Understanding Lipoprotein(a) and Heart Health
Learn why Lipoprotein(a) matters for your heart health and how to monitor it.
Natalie Telis, Hang Dai, Ashley Waring, David Kann, Dana Wyman, Simon White, Basil Khuder, Francisco Tanudjaja, Alexandre Bolze, Matthew E. Levy, Cassie Hajek, Lisa M. McEwen, Douglas Stoller, Christopher N. Chapman, C. Anwar A. Chahal, Daniel P. Judge, Douglas A. Olson, Joseph J. Grzymski, Nicole L. Washington, William Lee, Elizabeth T. Cirulli, Shishi Luo, Kelly Schiabor Barrett
― 6 min read
Table of Contents
- Why Should You Care About Lp(a)?
- How is Lp(a) Made?
- What's Considered High Lp(a)?
- How is Lp(a) Tested?
- Why is it Hard to Measure Lp(a)?
- Genetics: The New Frontier
- The Research So Far
- What They Found
- Different Groups, Different Risks
- Lp(a) and Heart Disease: The Connection
- Who Gets Tested?
- What Can Be Done?
- The Future of Lp(a) Testing
- Conclusion: The Takeaway
- The Importance of Getting Checked
- How Can You Improve Your Heart Health?
- Living with Knowledge
- The Wrap-Up
- Original Source
Lipoprotein(a), or Lp(a) for short, is a type of fat particle in your blood that can cause problems for your heart. You can think of Lp(a) as a delivery truck that carries Cholesterol, but unfortunately, it has a tendency to get stuck in your arteries, leading to heart issues.
Why Should You Care About Lp(a)?
Many people have never heard of Lp(a), and that’s a problem. High levels of this lipoprotein are linked to a higher chance of heart-related problems, including heart attacks and strokes. Researchers found that about 20% of the population has high levels of Lp(a). So, if you’re part of that 20%, you might want to pay attention.
How is Lp(a) Made?
The level of Lp(a) in your blood mostly comes from your Genetics. It’s like getting your eye color from your parents; you don’t have much say in the matter. Some people have much higher levels than others, and that’s generally due to variations in a gene called LPA. This gene tells your body how much Lp(a) to produce.
What's Considered High Lp(a)?
When doctors talk about high Lp(a) levels, they usually mean anything above 120 nanomoles per liter, or about 50 milligrams per deciliter. If you roll that number out at a party, you're likely to clear the room, but as boring as it may be, it’s crucial information because those with higher Lp(a) face a greater risk of Heart Disease.
How is Lp(a) Tested?
Unfortunately, doctors don’t often check for Lp(a) in routine blood tests. This is a bit surprising, given its importance. You’re more likely to get tested for cholesterol levels, which is like checking to see if your roof is leaking without considering whether the foundation is solid.
Why is it Hard to Measure Lp(a)?
Measuring Lp(a) levels accurately can be tricky. It’s not just about taking a blood sample; it’s also about the size of the Lp(a) particles, which varies between individuals. The current lab tests can struggle with this due to the complex nature of Lp(a).
Genetics: The New Frontier
Since Lp(a) levels are largely influenced by genes, researchers are exploring ways to estimate these levels through genetic testing. This is like getting a sneak peek into your future heart health based on your family tree. They are eager to make this genetic estimation a more practical option that could one day replace blood tests.
The Research So Far
Scientists have looked into various ways to measure Lp(a) and assess risk. They found that combining two specific genetic measures can give a clearer picture of your Lp(a) levels. Think of it as using both a map and a GPS to find your way instead of relying on just one.
What They Found
In a large study that included over 76,000 people, researchers found that looking at both genetic factors helped them predict who might have high Lp(a) levels. It's like figuring out who is likely to be late to a party based on how often they show up late to other events.
Different Groups, Different Risks
The research pointed out interesting differences between people of different backgrounds. For those whose ancestry is primarily European, genetic prediction tools worked well. However, for others, the tools weren’t as effective. This shows that we need to be careful and ensure that genetics works fairly for everyone.
Lp(a) and Heart Disease: The Connection
High Lp(a) levels aren't just numbers; they translate into real health risks. The study showed that people with higher genetic risk of high Lp(a) were more likely to develop heart conditions. This is like having a cloud of bad luck following you; the more Lp(a) you have, the more likely you are to face heart problems down the line.
Who Gets Tested?
Currently, only a small fraction of patients get their Lp(a) tested during routine check-ups. This is puzzling since many have their cholesterol checked regularly. Ignoring Lp(a) is like ignoring a potential elephant in the room; it’s there, and it might be causing trouble.
What Can Be Done?
There are a few options for treating high Lp(a), but they aren't as straightforward as popping a pill. While some medicines can help reduce Lp(a) levels, they usually don’t target it directly. Researchers are looking into new treatments, but we are still waiting for them to hit the market.
The Future of Lp(a) Testing
As we move toward genetic testing becoming a routine part of medical care, understanding Lp(a) will become even more accessible. Imagine a world where simply knowing your genetic risk could guide your heart health decisions, like having a medical crystal ball.
