What is lipoprotein (a)?

Lipoprotein (a), which is often abbreviated to Lp(a), is a type of particle that transports cholesterol in the bloodstream.

It is one of seven classes of lipoproteins – particles that transport lipids (i.e. fat and cholesterol) in the bloodstream between different tissues, such as the intestines, liver, skeletal muscle and adipose (fat) tissue.

We’ve encountered lipoproteins before in the Cholesterol and ageing trait and Blood fat level (APOA5) trait articles. Readers are encouraged to visit these articles for further background.

Source: Chaudhary, J., Bower, J., & Corbin, I. R. (2019). Lipoprotein drug delivery vehicles for cancer: rationale and reason. International journal of molecular sciences, 20(24), 6327.

To recap briefly, fat (in the form of triglycerides) is used by various tissues as an energy source (e.g. by muscles) or an energy store (e.g. in adipose tissue). Cholesterol is a fat-like substance used to make cell membranes, hormones (such as testosterone and oestrogen), and key signalling muscles.

Neither fats nor cholesterol are soluble in water, so have to be packaged into lipoprotein particles in order to be transported in the bloodstream between various tissues. As mentioned earlier, there are different classes of lipoprotein particles, which differ in their size, density, and composition of fat and cholesterol. Different lipoprotein particles also transport fat and cholesterol to different locations / tissues.

For example, chylomicrons are very large particles that mainly transport fat (in the form of triglycerides) from the intestines to peripheral tissues such as skeletal muscle and adipose tissue.

Low-density lipoproteins (LDL), as their name suggests, are lipoprotein particles that have a low density and transport cholesterol to peripheral tissues, including skeletal muscle, adrenal glands, ovaries, and testes. Cholesterol in LDL particles can also be deposited into fatty plaques in the linings of arterial walls. The build-up of fatty, cholesterol-rich plaques that narrow arteries is known as atherosclerosis.  

Given its propensity to form atherosclerotic plaques, the cholesterol transported in LDL particles (called LDL-cholesterol or LDL-C) is sometimes known as ‘bad’ cholesterol. Similarly, we say that LDL particles are pro-atherogenic.

The cholesterol transported by lipoprotein (a) (Lp(a)) particles can also be deposited in arteries. Lp(a) particles are very similar in size and structure to LDL particles. They are both of low density and transport cholesterol in the bloodstream. Given the similarities in size and density between Lp(a) and LDL particles, the cholesterol carried in Lp(a) particles is typically grouped under the banner of LDL-cholesterol. Blood tests that measure LDL-cholesterol levels, for example, typically includes both cholesterol carried in LDL and Lp(a) particles.

One key difference between LDL and Lp(a), however, is that Lp(a) particles have an additional apolipoprotein molecule on their surface. As discussed in the Blood fat level (APOA5) trait articles, apolipoproteins are molecules on the surface of lipoprotein particles that add structural support and guide the movement and metabolism of lipoproteins and their contents.

As shown in the diagram below, Lp(a) particles have an additional apolipoprotein (a) molecule attached to the apolipoprotein-B surface molecule.

This additional apolipoprotein (a) molecule makes Lp(a) particles more prone to deposit cholesterol into fatty arterial (atherosclerotic) plaques. Lp(a) particles are therefore more pro-atherogenic than LDL particles.  In line with this, as we’ll explain in the next section, high Lp(a) levels can cause the build-up of fatty plaques in blood vessels supplying the heart, causing heart disease.  

KEY POINTS

• Lipoprotein (a) (Lp(a)) is a particle that transports cholesterol in the bloodstream.
• Cholesterol transported in Lp(a) particles may be deposited into fatty plaques in arterial linings, causing atherosclerosis.
• Lp(a) particles are similar to LDL (Low-density lipoprotein) particles.

Why are high lipoprotein (a) levels bad for health?

High Lp(a) levels have been causally linked to a higher risk of atherosclerotic cardiovascular disease (ASCVD).

What is ASCVD?

As described in the previous section, atherosclerosis refers to the build-up of fatty, cholesterol rich plaques in the walls of arteries, causing them to become narrowed and blocked.

Atherosclerotic cardiovascular disease (ASCVD) is an umbrella term for the development atherosclerosis in different parts of the cardiovascular system, and includes coronary heart disease, stroke, and peripheral arterial disease.

Coronary heart disease (CHD)

Atherosclerotic plaques can build up in the blood vessels that supply the heart, known as the coronary arteries. When the coronary arteries become narrowed and blocked by atherosclerotic plaques, impairing blood flow to the heart, it is referred to as coronary heart disease (CHD).

