Inherited cardiovascular risk, Johannesburg
Lipoprotein(a): the inherited cardiovascular risk factor worth knowing.
Lp(a) is largely genetically determined, usually causes no symptoms and can materially alter cardiovascular risk even when a standard cholesterol panel looks reassuring.
In short
Lipoprotein(a), or Lp(a), is a largely genetically determined apoB-containing lipoprotein associated with increased atherosclerotic cardiovascular risk and aortic valve disease. Current 2026 AHA/ACC guidance recommends measuring Lp(a) at least once in adulthood. Levels are relatively stable in most people, and an elevated result should lead to more careful overall risk assessment and stronger control of modifiable risk factors rather than panic or unsupported treatment.
Medically reviewed by Dr Arnav Kapur, MBBCh Cum Laude
The approach
Understand first. Then treat.
Lp(a) is not part of most standard cholesterol panels, so a person can have an elevated inherited risk factor without knowing it. Because levels are largely genetic, family history can be especially relevant.
The result is interpreted as part of total cardiovascular risk. Lp(a) is not a binary 'safe or dangerous' test, and treatment focuses on the whole risk profile while dedicated Lp(a)-lowering therapies continue to evolve.
Why Lp(a) matters
- Inherited cardiovascular risk
- Premature heart attack or stroke in a patient or family
- Risk that is not fully explained by a standard lipid panel
- Aortic valve stenosis risk context
- Familial hypercholesterolaemia or very high LDL cholesterol
- Residual risk despite otherwise good risk-factor control
- Family screening when a markedly elevated level is identified
Why Lp(a) is different from LDL
Lp(a) is an LDL-like particle with an additional apolipoprotein(a) component. Its concentration is strongly influenced by genetics and is much less responsive to lifestyle than conventional LDL cholesterol.
Who should be tested?
The 2026 AHA/ACC dyslipidaemia guideline recommends measuring Lp(a) at least once in adulthood. Testing is particularly informative when there is premature cardiovascular disease, strong family history, familial hypercholesterolaemia or otherwise unexplained risk.
What does a high result mean?
Cardiovascular risk rises progressively with higher Lp(a), rather than changing abruptly at one cut-off. Current 2026 guidance treats approximately 125 nmol/L or 50 mg/dL and above as a risk-enhancing level. The result must still be interpreted alongside blood pressure, LDL cholesterol, ApoB, smoking, diabetes and the rest of the clinical picture.
What can be done now?
Lifestyle changes have major cardiovascular benefits even though they usually do not substantially lower Lp(a) itself. Current management therefore focuses on aggressive control of modifiable risk, especially LDL cholesterol and ApoB where indicated. Some lipid-lowering therapies can modestly reduce Lp(a), but there is not yet a generally approved medicine used solely to normalise Lp(a) for routine primary prevention.
Common questions
Answers before you book.
Can diet or exercise lower Lp(a)?
They usually have little effect on the Lp(a) concentration itself because the level is largely genetic. They remain important because they reduce other cardiovascular risk factors.
Should my family be tested if my Lp(a) is high?
Often yes, especially when the level is markedly elevated or there is premature cardiovascular disease in the family. Because Lp(a) is inherited, testing first-degree relatives can identify others at increased risk.
Do I need to repeat Lp(a) every year?
Usually not. Lp(a) is relatively stable across adulthood, so one measurement is often enough. Repeat testing may be useful in selected clinical situations or if future Lp(a)-targeted treatment is introduced.
Are there medicines specifically for high Lp(a)?
Several targeted therapies are in advanced development, but routine management today still centres on reducing overall cardiovascular risk and intensifying treatment of modifiable factors when appropriate.
This page provides general health information and does not replace individual cardiovascular assessment. Lp(a) results should be interpreted in the context of overall risk.
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