A little-known inherited cholesterol particle called Lp(a) may explain some unexplained heart risk and is becoming a major target for new treatments.
Most people know about “good” and “bad” cholesterol — but there’s another type that often goes undetected and could quietly raise the risk of heart attacks and strokes, even in otherwise healthy people.
Known as lipoprotein(a), or Lp(a), this little-known particle has become one of the most closely watched topics in cardiovascular research. It isn’t included in standard cholesterol tests and, until recently, there has been little doctors could do about it. Now, a new wave of experimental treatments is beginning to change that.
What is lipoprotein(a)?
Lipoprotein(a) is a cholesterol particle that carries lipoprotein, particles made of fats and proteins, through the bloodstream. It is similar in structure to LDL (low-density lipoprotein, or “bad” cholesterol), but it has an added protein called apolipoprotein(a).
This extra protein component seems to make Lp(a) more likely to contribute to the build-up of fatty deposits in arteries. It may also promote blood clotting. Together, these processes increase the likelihood of cardiovascular disease (heart disease and stroke).
Large-scale studies and international guidelines now recognize Lp(a) as a risk factor for heart disease and stroke.
What determines your Lp(a) levels?
Unlike most other cholesterol measures, Lp(a) is largely determined by genetics.
Around 70-90% of variation in Lp(a) levels is inherited. This is driven mainly by differences in the LPA gene, which controls the structure of apolipoprotein(a).
Because of this strong genetic control, Lp(a) levels are usually set early in life and remain relatively stable over time, with little influence from diet, exercise, or body weight.
There are some smaller influences. Levels can vary by sex, ethnicity, and hormonal changes, and may be slightly affected by factors such as menopause or kidney disease.
How does it affect your risk?
A growing body of research shows that higher Lp(a) levels are associated with an increased risk of heart attacks, strokes, and aortic valve disease.
Importantly, the relationship appears continuous. In long-term studies, cardiovascular risk rises step by step as Lp(a) levels increase.
Lp(a) also adds to overall risk. For example, someone with high LDL cholesterol and high Lp(a) is likely to be at higher risk than someone with elevated LDL cholesterol alone.
For people with higher Lp(a) levels, cardiovascular risk rises mainly when inflammation is elevated.
This helps explain why some people develop cardiovascular disease despite otherwise favorable risk profiles.
Can you lower lipoprotein(a)?
There are currently few options to lower Lp(a).
Lifestyle changes that improve heart health, such as eating well, being physically active, and not smoking, remain essential. But they have minimal effect on Lp(a) itself.
Most commonly used cholesterol-lowering medications, including statins, do not reduce Lp(a). In some cases, statins may even increase Lp(a) slightly. Despite this, statins still reduce overall cardiovascular risk and remain a cornerstone of treatment.
Some newer drugs, such as PCSK9 inhibitors, can lower Lp(a), but typically only by a modest amount of around 15–30%.
Several drug companies, including Novartis, Amgen, and Eli Lilly, are racing to develop treatments that specifically lower Lp(a). These new medicines work very differently from statins. Instead of helping the body clear cholesterol from the blood, they use a “gene silencing” approach that reduces how much Lp(a) the liver makes in the first place.
This means it switches off production of cholesterol rather than trying to remove what is already there.
In early clinical trials, these drugs have lowered Lp(a) levels by 80–90%, far more than existing treatments. This is why Lp(a) is suddenly getting attention.
If upcoming trials show these large reductions also lead to fewer heart attacks and strokes, it could change how cardiovascular risk is assessed and treated, especially for people whose risk is driven largely by genetics rather than lifestyle.
Should you get tested?
Lp(a) is not included in standard cholesterol tests. A specific blood test is required.
Medicare doesn’t cover these blood tests, so if your doctor orders one, you’ll have to pay out of pocket – around A$25 to $80—plus any costs associated with the consultation.
International guidelines now recommend measuring Lp(a) at least once in adulthood, particularly for people with a family history of early heart disease or unexplained cardiovascular risk.
Because levels are largely genetically determined and stable, a single measurement is often considered sufficient for most people.
What should you focus on?
Learning you have high Lp(a) can feel frustrating, especially given the limited options to lower it directly.
But it’s important to see Lp(a) as one part of your overall cardiovascular risk.
There are still many factors you can influence to lower your overall risk, and particularly your LDL cholesterol. These include:
- LDL (bad) cholesterol
- blood pressure
- smoking
- physical activity
- diet quality
- managing conditions such as diabetes
What happens next?
Research into Lp(a) is moving quickly. If current clinical trials show targeted therapies reduce cardiovascular events, testing and treatment may become more common.
For now, awareness is an important first step.
If you are concerned about your cardiovascular risk, it may be worth discussing Lp(a) testing with your doctor, especially if you have a strong family history of heart disease.
At the same time, the broader message to maximize heart health through healthy behaviors remains unchanged. Even as new risk factors emerge, the foundations of good heart health are still the things we can control.
Adapted from an article originally published in The Conversation.
Never miss a breakthrough: Join the SciTechDaily newsletter.
Follow us on Google and Google News.