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Lipoprotein(a) or Lp(a) with a tail in the blood stream.

The various large meta-analyses, Mendelian randomizations, and prospective population-based studies have found that Lipoprotein (a) is an independent risk factor for atherosclerosis, aortic valve stenosis, and thrombosis. The Lp(a) test is considered elevated when its value is >50 mg/dL or >100 nmol/L, corresponding to the top 20th percentile of the general population.

Currently, there are no approved specific therapies for Lp(a). The National Lipid Association (NLA) does not recommend the use of niacin, hormone replacement therapy (HRT), or lomitapide (microsomal triglyceride transfer protein inhibitor). Recent trials such as FOURIER and ODYSSEY have shown that the addition of PCSK9 inhibitors to statin therapy can lower Lp(a) by 30%.

However, various guidelines, including the 2018 American Heart Association/American College of Cardiology (AHA/ACC) and the 2019 NLA scientific statement, recommend the use of PCSK9 inhibitors only in the context of uncontrolled LDLc/non-HDLc in patients at high risk or very high risk for ASCVD events.

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Lipoprotein(a)

J. CLINICAL LIPIDOLOGY – Scientific Statement, April 2019

Pathogenesis

  • Apolipoprotein(a), attached to the Apo B segment of an LDL-like particle, is a unique protein contained within Lp(a).
  • Apo(a) has homology with plasminogen and may inhibit fibrinolysis, thus increasing thrombosis.
  • Through inhibition of fibrinolysis at sites of plaque rupture, Apo(a) has the potential to cause MI and ischemic stroke.
  • Thrombosis at sites of turbulent flow may promote atherosclerotic and valvular aortic stenosis.
  • Apo(a) possesses unique properties that promote initiation and progression of atherosclerosis and calcific valvular aortic stenosis through endothelial dysfunction and pro-inflammatory responses, and pro-osteogenic effects promoting calcification.
  • Many of these effects are likely attributable to the oxidized phospholipids, of which Lp(a) is the preferential carrier, and which are covalently attached to the apo(a) portion of Lp(a).

Studies

  • Meta-analyses of prospective, population-based studies of high Lp(a) demonstrate high risk of MI, CHD, and ischemic stroke.
  • Large prospective, population-based studies of high Lp(a) demonstrate high risk of MI, ischemic stroke, VAS, coronary artery stenosis, carotid stenosis, femoral artery stenosis, heart failure, cardiovascular mortality, and all-cause mortality.
  • Large Mendelian randomization and GWA studies confirm that high Lp(a) is a causal factor for MI, ischemic stroke, VAS, coronary artery stenosis, carotid stenosis, femoral artery stenosis, heart failure, cardiovascular mortality, and all-cause mortality.
  • These causal relationships are independent of concentrations of other lipids and lipoproteins, including LDLc.

Assays

  • Measurement of Lp(a) is currently not standardized or harmonized.
  • Available assays report Lp(a) in either mg/dL or nmol/L and may exhibit Lp(a) isoform-dependent bias.
  • Evidence is incomplete regarding the utility of using different cut points of Lp(a) based on age, gender, ethnicity, or the presence of comorbid conditions.
  • Elevated Lp(a) appears to confer elevated risk for ASCVD over a wide range of (“at any”) LDLc concentrations.
  • An Lp(a) level >50 mg/dL (>100 nmol/L) may be considered as a risk-enhancing factor favoring the initiation of statin therapy. This level corresponds to the top 20th percentile in populations which are predominantly Caucasian.
  • The corresponding top 20th population percentile in African Americans is approximately 150 nmol/L, but it is unclear whether a different risk threshold or cut-point should be applied.
  • Clinicians should be aware that African Americans have an approximately 3-fold higher median Lp(a) than Caucasian populations (75 nmol/L vs 20 nmol/L)

When to test

Lp(a) testing is reasonable to refine risk assessment for ASCVD events in adults with:

  • Family HX of 1st-degree relatives with premature ASCVD (<55 y of age in men; <65 y of age in women).
  • Personal HX of premature ASCVD (<55 y of age in men; <65 y of age in women).
  • Personal HX of severe hypercholesterolemia (LDLc ≥190 mg/dL) or suspected FH.

Published

By

Gerti Tashko, MD
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