Lp(a): The Heart Attack Risk Factor Your GP Isn't Testing

Imagine discovering that you carry a risk factor for heart attack and stroke that doubles or even triples your chances — one that's entirely genetic, present from birth, and affects roughly 1 in 5 people. Now imagine that your GP has almost certainly never tested for it, that the NHS doesn't include it in routine screening, and that most people who have it will never know until they have a cardiovascular event.

That risk factor is lipoprotein(a) — known as Lp(a) — and it's one of the most underappreciated dangers in cardiovascular medicine.

What Is Lp(a)?

Lp(a) is a type of lipoprotein — a particle that carries cholesterol through your bloodstream. It's structurally similar to LDL (the so-called "bad cholesterol"), but with a crucial difference: it has an additional protein called apolipoprotein(a) attached to it.

This extra protein makes Lp(a) uniquely dangerous for three reasons:

• It promotes atherosclerosis — Lp(a) particles deposit cholesterol into artery walls just like LDL, but they're harder for your body to clear
• It promotes blood clotting — the apolipoprotein(a) component has structural similarity to plasminogen, a protein involved in dissolving blood clots. Lp(a) interferes with this process, making clots more likely
• It promotes inflammation — Lp(a) carries oxidised phospholipids that trigger inflammatory responses in your blood vessels

In short, Lp(a) attacks your cardiovascular system on three fronts simultaneously: plaque build-up, clot formation, and vascular inflammation. That's why elevated Lp(a) is such a potent independent risk factor for heart attack and stroke.

Why Your GP Doesn't Test It

Here's the frustrating reality. Despite strong evidence that elevated Lp(a) significantly increases cardiovascular risk, the NHS does not include it in routine lipid screening. Your standard cholesterol test measures total cholesterol, LDL, HDL, and triglycerides — but Lp(a) is not part of that panel.

Why? Several reasons:

• Historical oversight — Lp(a) was identified decades ago but was long considered a "niche" marker. It's only in recent years that the evidence base has become overwhelming
• No approved drug therapy — until recently, there was no specific medication to lower Lp(a), which reduced the perceived clinical utility of testing it. The logic was: why test for something you can't treat?
• Cost and volume — adding Lp(a) to every NHS lipid panel would involve significant laboratory cost at scale
• Guideline lag — NICE guidelines for cardiovascular risk assessment haven't yet incorporated routine Lp(a) screening, even though the European Society of Cardiology and Heart UK now recommend it

The result is a strange paradox: we have a well-validated, highly prevalent, genetically determined risk factor for the UK's leading cause of death — and the vast majority of people will never be tested for it.

How Common Is Elevated Lp(a)?

More common than most people realise.

• Approximately 20% of the global population has Lp(a) levels above 50 mg/dL (or 125 nmol/L), the threshold generally considered elevated
• In the UK, that equates to roughly 13 million people
• Certain ethnic groups have higher average Lp(a) levels — people of South Asian and Black African or Caribbean descent tend to have higher levels than White European populations
• Lp(a) levels are 90% genetically determined — they're set by your genes and remain remarkably stable throughout your lifetime

Your diet, exercise, and lifestyle have virtually no effect on your Lp(a) level. This is purely genetic inheritance.

What the Research Says

The evidence linking elevated Lp(a) to cardiovascular disease is now extensive:

• The European Society of Cardiology's 2021 guidelines recommend measuring Lp(a) at least once in every adult's lifetime to identify those with very high inherited levels
• A European Atherosclerosis Society Consensus Statement concluded that Lp(a) is a causal, independent, and genetically determined risk factor for cardiovascular disease and aortic valve stenosis
• Heart UK states that elevated Lp(a) approximately doubles the risk of coronary heart disease and is associated with a 2–3 fold increased risk of heart attack when levels are very high
• Large genetic studies (Mendelian randomisation analyses) have confirmed that the association between Lp(a) and cardiovascular events is causal, not merely correlational

This isn't emerging science. This is settled evidence that hasn't yet translated into routine clinical practice.

Lp(a) Levels: What's Normal?