In many cases, atherosclerotic plaques in the coronary arteries may rupture and form blood clots, which can completely cut off blood (and therefore oxygen) supply to the heart muscle. This is what happens in a heart attack or myocardial infarction.

Stroke

Atherosclerosis can also occur in blood vessels supplying the brain. As with coronary artery disease and myocardial infarction, atherosclerotic plaques in blood vessels supplying the brain can rupture and form blood clots that completely block off blood flow. Consequently, parts of brain tissue become starved of oxygen and get damaged or die. This is what happens in an ischaemic stroke.

Peripheral arterial disease

Peripheral arteries are those blood vessels that carry blood away from the heart to other parts of the body e.g. our limbs. Atherosclerotic plaques can build-up in these arteries, most commonly in those supplying the legs and feet, thereby restricting blood flow to these areas. This is what happens in peripheral arterial disease.

Patients with peripheral arterial disease may complain of pain that occurs when walking but goes away with rest (termed ‘intermittent claudication’). This is because the atherosclerotic plaques block arteries supplying leg muscles and prevent adequate blood flow to exercising muscles.

Lp(a) levels and atherosclerotic cardiovascular disease (ASCVD)

Several studies have shown that higher Lp(a) levels are associated with a higher risk of ASCVD.

In one large prospective study, 460,506 subjects enrolled in the UK Biobank database had their blood Lp(a) levels measured and then were followed up for an average of 11.2 years to observe whether subjects developed an ASCVD event (e.g. a heart attack, coronary artery bypass surgery, an ischaemic stroke).

As shown in the graph below, there was a linear relationship between Lp(a) level and risk of an ASCVD event. The researchers found that every 50 nmol/L increase in Lp(a) level was associated with an 11% increase in risk of ASCVD event. This figure was similar across White, Black and South Asian subject groups.

Source: Patel, A. P., Wang, M., Pirruccello, J. P., Ellinor, P. T., Ng, K., Kathiresan, S., & Khera, A. V. (2021). Lp (a)(lipoprotein [a]) concentrations and incident atherosclerotic cardiovascular disease: new insights from a large national biobank. Arteriosclerosis, Thrombosis, and Vascular Biology, 41(1), 465-474.

The researchers also examined the effect of having ‘high’ Lp(a) levels – defined as an Lp(a) concentration greater than or equal to 150 nmol/L.

(To put these numbers in context, it’s worth noting that Lp(a) levels vary considerably in the human population – varying more than 1,000-fold between individuals. As shown in the left-hand graph below, the distribution of Lp(a) levels in the UK Biobank study had a positive skew: meaning more people tended to have lower Lp(a) levels. The median Lp(a) level for this cohort was 19.6 nmol/L).

Analysing subjects who did not have any ASCVD at baseline, those who had high Lp(a) levels (≥150 nmol/L) had a 50% higher risk of going on to have an ASCVD event. Broken down by individual diseases, this included a 63% higher risk of coronary artery disease and a 16% higher risk of ischaemic stroke.

As illustrated by the steeper gradient of red line in the right-hand graph below, those with high Lp(a) levels at baseline went on to develop more ASCVD events over the follow-up period

Crunching the numbers, the researchers found that individuals with high Lp(a) levels had a 4.2% cumulative 10-year risk of an ASCVD event. This cumulative risk was significantly greater than those with a lower (i.e. < 150 nmol/L) Lp(a) levels (2.8%).  

Source: Patel, A. P., Wang, M., Pirruccello, J. P., Ellinor, P. T., Ng, K., Kathiresan, S., & Khera, A. V. (2021). Lp (a)(lipoprotein [a]) concentrations and incident atherosclerotic cardiovascular disease: new insights from a large national biobank. Arteriosclerosis, Thrombosis, and Vascular Biology, 41(1), 465-474.

The relationship between Lp(a) levels and ASCVD risk is due to the pro-atherogenic properties of Lp(a) particles. As discussed previously, Lp(a) particles transport cholesterol in the bloodstream and can deposit cholesterol into arterial linings, causing the build-up of fatty, cholesterol-rich, atherosclerotic plaques. Higher Lp(a) levels, or, more accurately, greater amounts of cholesterol circulating in Lp(a) particles, therefore promote greater deposition of cholesterol into atherosclerotic plaques, driving atherosclerotic cardiovascular disease (ASCVD).

