Lp(a) and CVD

• 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.