Conclusion: The Takeaway
In a nutshell, Lp(a) is a significant player in the game of heart health. While genetics primarily controls your Lp(a) levels, being aware of this measurement is essential. The next time you get a chance to discuss your heart health with your doctor, don’t forget to ask about Lp(a). It just might be the key to a healthier future!
The Importance of Getting Checked
Don’t let Lp(a) catch you off guard. Since most people don’t think about it, awareness can go a long way. If you have a family history of heart disease, it’s worth checking into. Consider it another layer of protection for your heart!
How Can You Improve Your Heart Health?
Even if you find out that your Lp(a) levels are high, there are still things you can do. Eating a balanced diet, staying active, and keeping stress levels low are great starting points. These healthy choices can help manage other risk factors that contribute to heart disease.
Living with Knowledge
Armed with knowledge about Lp(a), you can take proactive steps for your heart health. This means being more informed about your body and understanding how your genetics play a role. After all, knowledge is power, and in this case, it might even save your life.
The Wrap-Up
In closing, Lp(a) might not be as well-known as cholesterol, but it plays a crucial role in heart disease risk. Don’t hesitate to talk to your doctor about Lp(a) and how it may apply to your health. The more you know, the better prepared you’ll be to take care of your heart!
Title: A novel method for predicting Lp(a) levels from routine outpatient genomic testing identifies those at risk of cardiovascular disease across a diverse cohort
Abstract: BackgroundLipoprotein(a) (Lp(a)) levels are a largely genetically determined and often an unmeasured predictor of future Atherosclerotic Cardiovascular Disease (ASCVD). With the increased use of exome sequencing in the clinical setting, there is opportunity to identify patients who have a high chance of having elevated Lp(a) and are therefore at risk of ASCVD. However, accurate genetic predictors of Lp(a) are challenging to design. In addition to single nucleotide variants (SNVs), which are often summarized as a combined genetic risk score, Lp(a) levels are significantly impacted by copy number variation in repeats of the kringle IV subtype 2 domain (KIV-2), which are challenging to quantify. KIV-2 copy numbers are highly variable across populations, and understanding their impact on Lp(a) levels is important to creating an equitable and reliable genetic predictor of Lp(a)-driven cardiovascular risk for all individuals. MethodsWe develop a novel method to quantify individuals total number of KIV-2 repeats from exome data, validate this quantification against measured Lp(a) levels, and then use this method, combined with a SNV-based genetic risk score, to genotype an entire all-comers cohort of individuals from health systems across the United States (Helix Research Network; N = 76,147) for an estimated Lp(a) level. ResultsOur combined genotyping strategy improved prediction of those with clinically-elevated Lp(a) measurements across the genetically diverse cohort, especially for individuals not genetically similar to European reference populations, where GRS-based estimates fall short (r2= 0.04 for GRS, r2 = 0.34 KIV2+GRS in non-European). Importantly, high combined genetic risk of high Lp(a) genotypes are significantly associated with earlier onset and increased incidence in ASCVD, compared to average and low combined genetic risk genotypes in a retrospective analysis of atherosclerotic diagnoses derived from electronic health records (EHRs). This holds in the cohort at large (CAD HRs=1.29, 1.58), in the European subcohort (HRs=1.30,1.61) as well as at trending levels of significance in individuals not genetically similar to Europeans (HRs=1.22,1.31). In addition, high combined genetic risk for high Lp(a) genotypes are at least 2-fold enriched amongst individuals with ASCVD diagnosis despite a lack of EHR-based evidence of traditional risk factors for cardiovascular disease. ConclusionsOur study demonstrates that genetically predicted Lp(a) levels, incorporating both SNV and our novel KIV-2 repeat estimate, may be a practical method to predict clinically elevated Lp(a). Supporting this, individuals with high combined genetic risk for high Lp(a) have an increased risk for ASCVD, as evidenced across data from seven US-based health systems.
Authors: Natalie Telis, Hang Dai, Ashley Waring, David Kann, Dana Wyman, Simon White, Basil Khuder, Francisco Tanudjaja, Alexandre Bolze, Matthew E. Levy, Cassie Hajek, Lisa M. McEwen, Douglas Stoller, Christopher N. Chapman, C. Anwar A. Chahal, Daniel P. Judge, Douglas A. Olson, Joseph J. Grzymski, Nicole L. Washington, William Lee, Elizabeth T. Cirulli, Shishi Luo, Kelly Schiabor Barrett
Last Update: 2024-11-04 00:00:00
Language: English
Source URL: https://www.medrxiv.org/content/10.1101/2024.11.01.24316526
Source PDF: https://www.medrxiv.org/content/10.1101/2024.11.01.24316526.full.pdf
Licence: https://creativecommons.org/licenses/by-nc/4.0/
Changes: This summary was created with assistance from AI and may have inaccuracies. For accurate information, please refer to the original source documents linked here.
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