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Updated: Aug 23, 2026

Isolation and Analysis of Plasma Lipoproteins by Ultracentrifugation
06:47

Isolation and Analysis of Plasma Lipoproteins by Ultracentrifugation

Published on: January 28, 2021

Lipoprotein(a) and the link between atherosclerosis and thrombosis

Marlys L Koschinsky1

  • 1Department of Biochemistry, Queen's University, Kingston, Ontario. mk11@post.queensu.ca

The Canadian Journal of Cardiology
|August 17, 2004
PubMed

Insights

Elevated lipoprotein(a) (Lp[a]) levels are a risk factor for atherosclerosis and thrombosis. Lp[a] may directly link these conditions by affecting endothelial function, impacting blood clotting and vessel health.

Area of Science:

  • Cardiovascular Medicine
  • Lipidology
  • Pathophysiology

Background:

  • Elevated lipoprotein(a) (Lp[a]) is a known risk factor for thrombotic and atherosclerotic disorders, including coronary artery disease.
  • The precise mechanisms by which Lp(a) exerts its pathophysiological effects are not fully understood.
  • Atherosclerosis and thrombosis are closely linked, with thrombotic events often arising from atherosclerotic plaque rupture.

Purpose of the Study:

  • To elucidate the mechanisms underlying Lp(a)'s role in cardiovascular disease.
  • To investigate Lp(a)'s potential to mediate the link between atherosclerosis and thrombosis.
  • To explore Lp(a)'s impact on endothelial function and its implications for atherogenesis and thrombosis.

Main Methods:

  • This study reviews existing literature and mechanistic data on Lp(a).
  • Analysis focuses on Lp(a)'s proatherogenic and prothrombotic properties.
  • Investigation includes Lp(a)'s effects on endothelial function, including coagulation balance, inflammation, and barrier integrity.

Main Results:

  • Lp(a) exhibits both proatherogenic and prothrombotic properties, suggesting a direct role in linking these processes.
  • Lp(a) significantly impacts endothelial function, altering the balance of anticoagulant/procoagulant and anti-inflammatory/pro-inflammatory mediators.
  • Lp(a) disrupts endothelial barrier function and affects vascular tone (vasorelaxation/vasoconstriction).

Conclusions:

  • Lp(a) acts as a crucial functional link between atherosclerosis and thrombosis.
  • Lp(a) contributes to atherogenesis and thrombosis by inducing endothelial dysfunction.
  • Understanding Lp(a)'s multifaceted effects on the endothelium is key to addressing its role in cardiovascular disease.

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