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Lipoprotein (a)

SI UNITS (recommended)

CONVENTIONAL UNITS

(Genetically Determined Atherogenic Lipoprotein – Key Risk Marker for ASCVD, Stroke & Aortic Stenosis)

Synonyms

  • Lipoprotein(a)
  • Lp(a)
  • LPA
  • Apo(a)-linked LDL particle
  • Atherogenic lipoprotein

Units of Measurement

  • g/L
  • mg/L
  • mg/dL
  • mg/100 mL
  • mg%
  • mg/mL

IMPORTANT NOTE

Lp(a) can be reported as:

  1. Mass concentration (mg/dL, mg/L) → traditional
  2. Molar concentration (nmol/L) → increasingly recommended (isoform-independent)

This article uses MASS units only, as requested.

Key Conversions

Mass ↔ molar conversion is unreliable due to apo(a) isoform size variability.

1 mg/dL = 10 mg/L
 1 mg/mL = 1 g/dL = 10 g/L
 mg% = mg/dL

Description

Lipoprotein(a) [Lp(a)] is a genetically determined LDL-like particle consisting of:

  • An LDL core
  • ApoB-100, and
  • A unique apolipoprotein(a) [apo(a)] attached by a disulfide bond

Apo(a) contains kringle IV repeats, giving Lp(a) its:

  • High atherogenicity
  • Thrombogenicity
  • Large inter-individual variability

Lp(a) levels are:

  • 90% genetically determined
  • Stable across life after age 5
  • Not significantly affected by diet, exercise, or statins

Physiological & Pathophysiological Role

1. Atherogenesis

Lp(a) promotes:

  • Arterial wall deposition
  • Foam cell formation
  • Oxidized phospholipid enrichment

2. Thrombosis

Competitively inhibits plasminogen → ↓ fibrinolysis.

3. Valve Calcification

Major driver of calcific aortic valve stenosis.

4. Carrier of Oxidized Phospholipids

Potent pro-inflammatory molecules.

Clinical Significance

HIGH Lp(a)

1. Atherosclerotic Cardiovascular Disease (ASCVD) Risk

Independent strong risk factor for:

  • Premature CAD
  • MI
  • Stroke
  • Peripheral arterial disease
  • Calcific aortic stenosis

Risk is continuous; no safe lower limit.

2. Family History of Premature Heart Disease

High Lp(a) is common in:

  • Early MI (<55 in men, <65 in women)
  • Familial hypercholesterolemia (FH)

3. Calcific Aortic Valve Stenosis

Lp(a) contributes to:

  • Valve inflammation
  • Calcification
  • Rapid progression

4. Stroke

Associated with:

  • Large artery stroke
  • Atherosclerotic plaque instability

5. Elevated in Certain Conditions

  • Nephrotic syndrome
  • CKD
  • Hypothyroidism
  • Inflammation (mildly)

LOW Lp(a)

Usually not clinically significant.
Genetically low levels may occur in:

  • Apo(a) null variants
  • Liver disease

Low Lp(a) does not cause deficiency syndromes.

Reference Intervals

(ESC/AHA guidelines + Mayo + ARUP + Tietz)

Mass-based reporting:

Optimal / Low Risk

  • < 30 mg/dL
     (= < 300 mg/L)

Intermediate Risk

  • 30 – 50 mg/dL
     (= 300 – 500 mg/L)

High Risk

  • > 50 mg/dL
     (= > 500 mg/L)
    → Considered causal risk factor for ASCVD

Very High Risk / Severe Elevation

  • > 90 mg/dL
     (= > 900 mg/L)
    → Extremely high genetically determined Lp(a)

Diagnostic Uses

1. ASCVD Risk Assessment

Lp(a) is recommended in:

  • Family history of early CAD
  • Premature MI / stroke
  • Recurrent cardiovascular events despite statins
  • Suspected heritable hypercholesterolemia

2. Calcific Aortic Valve Disease

High levels correlate with:

  • Faster progression
  • Earlier valve replacement

3. Stroke Risk

Especially large artery atherosclerosis.

4. Familial Hypercholesterolemia (FH)

Lp(a) worsens ASCVD risk even with normal LDL.

Treatment Considerations

  • Statins: do NOT lower Lp(a) (may raise slightly).
  • Niacin: lowers 20–30% (no proven outcome benefit).
  • PCSK9 inhibitors: reduce Lp(a) by ~20–30%.
  • Apheresis: in very high-risk patients.
  • Emerging therapies:
    • Antisense oligonucleotides (pelacarsen)
    • siRNA (olpasiran)
       These reduce Lp(a) by 80–95% (ongoing Phase 3 trials).

Analytical Notes

  • Stable fasting or non-fasting
  • Mass assays influenced by apo(a) isoform size (limitation)
  • Ideally measured once-in-a-lifetime unless monitoring therapy
  • Use the same lab/method for serial results

Clinical Pearls

  • Lp(a) is genetically fixed - lifestyle changes cannot lower it.
  • High Lp(a) amplifies risk even when LDL is normal.
  • Lp(a) carries oxidized phospholipids → highly pro-inflammatory.
  • In FH, Lp(a) elevation dramatically increases early MI risk.
  • Aortic stenosis patients often have very high Lp(a).

Interesting Fact

Lipoprotein(a) is present only in humans and a few primates-not found in most mammals—making it a uniquely human cardiovascular risk factor.

References

  1. Tietz Clinical Chemistry & Molecular Diagnostics, 8th Edition - Lipoproteins
  2. ESC Dyslipidemia Guidelines
  3. AHA/ACC Cholesterol Guidelines
  4. Mayo Clinic Laboratories - Lipoprotein(a)
  5. ARUP Consult - Cardiovascular Risk Markers
  6. NIH / MedlinePlus - Lp(a)
  7. Lancet & NEJM Lp(a) Genetic & Outcome Studies

Last updated: January 26, 2026

Reviewed by : Medical Review Board

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