Testing
Why, how, and in whom to measure Lp(a): a review makes the case for prioritising African and South Asian ancestry patients alongside familial and premature ASCVD groups (Diabetes Obes Metab 2025)
Original title: Why, how and in whom should we measure levels of lipoprotein(a): A review of the latest evidence and clinical implications
This narrative review by Razavi, Bhatia, Blumenthal, Shapiro and Mehta sets out the case for Lp(a) testing, summarising its pathophysiological links to atherogenesis, thrombosis and inflammation and its unique structural features driving a causal role in cardiovascular disease. The authors argue for a single lifetime measurement given Lp(a)'s genetic stability, and review guideline-based testing indications, highlighting high-risk populations including those with premature ASCVD, a family history of cardiovascular disease, and individuals of African or South Asian ancestry, groups with disproportionately high Lp(a) burden. They outline current risk-reduction strategies for elevated Lp(a), including lifestyle optimisation, statins, PCSK9 inhibitors and aspirin in select patients, and note that emerging antisense oligonucleotide and siRNA-based agents demonstrate Lp(a) reductions of up to 90% and are now in large-scale cardiovascular outcomes trials. The authors conclude that broader Lp(a) testing implementation, especially in high-risk groups, is central to advancing precision-medicine-based ASCVD prevention.
Original abstract
Lipoprotein(a) [Lp(a)] is a genetically determined, causal risk factor for atherosclerotic cardiovascular disease (ASCVD) and calcific aortic valve disease (CAVD). Despite robust evidence from epidemiological and genetic studies, Lp(a) remains underrecognised in clinical practice due to challenges in measurement, lack of guideline familiarity and limited therapeutic options. In this narrative review, we summarise the pathophysiological mechanisms linking Lp(a) to atherogenesis, thrombosis and inflammation, emphasising its unique structural features and causal role in cardiovascular disease. We discuss assay methodologies and make the case for a single lifetime measurement given the genetic stability of Lp(a). We review guideline-based indications for testing, highlighting high-risk populations such as those with premature ASCVD, a family history of cardiovascular disease and individuals of African or South Asian ancestry. We additionally outline clinical strategies to reduce ASCVD risk in individuals with elevated Lp(a), including lifestyle optimisation, statin therapy, PCSK9 inhibitors, and aspirin in select populations. Emerging targeted therapies, including antisense oligonucleotides and siRNA-based agents, demonstrate up to 90% Lp(a) reduction and are currently being evaluated in large-scale cardiovascular outcomes trials. As precision medicine advances, Lp(a) represents both a critical risk factor and a promising therapeutic target. Broader implementation of Lp(a) testing, particularly in high-risk individuals, will help improve ASCVD prevention efforts.
Summary written by lp-a.org from the published abstract; figures as published. Page updated 17 August 2026. Methods.