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Dr Kris Vijay, USA 02 January 2023

High levels of lipoprotein are an independent causal risk factor for ASCVDs.
Mechanisms include increased atherogenesis, inflammation and thrombosis.
Lipoprotein(a) [Lp(a)] is predominantly a monogenic CV risk determinant, with =70% to ≥90% of interindividualized heterogeneity in levels being genetically determined.
The two major protein components of Lp(a) particles are apoB100 and apolipoprotein (a).
Lp(a) remains a risk factor for CVD development even in the setting of effective reduction of plasma LDL-C and apoB100.
Despite its demonstrated contribution to ASCVD burden, we presently lack standard and harmonization of assays, universal guidelines for diagnosing and providing risk assessment, and targeted treatments to lower Lp(a).
There is a clinical need to understand the genetic and biological basis for variation in Lp(a) levels and its relationship to disease in different ancestry groups.
Lipoprotein apheresis is approved for reduction of levels if Lp(a) is >60 mg/dL.
New targeted therapies will hopefully provide insights into the prevention of ASCVD.

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