Lp(a) is measured in either mg/dL or nmol/L. The two units are not directly interchangeable due to variations in Lp(a) particle size, but approximate categories are:

Risk Category	Lp(a) in nmol/L	Lp(a) in mg/dL	Interpretation
Desirable	Below 75	Below 30	Low cardiovascular risk from Lp(a)
Borderline	75–125	30–50	Mildly elevated; consider overall risk profile
High	125–250	50–100	Significantly elevated; warrants aggressive risk factor management
Very high	Above 250	Above 100	Substantially increased risk; specialist review recommended

Important note: Unlike LDL cholesterol, there is currently no specific target to "lower Lp(a) to." The clinical approach is to identify elevated levels, then aggressively manage all other modifiable cardiovascular risk factors to offset the additional genetic risk.

Can You Lower Lp(a)?

This is where things get honest — and slightly frustrating. Because Lp(a) is genetically determined:

• Diet and exercise have no meaningful effect on Lp(a) levels
• Statins don't lower Lp(a) — in fact, some studies suggest they may slightly increase it
• Niacin (vitamin B3) can reduce Lp(a) by 20–30%, but clinical trials have not shown that this translates into reduced cardiovascular events, and niacin has significant side effects
• PCSK9 inhibitors (evolocumab, alirocumab) reduce Lp(a) by approximately 20–30% as a secondary effect, but they're not prescribed specifically for this purpose
• Lipoprotein apheresis — a dialysis-like procedure that physically removes Lp(a) from the blood — is available in extreme cases but is expensive, time-consuming, and limited to specialist centres

The honest answer today is: you cannot effectively lower Lp(a) with currently available treatments. But knowing your level is still profoundly important — because it changes how aggressively you and your doctor should manage everything else.

New Treatments on the Horizon

This is the reason cardiovascular researchers are genuinely excited. Several purpose-built Lp(a)-lowering therapies are in advanced clinical trials:

• Olpasiran — an RNA interference (RNAi) therapy that reduces Lp(a) by approximately 95% in clinical trials. Phase 3 results are expected soon
• Lepodisiran — another RNAi-based therapy showing reductions of up to 96% in Lp(a) levels
• Pelacarsen — an antisense oligonucleotide (ASO) that reduces Lp(a) by approximately 80%. The HORIZON trial (a large cardiovascular outcomes trial) is nearing completion

If these trials demonstrate that lowering Lp(a) reduces heart attacks and strokes — which many experts anticipate — the treatment landscape will transform. Knowing your baseline Lp(a) level now will position you to benefit from these therapies as they become available.

Who Should Get Tested

Based on current European Society of Cardiology and Heart UK recommendations, Lp(a) testing is particularly important if you:

• Have a family history of premature cardiovascular disease (heart attack or stroke before age 55 in men or 65 in women)
• Have established cardiovascular disease disproportionate to your conventional risk factors
• Have familial hypercholesterolaemia — elevated Lp(a) is common in this population
• Are of South Asian or Black African/Caribbean descent — groups with higher average levels
• Have recurrent cardiovascular events despite optimal statin therapy
• Have aortic valve stenosis — Lp(a) is causally linked to calcific aortic valve disease

In practice, the ESC recommends measuring Lp(a) at least once in every person's lifetime. It costs very little, requires a single blood draw, and could fundamentally change your risk management strategy.

You Only Need to Test Once

Here's the good news. Because Lp(a) levels are genetically determined and remain stable throughout your life, you only need to test it once. Unlike LDL cholesterol or triglycerides, which fluctuate with diet, weight, and medication, your Lp(a) level at age 30 will be essentially the same at age 60.

One test. One result. A lifetime of actionable information.

If your Lp(a) is low, you can rule it out as a risk factor permanently. If it's elevated, you and your doctor can adjust your overall cardiovascular prevention strategy accordingly — and you'll be ready to benefit from targeted therapies as they reach the market.

The question isn't whether you can afford to test Lp(a). It's whether you can afford not to.

Book Your Test

Ready to take control of your health? Book your lp(a): the heart attack risk factor your gp isn't testing test today and get results within days.