KEY POINTS

• Lp(a) particles are pro-atherogenic - they cause atherosclerosis, which can block blood vessels.
• Higher Lp(a) levels are linked to an increased risk of atherosclerotic cardiovascular disease (ASCVD).
• Atherosclerotic cardiovascular disease (ASCVD) includes coronary heart disease, heart attack, stroke, and peripheral vascular disease.
• There is a linear relationship between Lp(a) levels and ASCVD risk.

What are “healthy” lipoprotein (a) levels?

As explained in the preceding section, there appears to be a linear relationship between lipoprotein (a) (Lp(a)) levels and risk of atherosclerotic cardiovascular disease (ASCVD).

Furthermore, Lp(a) levels vary more than 1,000 fold in the general population, ranging from less than 0.1 mg/dL (0.2 nmol/L) to more than 200mg/dL (432 nmol/L). Accordingly, there is no clear-cut border between “healthy” and “unhealthy” Lp(a) levels.

Generally speaking, in terms of cardiovascular risk, the lower the Lp(a) level, the healthier. A consensus statement from the European Atherosclerosis Society suggested that a desirable Lp(a) level is < 50 mg/dL (105 nmol/L).

Several other cardiologists recommend a healthy Lp(a) level of < 30 mg/dL (62 nmol/L).  

An Lp(a) level of < 10 mg/dL (18 nmol/L) has been considered to be low cardiovascular risk by many US lipidologists.

Despite these figures, it is worth pointing out that studies suggest it is very difficult to target and reduce Lp(a) levels directly. Dietary changes and cholesterol-lowering drugs such as statins do not seem to have much effect on Lp(a) levels.

There is some evidence that a procedure known as apheresis – which involves passing blood through a specialised machine to filter out lipoprotein particles – can lower Lp(a) levels. Treatment with niacin has also been shown to reduce Lp(a) levels by between 25-30%. Both of these treatments, however, also reduce levels of LDL particles. The beneficial effects of these treatments on cardiovascular risk may therefore be also explained by reductions in LDL-cholesterol.

KEY POINTS

• Lower Lp(a) levels confer a lower risk of cardiovascular disease.
• Opinions vary on what is a healthy Lp(a) level.
• An Lp(a) level of less than 10 mg/dL (18 nmol/L) is widely considered to be low cardiovascular risk.
• Lp(a) levels are difficult to reduce specifcally with diet, exercise, and statins.

What is the LPA gene?

The LPA gene encodes apolipoprotein (a), one of the surface molecules on lipoprotein (a) (Lp(a)) particles.

This gene is interesting because it plays a significant role in controlling Lp(a) levels. Studies suggest that Lp(a) levels are strictly regulated by the LPA gene and are not largely influenced by lifestyle factors such as diet and exercise.

On this note, it has been estimated that between 75-90% of differences in Lp(a) levels are attributable to genetic factors. Of this variance, around 73% is due to the LPA gene specifically.

As we’ll explore in the following sections, the variants of the LPA gene that we inherit can affect our Lp(a) levels and our risk of atherosclerotic cardiovascular disease (ASCVD) such as coronary heart disease.

KEY POINTS

• The LPA gene encodes a surface molecule (apolipoprotein (a)) on Lp(a) particles.
• LPA gene variants have a strong effect on Lp(a) levels in the bloodstream.

How do LPA gene variants affect lipoprotein (a) levels?

Different variants of the LPA gene strongly affect circulating levels of lipoprotein (a) (Lp(a)).

Of genetic variations within the LPA gene known to affect Lp(a) levels, the Kringle IV (KIV) repeat polymorphism is likely to be the most important. This polymorphism causes changes in the number of a specific DNA sequence (called KIV-2) in the LPA gene, which in turn alters the size of the apolipoprotein (a) surface molecule produced on the surface of Lp(a) particles.

Source: Kronenberg, F. (2016). Human genetics and the causal role of lipoprotein (a) for various diseases. Cardiovascular drugs and therapy, 30(1), 87-100.

LPA variants with more KIV-2 repeats code for a larger, or higher molecular weight, apolipoprotein (a) molecule. This is linked to lower Lp(a) levels, as shown by the blue bars on the chart below.

By contrast, LPA gene variants with fewer KIV-2 repeats code for smaller, or lower molecular weight, apolipoprotein (a) molecules. People with these variants have higher Lp(a) levels, as shown by the red bars in the chart below.

