Use of Lipoprotein(a) in clinical practice: A biomarker whose time has come. A scientific statement from the National Lipid Association

HEART UK consensus statement on Lipoprotein(a): A call to action

“…Although Lipoprotein(a) (Lp(a)) is now established as a causal risk factor for cardiovascular disease (CVD) [1][2][3], there is little consensus between the different national guidelines on how to use this information on Lp(a) to more accurately estimate and modify cardiovascular risk [4,5]. For instance, the 2012 Australian Guideline does not mention Lp(a) [6].…”

The dedicated “Lp(a) clinic”: A concept whose time has arrived?

“…Despite population means being different across races and ethnicities, Lp(a) remains a risk factors in most races/ethnicities studied if elevated [37][38][39][40]. Lp(a) in molar concentration (nmol/L) lacks sufficient clinical data to give confidence on risk thresholds, although a recent study suggested the risk is at > 105 nmol/L [41] and the NLA recommended Lp(a) > 100 nmol/L as the 80th percentile of population risk thresholds in Caucasians [42]. To minimize confusion on what is the risk threshold for Lp(a) molar concertation (> 100 nmol/L, > 105 nmol/L or > 125 nmol/L), empiric studies are needed to determine the appropriate risk threshold.…”

Molecular, Population, and Clinical Aspects of Lipoprotein(a): A Bridge Too Far?

“…Both the IFCC and the World Health Orgnisation (WHO) approved a primary reference material. However, when this was used to calibrate different commercial assays that were testing a range of Lp(a) concentrations and apo(a) isoform sizes, considerable heterogeneity remained [87,88]. The bias created by the variation in repeat units in differently sized apo(a) isoforms typically manifests as an underestimation of the levels with small Lp(a) isoforms and an overestimation with the large Lp(a) isoforms [88].…”

“…However, when this was used to calibrate different commercial assays that were testing a range of Lp(a) concentrations and apo(a) isoform sizes, considerable heterogeneity remained [87,88]. The bias created by the variation in repeat units in differently sized apo(a) isoforms typically manifests as an underestimation of the levels with small Lp(a) isoforms and an overestimation with the large Lp(a) isoforms [88]. A recent comparison of six commercially available Lp(a) immunoassays has further highlighted how the biases between assays differ significantly across the clinically relevant concentration range in a nonlinear manner, highlighting the need for harmonisation of the Lp(a) assays [89].…”

“…Lp(a)-induced inhibition of fibrinolysis may increase risk of thrombosis, which at sites of plaque rupture may lead to increased risk of myocardial infarction and ischaemic stroke. Thrombosis at sites of turbulent blood flow may also contribute to both atherosclerotic and valvular aortic stenosis [88]. The true nature of the role of Lp(a) in thrombosis remains unclear, predominantly because, although elevated Lp(a) predisposes to thrombotic events in the aterial tree, these events are generally confounded by underlying atherosclerosis [101].…”