PCSK9 inhibition
Testing and treating Lp(a) is clinically actionable today via cascade screening and PCSK9 inhibition or apheresis, a review argues (Curr Cardiol Rep 2023)
Original title: Is Lipoprotein(a) Clinically Actionable with Today's Evidence? The Answer is Yes
This review argues that current evidence already supports Lp(a) testing and management as clinically actionable. Genome-wide association and Mendelian randomisation studies establish causal links between elevated Lp(a) and cardiovascular disease, including coronary artery disease and calcific aortic valve disease. Lp(a) testing identifies patients with risk comparable to heterozygous familial hypercholesterolaemia, refines risk stratification in those with borderline or intermediate traditional risk, and enables cascade screening of relatives when family history of elevated Lp(a) is known. Non-targeted therapies, PCSK9 inhibition and lipoprotein apheresis, reduce atherosclerotic cardiovascular disease risk in ways likely attributable to Lp(a) lowering, while more potent targeted therapies are in development. The authors conclude that Lp(a) can already guide primary and secondary prevention intensification and family cascade screening.
Original abstract
Purpose Of Review: Lipoprotein(a) is an independent risk factor for cardiovascular disease. We review the ongoing shifts in consensus guidelines for the testing and management of Lp(a) and provide insight into whether current evidence suggests that awareness and testing of Lp(a) is clinically actionable.
Recent Findings: GWAS and Mendelian randomization studies have established causal links between elevated Lp(a) and forms of CVD, including CAD and calcific aortic valve disease. Testing of Lp(a) identifies patients with similar risk to that of heterozygous FH, enhances risk stratification in patients with borderline/intermediate risk as determined through traditional factors, and facilitates the assessment of inherited CVD risk through cascade screening in patients with known family history of elevated Lp(a). Reductions in Lp(a) through non-targeted therapies including PCSK9 inhibition and lipoprotein apheresis have demonstrated reductions in ASCVD risk that are likely attributable to lowering Lp(a). Targeted therapies to potently lower Lp(a) are in clinical development. Lp(a) is actionable, and can be used to identify high risk patients for primary prevention and their family members through cascade screening, and to guide intensification of therapy in primary and secondary prevention of ASCVD.
cascade screeningguidelinesPCSK9 inhibition
Summary written by lp-a.org from the published abstract; figures as published. Page updated 18 August 2026. Methods.