Lipoprotein(a): The Test Worth Doing Once in Your Life

Lipoprotein(a) does not appear on a standard lipid panel, and most people have never heard of it. Yet it is an independent, inherited cardiovascular risk factor that explains a portion of early heart attacks in people whose bloodwork looks immaculate. Since 2022 the European Atherosclerosis Society has recommended measuring it at least once in every adult's life — a rare case where a single test genuinely suffices.

What the particle is#

Lipoprotein(a) is assembled like an ordinary LDL particle: a cholesteryl ester core, a surface coat, and apolipoprotein B-100. One thing differs — a second protein, apolipoprotein(a), is bonded to apoB by a disulfide bridge. That addition turns a familiar particle into a distinct risk factor.

Apo(a) is structurally similar to plasminogen, the precursor of plasmin, which dissolves clots. The resemblance has consequences: Lp(a) competes with plasminogen and impairs fibrinolysis. The particle also carries oxidised phospholipids with pro-inflammatory effects on the vessel wall.

Two separate contributions to risk follow. Atherogenic — Lp(a) participates in plaque formation and growth just as LDL does. Prothrombotic — it hinders the breakdown of clots that have already formed. A third, less familiar contribution involves aortic valve calcification: genetic studies have linked LPA variants to the development of aortic stenosis.

Who should measure it, and when#

Situation	Strength of indication	Why
Any adult, once in a lifetime	Recommended (EAS, 2022)	The level never changes; knowing it shifts risk assessment
Early heart attack or stroke in close relatives	High priority	Inherited factor; likely to be found
Your own event at a young age	High priority	Lp(a) explains a share of unexplained cases
Familial hypercholesterolaemia	Essential	The risks compound
Borderline calculated risk	Useful	May change the statin decision
Atherosclerosis progressing at normal LDL	Indicated	Looking for the missing factor
Family history of aortic stenosis	Useful	Linked to valve calcification

Elevated levels occur in around 20% of the population, making Lp(a) one of the most common genetic cardiovascular risk factors there is. Average levels differ between ethnic groups: people of African descent typically run considerably higher.

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Reading the result#

Level, nmol/L	Level, mg/dL	Interpretation
< 75	< 30	Low risk
75–125	30–50	Borderline
125–200	50–80	Elevated
> 200	> 80	High
> 430	> 180	Very high: risk comparable to familial hypercholesterolaemia

Units deserve a note of their own. Apo(a) exists in dozens of isoforms of different sizes, so particle mass varies and the mg/dL to nmol/L conversion factor is not universal. Current guidance prefers nmol/L. If you retest, use the same laboratory and the same assay.

Some situations do shift the level temporarily: pregnancy raises Lp(a), as do marked inflammation and acute illness; severe renal failure can raise it substantially and hepatic failure can lower it. Otherwise the value is stable for life.

What to do about a high level#

The unwelcome truth is that nothing in routine practice lowers Lp(a) itself. Diet, physical activity and weight loss move it by a few percent. Statins do not touch it and in some studies raised it slightly. Niacin genuinely lowers Lp(a) by 20–30%, but large trials found no clinical benefit alongside meaningful side effects, so it is not recommended. Lipoprotein apheresis exists but serves a very narrow group of patients.

Hence the logic of management: since one component of risk cannot be removed, every other one is reduced harder.

Target	What to do	Why it matters more with high Lp(a)
LDL	Lower targets, statin ± ezetimibe ± PCSK9 inhibitor	Reduces total apoB particle burden
Blood pressure	Tight control	Synergy with the atherogenic effect
Smoking	Complete cessation	Smoking amplifies the prothrombotic contribution
Glucose and weight	Diabetes prevention	Diabetes multiplies the risk
Activity	150–300 minutes a week	Improves the rest of the profile
Aspirin	Only on medical advice	Under discussion in high Lp(a), not for everyone
Family	Test first-degree relatives	Inherited in an autosomal codominant pattern

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What is coming#

This is one of the few areas in cardiology where waiting is genuinely warranted. Drugs that specifically suppress hepatic apo(a) synthesis are in development: antisense oligonucleotides and small interfering RNAs. In phase 2 studies they reduced Lp(a) by 80% or more.

The open question is whether that reduction translates into fewer heart attacks and strokes. Ongoing phase 3 trials should answer it. Until they report, none of these agents is standard care, and promises of a cure for Lp(a) run ahead of the evidence.

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The bottom line#

Lipoprotein(a) is an inherited, independent cardiovascular risk factor elevated in roughly one person in five. It contributes to atherosclerosis, to thrombosis and to aortic valve calcification, and its level is genetically fixed and essentially immune to lifestyle change.

The practical conclusion is straightforward: measure it once, ideally when young, and use the result to sharpen your risk assessment. Where it is high, work harder on everything else and have close relatives tested. Targeted therapy will probably arrive within a few years, but decisions today are made on the evidence that exists today.