Biology, pathophysiology and current therapies that affect lipoprotein (a) levels

Thampi Rawther1, Fatiha Tabet1

  • 1School of Medical Sciences, Faculty of Medicine, UNSW Sydney, Sydney, NSW 2052, Australia.

Insights

Elevated Lipoprotein (a) [Lp(a)] is a genetic risk factor for cardiovascular disease. This review explores Lp(a) biology and its reduction via lipid-lowering therapies like statins and PCSK9 inhibitors.

Area of Science:

  • Cardiology
  • Genetics
  • Pharmacology

Background:

  • Lipoprotein (a) [Lp(a)] is a recognized genetic risk factor for cardiovascular and calcific aortic valve diseases.
  • High prevalence of elevated Lp(a) highlights knowledge gaps in its biology and treatment.
  • Lp(a) levels are genetically determined and unresponsive to lifestyle modifications.

Purpose of the Study:

  • To review current understanding of Lipoprotein (a) [Lp(a)] biology, pathophysiology, and metabolism.
  • To summarize the efficacy of various lipid-lowering therapies in reducing Lp(a) levels.
  • To consolidate knowledge on Lp(a) response to statins, apheresis, PCSK9 inhibitors, CETP inhibitors, and ASOs.

Main Methods:

  • Literature review of current scientific knowledge on Lp(a).
  • Analysis of studies investigating Lp(a) reduction strategies.
  • Synthesis of data on Lp(a) response to different therapeutic classes.

Main Results:

  • Lp(a) is a significant independent risk factor for cardiovascular disease.
  • Plasma Lp(a) levels are primarily genetically determined.
  • Various lipid-lowering therapies demonstrate differential effects on Lp(a) levels.

Conclusions:

  • Further research into Lp(a) biology and pathophysiology is warranted.
  • Targeting Lp(a) represents a potential therapeutic strategy for cardiovascular disease prevention.
  • Understanding Lp(a) response to different treatments is crucial for clinical application.

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