Source: Kronenberg, F. (2016). Human genetics and the causal role of lipoprotein (a) for various diseases. Cardiovascular drugs and therapy, 30(1), 87-100.

Interestingly, people with the same number of KIV-2 repeats still show widely different Lp(a) levels, suggesting the role of other genetic factors in the control of Lp(a) levels. On this note, two SNPs (Single Nucleotide Polymorphisms) within the LPA gene have been linked to higher Lp(a) levels: rs10455872 and rs3798220.

Your FitnessGenes LPA and Heart Health trait focusses on these two SNPs.

- Rs10455872

This SNP causes an A --> G change in the LPA DNA sequence, giving rise to two LPA gene variants or ‘alleles’: the ‘A’ allele and the ‘G’ allele.

Several studies have shown that people who carry the ‘G’ allele (i.e. those with AG and GG genotypes) have significantly higher Lp(a) levels. For example, a study of Old Order Amish subjects found that ‘G’ allele carriers had 1.73 times higher Lp(a) levels compared to age and ex-matched non-carriers. This is shown in the scatter plot below ('G' allele carriers are those with the AG genotype).

Source: Wang, H., Hong, C. E., Lewis, J. P., Zhu, Y., Wang, X., Chu, X., ... & Fu, M. (2016). Effect of two lipoprotein (a)-associated genetic variants on plasminogen levels and fibrinolysis. G3: Genes, Genomes, Genetics, 6(11), 3525-3532.

- Rs3798220

This SNP causes a T --> C change in the LPA DNA sequence, giving rise to two LPA gene variants or ‘alleles’: the ‘T’ allele and the ‘C’ allele.

‘C’ allele carriers have been found to have significantly higher Lp(a) levels. In the aforementioned study of Amish subjects, researchers found that Lp(a) levels were 2.62 times higher in ‘C’ allele carriers compared to non-carriers. This is illustrated in the scatter plot below ('C' allele carriers are those with the CT genotype).

Another study of people with Eastern European, Northern European or Caucasian other ancestry reported that 'C' allele carriers had 5-7 times higher median Lp(a) levels compared to non-carriers.

Source: Wang, H., Hong, C. E., Lewis, J. P., Zhu, Y., Wang, X., Chu, X., ... & Fu, M. (2016). Effect of two lipoprotein (a)-associated genetic variants on plasminogen levels and fibrinolysis. G3: Genes, Genomes, Genetics, 6(11), 3525-3532.

It is not fully understood how the rs10455872 and rs3798220 SNPs bring about an increase in Lp(a) levels. Some studies suggest that neither of the SNPs alter the number of Kringle IV repeats and size of the apolipoprotein (a) surface molecule attached to Lp(a) particles.

Other studies, however, suggest that both SNPs do indeed alter the number of KIV repeats and are linked to smaller, more pro-atherogenic Lp(a) particles. Outside of this debate, there is some evidence that the rs10455872 SNP enhances LPA gene expression, which may elevate Lp(a) levels.

KEY POINTS

• LPA gene variants can affect the size of Lp(a) particles. Smaller particles are associated with higher Lp(a) levels.
• Your LPA and Heart Health trait looks at SNPs in the LPA gene: rs10455872 and rs3798220.
• The 'G' risk allele created by the rs10455872 SNP is linked to higher Lp(a) levels.
• The 'C' risk allele created by the rs3798220 SNP is also linked to higher Lp(a) levels.

How do LPA variants affect risk of coronary heart disease?

To recap what we’ve learned so far:

• Lp(a) is a pro-atherogenic particle that deposits cholesterol into fatty plaques in arterial walls.

• higher Lp(a) levels are linked to a higher risk of atherosclerotic cardiovascular disease (ASCVD), including coronary heart disease.

• Certain LPA gene variants (e.g. the ‘G’ (rs10455872) and ‘C’ (rs3798220) alleles) are independently linked to higher Lp(a) levels.

Putting these observations together, we may expect LPA gene variants associated with higher Lp(a) levels to also increase the risk of ASCVD. This is exactly what studies have found.

One large study, known as the PROCARDIS (Precocious Coronary Artery Disease) study, compared the LPA genotypes of European subjects with a diagnosis of coronary artery disease before the age of 66, to those of healthy control subjects.

An analysis of this cohort and other replication cohorts, found that carrying the rs10455872 risk allele was associated with a 47% higher risk of coronary artery disease. The rs3798220 risk allele was linked to a 68% higher risk of coronary artery disease. Both of these findings are illustrated in the right-hand Forest plot below.

