Lipoprotein (a) (Lp[a]) is a known causal risk factor for cardiovascular (CV) disease, but on an international level, published guidelines differ in recommendations for its use in clinical settings to estimate or modify CV risk. To summarize key strategies for Lp(a) management, HEART UK published a consensus statement in Atherosclerosis outlining recommendations for Lp(a) measurement and treatment in patients with elevated concentrations.

“In this statement,” wrote the researchers, “we advocate more widespread clinical use of Lp(a) data to refine assessment of cardiovascular risk…based on its accurate and reliable measurement.”

Supporting evidence for the review was found through searches in PubMed, Web of Science, and references in relevant literature.

The 10 principal statements are:


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  1. Lp(a) is an independent risk factor for both CV disease and calcific aortic valve stenosis.
  2. Serum levels of Lp(a) should be used to determine CV risk linked to Lp(a). HEART UK outlines Lp(a) levels of 32 to 90 nmol/L as being associated with minor risk, 90 to 200 nmol/L associated with moderate risk, 200 to 400 nmol/L associated with high risk, and >400 nmol/L associated with very high risk.
  3. Genetics predominantly control Lp(a) levels through autosomal co-dominant inheritance.
  4. Clinicians should determine secondary causes of high Lp(a) and treat them if possible.
  5. To measure serum Lp(a) concentrations, clinicians should use a method that minimizes the effect of isoform size using appropriate antibodies with calibrators certified for traceability of Lp(a) values to World Health Organization (WHO)/International Federation of Clinical Chemistry and Laboratory Medicine  (IFCC) reference material. Concentrations should be expressed in nmol/L of Lp(a) particles, as converting mass units to molar units can introduce inaccuracies. Currently, the only recommended assays are based on Denka regents with calibrators traceable in nmol/L to WHO/IFCC reference material.
  6. Clinicians need only measure Lp(a) once, unless a secondary cause is suspected or Lp(a)-lowering treatment has been initiated.
  7. Clinicians should measure serum Lp(a) levels in patients with a personal or family history of premature atherosclerotic CV disease, first degree relatives with raised serum Lp(a) levels, familial hypercholesterolemia or other genetic dyslipidemias, calcific aortic valve stenosis, or a borderline increased (<15%) 10-year risk for a CV event.
  8. The recommended management of patients with increased Lp(a) levels (>90 nmol/L) includes reducing overall atherosclerotic risk and controlling hyperlipidemia (ie, not specifically targeting Lp[a] levels). In addition, lipoprotein apheresis should be considered in individuals who have progressive coronary disease, Lp(a) level >150 nmol/L (>60 mg/dL), and persistently high low-density lipoprotein level (>125 mg/dL) despite lipid-lowering treatment.
  9. The ideal level for non-high-density lipoprotein cholesterol is <100 mg/dL in patients with raised Lp(a) levels.
  10. Future research should focus on the development of commercial isoform-insensitive assays, the role of antiplatelet therapy in primary prevention for patients with elevated Lp(a), and creation of reference ranges for Lp(a) in different ethnic groups. Randomized controlled studies that investigate the effect of selectively lowering Lp(a) on atherosclerotic CV disease are also needed.

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Disclosure: Several study authors declared affiliations with the pharmaceutical industry. Please see the original reference for a full list of authors’ disclosures.

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Reference

Cegla J, Neely RDG, France M, et al. HEART UK consensus statement on lipoprotein(a): a call to action [published online October 14, 2019]. Atherosclerosis. doi:10.1016/j.atherosclerosis.2019.10.011