Recent Updates of Lipoprotein(a) and Cardiovascular Disease

Taili Liu1, Won-Sik Yoon1, Sang-Rok Lee1

  • 1Division of Cardiology, Department of Internal Medicine, Chonbuk National University Hospital, Jeonju, Korea.

Chonnam Medical Journal
|February 4, 2021
PubMed

Insights

Lipoprotein(a) [Lp(a)] is linked to cardiovascular disease (CVD) risk. New therapies, including PCSK9 inhibitors, now effectively lower Lp(a) levels, offering potential treatment options.

Area of Science:

  • Cardiovascular Science
  • Lipidology
  • Pharmacology

Background:

  • Epidemiological, GWAS, and Mendelian randomization studies confirm elevated lipoprotein levels increase coronary heart disease and cardiovascular disease (CVD) risk.
  • Lipoprotein(a) [Lp(a)] is recognized as an independent risk factor for atherosclerotic cardiovascular disease (ASCVD).
  • Current clinical guidelines do not recommend direct reduction of plasma Lp(a) due to a lack of effective therapies.

Purpose of the Study:

  • To review the structure, pathogenicity, and prognostic evidence of Lp(a).
  • To present recent advances in therapeutic drugs targeting Lp(a) levels.
  • To highlight the emergence of effective treatments for lowering Lp(a).

Main Methods:

  • Review of recent clinical trials and epidemiological data.
  • Analysis of genetic and molecular studies on Lp(a).
  • Evaluation of pharmacological interventions for Lp(a) reduction.

Main Results:

  • Proprotein convertase subtilisin/kexin-type 9 (PCSK9) inhibitors and second-generation antisense oligonucleotides demonstrate efficacy in reducing plasma Lp(a) levels.
  • These findings challenge previous therapeutic limitations for managing Lp(a)-associated cardiovascular risk.
  • Emerging treatments offer new hope for patients with elevated Lp(a).

Conclusions:

  • Lp(a) remains a significant, independent risk factor for ASCVD.
  • Recent therapeutic advancements, particularly PCSK9 inhibitors and ASOs, provide effective means to lower Lp(a).
  • These developments pave the way for guideline revisions and improved clinical management of Lp(a)-driven cardiovascular risk.

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