Source: Clarke, R., Peden, J. F., Hopewell, J. C., Kyriakou, T., Goel, A., Heath, S. C., ... & Farrall, M. (2009). Genetic variants associated with Lp (a) lipoprotein level and coronary disease. New England Journal of Medicine, 361(26), 2518-2528.

Other studies have reported similar findings with these LPA variants. A 2011 meta-analysis combined the results of several of these studies, which largely involved Caucasian subjects. After restricting their analysis to studies that did not involve substantial use of aspirin, the ‘C’ allele (rs3798220) was associated with a 69% greater risk of coronary heart disease. Similarly, the ‘G’ allele (rs10455872) was linked to a 42% higher risk of coronary heart disease.

It’s worth noting that the two different LPA SNPs (rs10455872 and rs3798220) are each independently linked to higher Lp(a) levels and greater risk of coronary heart disease. The SNPs are not in strong linkage disequilibrium, meaning they are not non-randomly coinherited together

Some people, of course, will carry both SNPs. Such carriers of both the ‘G’ (rs10455872) and ‘C’ (rs3798220) alleles are shown to have a higher risk of coronary heart disease compared to carriers of only one risk allele.

Source: Clarke, R., Peden, J. F., Hopewell, J. C., Kyriakou, T., Goel, A., Heath, S. C., ... & Farrall, M. (2009). Genetic variants associated with Lp (a) lipoprotein level and coronary disease. New England Journal of Medicine, 361(26), 2518-2528.

For example, in the PROCARDIS study cohort, carriers of two variant alleles had a 4.87-times higher risk of coronary artery disease. This is illustrated in the graph above. When the analysis was extended to include other cohorts, carriers of two or more variant alleles had a 2.57-times higher risk.

KEY POINTS

• The 'G' risk allele (rs10455872) is associated with a higher risk (42% higher according to one meta-analysis) of coronary heart disease.
• The 'C' risk allele (rs3798220) is associated with a higher risk (69% higher according to one meta-analysis) of coronary heart disease.
• Carrying both the 'G' and 'C' risk alleles confers an even higher (2.57 times higher risk according to one meta-analsysi) of coronary heart disease than carrying just one risk allele.

How do LPA variants affect response to aspirin?

Aspirin, also known as acetylsalicylic acid, is a common drug that is often used for its ‘antiplatelet effects’. Platelets are small cell fragments in the blood that are responsible for forming blood clots and preventing bleeding.

You may have heard of aspirin described as a “blood-thinning” medication. In reality, aspirin acts to reduce the stickiness of platelets, thereby preventing the formation of blood clots. As you will recall from previously, atherosclerotic plaques can rupture and form blood clots, thereby blocking off blood supply to organs such as the heart and brain.

For this reason, low dose aspirin (e.g. 75 mg per day) is often used in the prevention of atherosclerotic cardiovascular disease (ASCVD), such as coronary heart disease, myocardial infarction (heart attack), ischaemic stroke, and peripheral arterial disease.

Studies suggest, however, that LPA gene variants can affect the therapeutic effect of aspirin. Specifically, compared to non-carriers, people who carry the ‘C’ allele (rs3798220) are shown to have greater reductions in risk of cardiovascular events (e.g. heart attacks) when taking aspirin.

In the Women’s Health Study, 25,131 Caucasian women were given either aspirin or a placebo and then followed over 9.9 years. The researchers recorded whether the women suffered from a major cardiovascular event, which included myocardial infarction (heart attack), ischaemic stoke, or cardiovascular death.

In line with previously described studies, carriers of the ‘C’ allele (rs3798220) had higher Lp(a) levels and a greater (about 2.2 times higher) risk of major cardiovascular events. When these carriers took aspirin, however, they had a significantly greater risk reduction compared to non-carriers.

In non-carriers of the ‘C’ allele (rs3798220), those in the placebo and aspirin groups had an absolute risk of major cardiovascular event over 9.9 years of 2.25% and 2.13%, respectively. Therefore, taking aspirin was not associated with a large  

By contrast, among ‘C’ allele carriers, those in the placebo and aspirin groups, had an absolute risk of 4.83% and 2.14%, respectively. This represents a 56% reduction in relative risk of major cardiovascular event from taking aspirin.

Source: Li, Y., Luke, M. M., Shiffman, D., & Devlin, J. J. (2011). Genetic variants in the apolipoprotein (a) gene and coronary heart disease. Circulation: Cardiovascular Genetics, 4(5), 565-573.

