Design
Review
Answers are grounded in this paper and cite their sources.
High Lp(a) warrants modifiable risk optimization; confirms dual mechanisms but leaves targeted therapy trials open.
Lipoprotein(a) or Lp(a) represents a class of lipoprotein particles having lipid composition similar to low-density lipoprotein (LDL) and a protein moiety, apoB100, covalently linked to apo(a), a glycoprotein with striking structural similarities to plasminogen. High plasma levels of Lp(a) are associated with an increased risk for atherosclerotic cardiovascular disease (ASCVD) by mechanisms yet to be determined. From in vitro and ex vivo observations it is apparent that because of its structural properties, Lp(a) can have both atherogenic and thrombogenic potentials. Means for correcting the high plasma levels of Lp(a) are still limited in effectiveness. The emerging notion that the pathogenicity of Lp(a) is increased in the presence of other risk factors, invites development of approaches for their correction, particularly in subjects with personal and/or family history of ASCVD.
No takes yet. Share an insight, caveat, or question.
A M Scanu (1991) studied this question.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: