(a) synthesis and Lp(a) production.
  • Understanding Lp(a) kinetics is crucial for developing effective cardiovascular disease prevention strategies.
Abstract

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