The Kaplan-Meier graph above shows the differences in the cumulative fraction of subjects with a major cardiovascular event over the 9.9 years according to genotype and treatment status. As you can see by comparing the blue and red lines, carriers (blue line) had a much greater reduction in cardiovascular events when taking asprin (dotted blue) compared to placebo (solid blue).

The underlying reason that ‘C’ allele carriers respond better to aspirin remains to be fully explained. Lp(a) particles play a direct role in the formation of blood clots around atherosclerotic plaques. It is possible that aspirin also reduces the expression of apolipoprotein (a), one of the surface molecules on Lp(a) particles that gives them their pro-atherogenic properties.

KEY POINTS

• Aspirin is a drug that inhibits the formation of blood clots and is used in the prevention of cardiovascular disease.
• People who carry the 'C' allele (rs3798220) of the LPA gene show a greater reduction in risk of cardiovascular disease when taking aspirin.

How do LPA variants affect response to statins?

Statins are drugs used to lower LDL-cholesterol levels. As explained previously, cholesterol carried in low density lipoprotein (LDL) particles can be deposited in arterial linings forming fatty, atherosclerotic plaques. This can cause atherosclerotic cardiovascular disease (ASCVD).

Statins are therefore often prescribed for the prevention of ASCVD. They work by blocking an enzyme called HMG-CoA-reductase, which is responsible for producing cholesterol in the liver. Blocking liver production of cholesterol means less is packaged into LDL particles to circulate in the bloodstream.

Furthermore, the liver compensates for reduced cholesterol production by removing and taking up LDL particles from the bloodstream and using the packaged cholesterol. The combination of both these effects leads to a reduction in LDL-cholesterol levels in response to treatment with statins.

This cholesterol-lowering effect of statins, however, is shown to be influenced by LPA gene variants. In response to statin, carriers of the ‘G’ allele (rs10455872) have been found to have poorer reductions in LDL-cholesterol levels and smaller reductions in risk of coronary heart disease.

A meta-analysis of over 10,000 subjects found that statin treatment effected an average of a 1.98 mmol/L absolute reduction in LDL-cholesterol levels. (To put this figure in context, a healthy LDL cholesterol level is considered to be below 3 mmol/L).

Carriers of the ‘G’ allele, however, had a 0.1mmol/L higher-on-treatment LDL-cholesterol level (per allele). This poorer cholesterol-lowering response is illustrated in the Forest plot below.

Source: Donnelly, L. A., van Zuydam, N. R., Zhou, K., Tavendale, R., Carr, F., Maitland-van der Zee, A. H., ... & Palmer, C. N. (2013). Robust association of the LPA locus with LDLc lowering response to statin treatment in a meta-analysis of 30,467 individuals from both randomised control trials and observational studies and association with coronary artery disease outcome during statin treatment. Pharmacogenetics and genomics, 23(10), 518.

Even after adjusting for the poorer reduction LDL-cholesterol levels, however, the researchers found that the ‘G’ allele was associated with only a 2% reduction in risk of coronary heart disease with statin treatment.

This suggests that, as well as having a poorer cholesterol-lowering response to statins, ‘G’ allele carriers have an increased cardiovascular disease risk that is largely independent of LDL-cholesterol levels.

KEY POINTS

• Statins are drugs used to lower levels of LDL-cholesterol.
• People who carry the 'G' allele (rs10455872) of the LPA gene are shown to have poorer reductions in LDL-cholesterol levels when taking statins.
• 'G' allele carriers also show poorer reductions in cardiovascular disease risk when taking statins.

Your LPA and heart health trait

Your LPA and heart health trait looks at two key SNPs in the LPA gene: rs10455872 and rs3798220. These create the ‘G’ and ‘C’ risk alleles, respectively, which are both independently linked to higher Lp(a) levels and higher risk of coronary heart disease.

Depending on your DNA results, you will be classified into one of three groups:

• Increased cardiovascular disease risk: you carry both SNPs/risk alleles associated with higher Lp(a) levels and increased risk of coronary heart disease (and other atherosclerotic cardiovascular diseases).

• Moderately increased cardiovascular disease risk: you carry one of the SNPs/risk alleles linked to higher Lp(a) levels and increased risk of coronary heart disease (and other ASCVD). Your cardiovascular disease risk will not be as high as those in the “increased” band above.

• Average cardiovascular disease risk: you do not carry either of the SNPs/risk alleles linked to higher Lp(a) levels and cardiovascular disease risk.

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